subject:(NLR Family Pyrin Domain Containing 3 Protein)

1. 山本, 梓司. Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果.

Degree: 博士(医学), 2018, Saitama Medical University / 埼玉医科大学

URL: http://id.nii.ac.jp/1386/00000615/

►

Multiple sclerosis is a neuroinflammatory demyelinating and neurodegenerative disease of the central nervous system characterized by recurrent and progressive demyelination/remyelination cycles, neuroinflammation, oligodendrocyte loss, demyelination,… (more)

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Multiple sclerosis is a neuroinflammatory demyelinating and neurodegenerative disease of the central nervous system characterized by recurrent and progressive demyelination/remyelination cycles, neuroinflammation, oligodendrocyte loss, demyelination, and axonal degeneration. Cyclic phosphatidic acid (cPA) is a natural phospholipid mediator with a unique cyclic phosphate ring structure at the sn-2 and sn-3 positions of the glycerol backbone. We reported earlier that cPA elicits a neurotrophin-like action and protects hippocampal neurons from ischemia-induced delayed neuronal death. We designed, chemically synthesized, and metabolically stabilized derivatives of cPA: 2-carba-cPA (2ccPA), a synthesized compound in which one of the phosphate oxygen molecules is replaced with a methylene group at the sn-2 position. In the present study, we investigated whether 2ccPA exerts protective effects in oligodendrocytes and suppresses pathology in the two most common mouse models of multiple sclerosis.

To evaluate whether 2ccPA has potential beneficial effects on the pathology of multiple sclerosis, we investigated the effects of 2ccPA on oligodendrocyte cell death in vitro and administrated 2ccPA to mouse models of experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced demyelination.

We demonstrated that 2ccPA suppressed the CoCl

-induced increase in the Bax/Bcl-2 protein expression ratio and phosphorylation levels of p38MAPK and JNK protein. 2ccPA treatment reduced cuprizone-induced demyelination, microglial activation, NLRP3 inflammasome, and motor dysfunction. Furthermore, 2ccPA treatment reduced autoreactive T cells and macrophages, spinal cord injury, and pathological scores in EAE, the autoimmune multiple sclerosis mouse model.

We demonstrated that 2ccPA protected oligodendrocytes via suppression of the mitochondrial apoptosis pathway. Also, we found beneficial effects of 2ccPA in the multiperiod of cuprizone-induced demyelination and the pathology of EAE. These data indicate that 2ccPA may be a promising compound for the development of new drugs to treat demyelinating disease and ameliorate the symptoms of multiple sclerosis.

平成29年度

Subjects/Keywords: Animals; Anti-Inflammatory Agents; Apoptosis; Cell Differentiation; Cell Line, Transformed; Cuprizone; Demyelinating Diseases; Disease Models, Animal; Female; Gene Expression Regulation; Humans; MAP Kinase Signaling System; Male; Mice; Mice, Inbred C57BL; Monoamine Oxidase Inhibitors; Myelin Sheath; NLR Family, Pyrin Domain-Containing 3 Protein; Phosphatidic Acids; Proto-Oncogene Proteins c-bcl-2; p38 Mitogen-Activated Protein Kinases

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

山本, �. (2018). Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果. (Thesis). Saitama Medical University / 埼玉医科大学. Retrieved from http://id.nii.ac.jp/1386/00000615/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

山本, 梓司. “Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果.” 2018. Thesis, Saitama Medical University / 埼玉医科大学. Accessed February 28, 2021. http://id.nii.ac.jp/1386/00000615/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

山本, 梓司. “Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果.” 2018. Web. 28 Feb 2021.

Vancouver:

山本 �. Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果. [Internet] [Thesis]. Saitama Medical University / 埼玉医科大学; 2018. [cited 2021 Feb 28]. Available from: http://id.nii.ac.jp/1386/00000615/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

山本 �. Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果. [Thesis]. Saitama Medical University / 埼玉医科大学; 2018. Available from: http://id.nii.ac.jp/1386/00000615/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas A&M University

2. Akoolo, Lavoisier. Role of Brucella Toll/Interleukin-1 Receptor (TIR) Domain Containing Protein (∆TcpB) Deletion Mutant in Protective Immunity against Brucellosis.

Degree: PhD, Veterinary Microbiology, 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/155602

► Brucellosis is an important zoonotic disease affecting about 500,000 people annually. The development of safer and more efficacious Brucella Live attenuated vaccines addresses safety concerns… (more)

▼ Brucellosis is an important zoonotic disease affecting about 500,000 people annually. The development of safer and more efficacious Brucella Live attenuated vaccines addresses safety concerns that include the identification of reproducible and reliable surrogates of protection and mechanisms to bolster longevity. Brucella encodes a toll interleukin receptor domain containing protein (TcpB/Btp-1). These proteins subvert host innate immunity by abrogating NF-κB mediated cytokine production, by binding to and/or causing the degradation of signaling molecules TIRAP (MAL) and MyD88. TcpB has also been shown to directly reduce the CTL killing activity of infected host cells. In the current study, we investigated the effect of deleting tcpB from Brucella on invitro and invivo immune responses. We also evaluated an in vitro murine Brucella growth inhibition co-culture assay to determine the capacity of immune splenocytes from mice exposed to the tcpB mutant or wild type to control the growth of Brucella melitensis in murine bone marrow derived macrophages. A tcpB knockout constructed by gene replacement in the Brucella abortus S19 genetic background was used to vaccinate C57BL/6 mice assessed for development of CD4+ memory T cells. Mice vaccinated with the mutant displayed an elevated Th1 response, compared to the parental S19 and non- vaccinated controls, as manifested by multiple factors. These include; elevated IFN-γ early post vaccination, and a significant elevation of memory CD4+CD44+CD62L+ within CD4+T cell population in splenocytes derived from mice vaccinated with the mutant. S19 and S19ΔtcpB strains induced a significant increase in the IgG2a levels post vaccination. Consistent with a shift to a Th1 response, S19ΔtcpB induced a higher response later in vaccination. Splenocytes obtained from mice vaccinated with the S19ΔtcpB mutant exhibited significantly higher levels of killing activity compared to cells derived from S19 vaccinated mice and PBS controls. Consistent with enhanced immune protection, fewer bacteria were recovered from the spleens of mice vaccinated with the S19ΔtcpB mutant, which had reduced inflammatory lesions consistent with reduced bacterial burden. These results provide strong evidence that tcpB deletion improves immunogenicity, longevity and protective efficacy of S19 and that ex vivo co- cultivation may be employed to predict potential vaccine efficacy. Advisors/Committee Members: Ficht, Thomas A (advisor), Adams, Garry L (committee member), McMurray, David N (committee member), Zhu, Guan (committee member).

Subjects/Keywords: Brucella; Toll interleukin-1 receptor domain containing protein; Immunity; vaccine

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Akoolo, L. (2015). Role of Brucella Toll/Interleukin-1 Receptor (TIR) Domain Containing Protein (∆TcpB) Deletion Mutant in Protective Immunity against Brucellosis. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155602

Chicago Manual of Style (16^th Edition):

Akoolo, Lavoisier. “Role of Brucella Toll/Interleukin-1 Receptor (TIR) Domain Containing Protein (∆TcpB) Deletion Mutant in Protective Immunity against Brucellosis.” 2015. Doctoral Dissertation, Texas A&M University. Accessed February 28, 2021. http://hdl.handle.net/1969.1/155602.

MLA Handbook (7^th Edition):

Akoolo, Lavoisier. “Role of Brucella Toll/Interleukin-1 Receptor (TIR) Domain Containing Protein (∆TcpB) Deletion Mutant in Protective Immunity against Brucellosis.” 2015. Web. 28 Feb 2021.

Vancouver:

Akoolo L. Role of Brucella Toll/Interleukin-1 Receptor (TIR) Domain Containing Protein (∆TcpB) Deletion Mutant in Protective Immunity against Brucellosis. [Internet] [Doctoral dissertation]. Texas A&M University; 2015. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1969.1/155602.

Council of Science Editors:

Akoolo L. Role of Brucella Toll/Interleukin-1 Receptor (TIR) Domain Containing Protein (∆TcpB) Deletion Mutant in Protective Immunity against Brucellosis. [Doctoral Dissertation]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155602

Queensland University of Technology

3. Ashton, Nicholas W. Characterisation of human single-stranded DNA-binding protein 1 (hSSB1) regulation by post-translational modifications.

Degree: 2016, Queensland University of Technology

URL: https://eprints.qut.edu.au/98660/

► Human single-stranded DNA-binding protein 1 (hSSB1) is required for the timely repair of double-strand DNA breaks, as well as the stabilisation and restart of stalled… (more)

Subjects/Keywords: Human single-stranded DNA-binding protein 1; Nucleic acid-binding protein 2; OB-fold containing protein 2B; Sensor of single-stranded DNA complex subunit B; DNA-dependent protein kinase (DNA-PK); PPP-family protein phosphatases; Integrator complex subunit 3 (INTS3); hSSB1; NABP2; OBFC2B

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ashton, N. W. (2016). Characterisation of human single-stranded DNA-binding protein 1 (hSSB1) regulation by post-translational modifications. (Thesis). Queensland University of Technology. Retrieved from https://eprints.qut.edu.au/98660/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ashton, Nicholas W. “Characterisation of human single-stranded DNA-binding protein 1 (hSSB1) regulation by post-translational modifications.” 2016. Thesis, Queensland University of Technology. Accessed February 28, 2021. https://eprints.qut.edu.au/98660/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ashton, Nicholas W. “Characterisation of human single-stranded DNA-binding protein 1 (hSSB1) regulation by post-translational modifications.” 2016. Web. 28 Feb 2021.

Vancouver:

Ashton NW. Characterisation of human single-stranded DNA-binding protein 1 (hSSB1) regulation by post-translational modifications. [Internet] [Thesis]. Queensland University of Technology; 2016. [cited 2021 Feb 28]. Available from: https://eprints.qut.edu.au/98660/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ashton NW. Characterisation of human single-stranded DNA-binding protein 1 (hSSB1) regulation by post-translational modifications. [Thesis]. Queensland University of Technology; 2016. Available from: https://eprints.qut.edu.au/98660/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

NSYSU

4. Hsiao, Hsuan-Yi. Exercise protein irisin promotes angiogenesis in endothelial cells.

Degree: Master, Institute of Biomedical Sciences, 2014, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0805114-103028

► Myokinesis a critical cytokines in organism major secretes from muscle cells after doing exercise. Myokines involved in angiogenesis, tissue regenerate and repair, preserved normal functions… (more)

Subjects/Keywords: Angiogenesis; white adipose; brown adipose; FNDC5 (Fibronectin type III domain-containing protein 5); endothelial cells

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APA (6^th Edition):

Hsiao, H. (2014). Exercise protein irisin promotes angiogenesis in endothelial cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0805114-103028

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hsiao, Hsuan-Yi. “Exercise protein irisin promotes angiogenesis in endothelial cells.” 2014. Thesis, NSYSU. Accessed February 28, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0805114-103028.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hsiao, Hsuan-Yi. “Exercise protein irisin promotes angiogenesis in endothelial cells.” 2014. Web. 28 Feb 2021.

Vancouver:

Hsiao H. Exercise protein irisin promotes angiogenesis in endothelial cells. [Internet] [Thesis]. NSYSU; 2014. [cited 2021 Feb 28]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0805114-103028.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hsiao H. Exercise protein irisin promotes angiogenesis in endothelial cells. [Thesis]. NSYSU; 2014. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0805114-103028

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of the Western Cape

5. Phillips, Kyle. Characterization of the role of Zea mays burp domain-containing genes in maize drought responses .

Degree: 2016, University of the Western Cape

URL: http://hdl.handle.net/11394/5339

► Global climate change has resulted in altered rainfall patterns, causing annual losses in maize crop yield due to water deficit stress. Therefore, it is important… (more)

▼ Global climate change has resulted in altered rainfall patterns, causing annual losses in maize crop yield due to water deficit stress. Therefore, it is important to produce maize cultivars which are more drought-tolerant. This not an easily accomplished task as plants have a plethora of physical and biochemical adaptation methods. One such mechanism is the drought-induced expression of enzymatic and non-enzymatic proteins which assist plants to resist the effects of water deficit stress. The RD22-like protein subfamily is expressed in response to water deficit stress. Members of the RD22-like subfamily include AtRD22, GmRd22 and BnBDC1 which have been identified in Arabidopsis thaliana, Glycine max and Brassica napus respectively. This study aims at characterising two putative maize RD22-like proteins (designated ZmRd22A and ZmRd22B) by identifying sequence/domain features shared with characterised RD22-like proteins. Semi-quantitative and quantitative PCR techniques were used to examine the spatial and temporal expression patterns of the two putative maize Rd22-like proteins in response to, water deficit stress and exogenously applied abscisic acid in the roots and 2nd youngest leaves of maize seedlings. Using an in silico approach, sequence homology of the two putative maize Rd22- like proteins with AtRD22, GmRD22 and BnBDC1 has been analysed. Online bioinformatic tools were used to compare the characteristics of these Rd22-like proteins with those of the two maize proteins. It was shown that the putative maize RD22-like proteins share domain organisation with the characterised proteins, these common features include a N-terminal hydrophobic signal peptide, followed by a region with a conserved amino acid sequence, a region containing several TxV (x is any amino acid) repeat units and a C-terminal BURP domain-containing the conserved X₅-CH-X₁₀-CH-X₂₃-₂₇-CH-X₂₃-₂₆-CH-X₈-W motif. The putative maize Rd22-like protein appears to be localized in the apoplast, similarly to AtRD22, GmRD22 and BnBDC1. Analysis of the gene's promotor regions reveals cis-acting elements suggestive of induction of gene expression by water deficit stress and abscisic acid (ABA). Semi-quantitative and quantitative real time PCR analysis of the putative maize RD22-like gene revealed that the genes are not expressed in the roots. Exposure to water deficit stress resulted in an increase of ZmRD22A transcript accumulation in the 2nd youngest leaves of maize seedlings. ZmRD22A was shown to be non-responsive to exogenous ABA application. ZmRD22B was highly responsive to exogenous ABA application and responded to water deficit stress to a lesser degree. Transcript accumulation studies in three regions of the 2nd youngest leaves in response to water deficit stress showed that ZmRd22A transcripts accumulate mainly at the base and tips of the leaves. A restricted increase in ZmRD22A transcript accumulation in the middle of the leaves was observed. ZmRD22B showed a similar, but weaker transcript accumulation pattern in response to water deficit… Advisors/Committee Members: Ludidi, Ndiko (advisor).

Subjects/Keywords: BURP-domain containing protein; RD22-like proteins; Water deficit stress; Transcript accumulation; Maize; Abscisic acid

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Phillips, K. (2016). Characterization of the role of Zea mays burp domain-containing genes in maize drought responses . (Thesis). University of the Western Cape. Retrieved from http://hdl.handle.net/11394/5339

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Phillips, Kyle. “Characterization of the role of Zea mays burp domain-containing genes in maize drought responses .” 2016. Thesis, University of the Western Cape. Accessed February 28, 2021. http://hdl.handle.net/11394/5339.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Phillips, Kyle. “Characterization of the role of Zea mays burp domain-containing genes in maize drought responses .” 2016. Web. 28 Feb 2021.

Vancouver:

Phillips K. Characterization of the role of Zea mays burp domain-containing genes in maize drought responses . [Internet] [Thesis]. University of the Western Cape; 2016. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/11394/5339.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Phillips K. Characterization of the role of Zea mays burp domain-containing genes in maize drought responses . [Thesis]. University of the Western Cape; 2016. Available from: http://hdl.handle.net/11394/5339

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Georgia

6. Chandrayan, Puja. Biochemical characterization of a pectate lyase from Caldicellulosiruptor bescii.

Degree: 2014, University of Georgia

URL: http://hdl.handle.net/10724/29729

► Caldicellulosiruptor bescii is a gram-positive thermophilic bacterium with the ability to grow on untreated plant biomass. Upon growth on switchgrass at 78°C, a set of… (more)

Subjects/Keywords: Caldicellulosiruptor bescii, Cbes_1854; Pectinolytic enzymes, Polysaccharide lyase family 3; Catalytic domain (PL3), Full-length protein (X-PL3); E. coli, Cellulase (Cel A)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chandrayan, P. (2014). Biochemical characterization of a pectate lyase from Caldicellulosiruptor bescii. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/29729

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chandrayan, Puja. “Biochemical characterization of a pectate lyase from Caldicellulosiruptor bescii.” 2014. Thesis, University of Georgia. Accessed February 28, 2021. http://hdl.handle.net/10724/29729.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chandrayan, Puja. “Biochemical characterization of a pectate lyase from Caldicellulosiruptor bescii.” 2014. Web. 28 Feb 2021.

Vancouver:

Chandrayan P. Biochemical characterization of a pectate lyase from Caldicellulosiruptor bescii. [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10724/29729.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chandrayan P. Biochemical characterization of a pectate lyase from Caldicellulosiruptor bescii. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/29729

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

7. Goulet, Isabelle. New Roles for Arginine Methylation in RNA Metabolism and Cancer .

Degree: 2011, University of Ottawa

URL: http://hdl.handle.net/10393/20293

► Because it can expand the range of a protein’s interactions or modulate its activity, post-translational methylation of arginine residues in proteins must be duly coordinated… (more)

Subjects/Keywords: Arginine methylation; Protein arginine methyltransferases; Protein arginine methyltransferase 1; Tudor domain-containing proteins; TDRD3; PRMT1; Breast cancer; RNA metabolism; Stress granules; RNA processing; Tudor domain-containing protein 3; Tudor domain

…member of the PRMT family, PRMT1, and of the novel Tudor domain-containing protein 3 (… …activating protein (SH3 domain) binding protein 1 xviii GAPDH glyceraldehyde-3… …domain containing protein 2A KH K homology domain KLH keyhole limpet hemocyanin KSRP KH… …domain containing, octamer-binding (NONO) PABP-1 poly(A) binding protein… …binding protein 1 SG stress granule SH3 SRC homology domain 3 shRNA small hairpin…

10 more images…

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APA (6^th Edition):

Goulet, I. (2011). New Roles for Arginine Methylation in RNA Metabolism and Cancer . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/20293

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Goulet, Isabelle. “New Roles for Arginine Methylation in RNA Metabolism and Cancer .” 2011. Thesis, University of Ottawa. Accessed February 28, 2021. http://hdl.handle.net/10393/20293.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Goulet, Isabelle. “New Roles for Arginine Methylation in RNA Metabolism and Cancer .” 2011. Web. 28 Feb 2021.

Vancouver:

Goulet I. New Roles for Arginine Methylation in RNA Metabolism and Cancer . [Internet] [Thesis]. University of Ottawa; 2011. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10393/20293.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Goulet I. New Roles for Arginine Methylation in RNA Metabolism and Cancer . [Thesis]. University of Ottawa; 2011. Available from: http://hdl.handle.net/10393/20293

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Western Ontario

8. Dunn, Henry A. Regulation of CRFR1 and 5-HT2AR by PDZ Domain-Containing Proteins SAP97 and PSD-95.

Degree: 2014, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/2585

► Previous studies identified a crosstalk mechanism whereby CRFR1 sensitized 5-HT2AR-mediated signaling via interactions with PDZ domain-containing proteins: a mechanism that may underlie stress-induced anxiety and… (more)

▼ Previous studies identified a crosstalk mechanism whereby CRFR1 sensitized 5-HT2AR-mediated signaling via interactions with PDZ domain-containing proteins: a mechanism that may underlie stress-induced anxiety and depression. This prompted an investigation into uncovering which PDZ domain-containing proteins could regulate the crosstalk between these two receptors, and how they could be regulated individually. In the current studies, a subset of PDZ domain-containing proteins were identified that may interact with CRFR1 and 5-HT2AR. The focus narrowed to two candidates previously implicated in psychiatric disease: SAP97 and PSD-95. We confirmed SAP97 and PSD-95 as interacting partners of CRFR1 in adult mouse cortex via co-immunoprecipitation. Both proteins exhibited functional regulation of CRFR1 by antagonizing CRFR1 endocytosis in HEK293 cells, measured by flow cytometry. Additionally, PSD-95 suppressed β-arrestin2 recruitment, thereby providing a potential mechanism for antagonizing endocytosis. Although neither SAP97 nor PSD-95 appeared to play a significant role in CRFR1-mediated cAMP signaling, endogenous SAP97 was integral for CRF-mediated ERK1/2 phosphorylation in HEK293 and AtT20 cells. Despite extensive sequence homology between SAP97 and PSD-95, PSD-95 did not appear to play a significant role in CRF-mediated ERK1/2 phosphorylation. Thus, we begin to understand subtle signaling biases between these two proteins. As PSD-95 was already documented to regulate 5-HT2AR, we investigated if SAP97 could play a role in regulating 5-HT2AR function. The interaction between SAP97 and 5-HT2AR was confirmed in adult mouse cortex. As was seen with CRFR1, SAP97 antagonized 5-HT2AR endocytosis. Although SAP97 did not appear to significantly modulate Gs-coupled signaling via CRFR1, the endogenous expression of SAP97 was integral for maximal Gq-coupled signaling via 5-HT2AR. Endogenous SAP97 was also required for ERK1/2 phosphorylation, and this regulatory role appears to be downstream of receptor interactions. Finally, we were unable to prevent the CRFR1-mediated sensitization of 5-HT2AR-mediated signaling by knocking down either SAP97 or PSD-95 using shRNA. Therefore, neither SAP97 nor PSD-95 appear to be exclusively involved in this heterologous crosstalk mechanism. Nevertheless, we have identified SAP97 and PSD-95 as novel regulators of CRFR1 function, and SAP97 as a novel regulator of 5-HT2AR function. These functional interactions may be targeted for the treatment of CRFR1- and 5-HT2AR-mediated mood disorders.

Subjects/Keywords: G protein-coupled receptors; PDZ domain-containing proteins; ERK signalling; receptor endocytosis; ßarrestin recruitment; mental health; Medical Molecular Biology

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APA (6^th Edition):

Dunn, H. A. (2014). Regulation of CRFR1 and 5-HT2AR by PDZ Domain-Containing Proteins SAP97 and PSD-95. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/2585

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dunn, Henry A. “Regulation of CRFR1 and 5-HT2AR by PDZ Domain-Containing Proteins SAP97 and PSD-95.” 2014. Thesis, University of Western Ontario. Accessed February 28, 2021. https://ir.lib.uwo.ca/etd/2585.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dunn, Henry A. “Regulation of CRFR1 and 5-HT2AR by PDZ Domain-Containing Proteins SAP97 and PSD-95.” 2014. Web. 28 Feb 2021.

Vancouver:

Dunn HA. Regulation of CRFR1 and 5-HT2AR by PDZ Domain-Containing Proteins SAP97 and PSD-95. [Internet] [Thesis]. University of Western Ontario; 2014. [cited 2021 Feb 28]. Available from: https://ir.lib.uwo.ca/etd/2585.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dunn HA. Regulation of CRFR1 and 5-HT2AR by PDZ Domain-Containing Proteins SAP97 and PSD-95. [Thesis]. University of Western Ontario; 2014. Available from: https://ir.lib.uwo.ca/etd/2585

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of the Western Cape

9. Mulaudzi, Takalani. Structural and functional characterisation of a novel signalling molecule in Arabidopsis thaliana .

Degree: 2011, University of the Western Cape

URL: http://hdl.handle.net/11394/3608

► Nitric Oxide (NO) influences a wide range of physiological processes in plants including growth and development, responses to abiotic and biotic stress and pathogen responses.… (more)

▼ Nitric Oxide (NO) influences a wide range of physiological processes in plants including growth and development, responses to abiotic and biotic stress and pathogen responses. NO binds to the heme group of the mammalian soluble guanylyl cyclase, which activates the enzyme to convert guanosine 5’ triphosphate (GTP) to a second messenger guanosine 3’, 5’ cyclic monophosphate (cGMP). Cyclic GMP further activates other signalling cascades including the regulation of protein kinases, ion gated channels and phosphodiesterases. In plants, a few GCs have been identified and these include AtGC1, AtBRI1, AtWAKL10, and AtPSKR1, however, a GC that contains a heme binding motif that senses NO has yet to be identified. In order to identify such molecules, a search motif based on conserved HNOX domains and the conserved and functionally assigned amino acid residues in the catalytic centres of annotated GCs was designed and used to search the Arabidopsis thaliana proteome. Several candidate molecules were identified including a flavin-containing monooxygenase (FMO)-like protein and the At5g57690 which is currently annotated as a diacylglycerol kinase. FMOs found in bacteria, yeast, and animals are the most important monooxygenases since they are involved in xenobiotic metabolism and variability in drug response. FMOs in plants are implicated in catalysing specific steps in auxin biosynthesis,metabolism of glucosinolates and pathogen defense mechanisms. The human diacylglycerol kinase acts as a lipid kinase that mediates a wide range of biological processes which include cell proliferation, differentiation and turmogenesis. In prokaryotes, the structure of Escherichia coli lipid kinase has been solved however, its function has not yet been demonstrated. So far, the occurrence of the diacylglycerol kinases in plants has not yet been reported, and their structure and function also remain elusive. The domain architecture of the 2 molecules (AtNOGC1 and At5g57690) identified by the HNOX-based search strategy revealed that these molecules contain a GC and a heme-binding motif that is conserved among all known heme-binding proteins.In this study, the role of AtNOGC1, a novel NO binding protein in higher plants was investigated and the results showed that this molecule contains an NO-dependant active GC domain. The sequence was first analysed and the location of the HNOX and the GC motifs highlighted. The protein was then recombinatly expressed as a His-SUMO fusion protein and the purification optimised by a second step of ion exchange chromatography. Electrochemical techniques such as cyclic voltammetry and square wave voltammetry were used to demonstrate the binding of NO and O2 to the AtNOGC1. Electrochemical data revealed that AtNOGC1 has a lower affinity for O2 and a higher affinity for NO, an important signalling molecule in plants.The presence of the GC activity in AtNOGC1 was investigated by conducting GC activity assays in vitro in the presence or absence of NO. The GC activity assays demonstrated that AtNOGC1 can synthesize… Advisors/Committee Members: Gehring, Christoph A (advisor), Iwuoha, Emmanuel (advisor).

Subjects/Keywords: Recombinant protein; H-NOX domain; Signalling molecule; Flavin-containing monooxygenase; Nitric oxide; Oxygen; Electrochemistry; Guanylyl cyclase; cGMP assays; Homology modelling

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mulaudzi, T. (2011). Structural and functional characterisation of a novel signalling molecule in Arabidopsis thaliana . (Thesis). University of the Western Cape. Retrieved from http://hdl.handle.net/11394/3608

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mulaudzi, Takalani. “Structural and functional characterisation of a novel signalling molecule in Arabidopsis thaliana .” 2011. Thesis, University of the Western Cape. Accessed February 28, 2021. http://hdl.handle.net/11394/3608.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mulaudzi, Takalani. “Structural and functional characterisation of a novel signalling molecule in Arabidopsis thaliana .” 2011. Web. 28 Feb 2021.

Vancouver:

Mulaudzi T. Structural and functional characterisation of a novel signalling molecule in Arabidopsis thaliana . [Internet] [Thesis]. University of the Western Cape; 2011. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/11394/3608.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mulaudzi T. Structural and functional characterisation of a novel signalling molecule in Arabidopsis thaliana . [Thesis]. University of the Western Cape; 2011. Available from: http://hdl.handle.net/11394/3608

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Illinois – Urbana-Champaign

10. Rosenberger, Christina Laura. Regulation of mTORC1 by phosphatidic acid: mechanism and structural insight.

Degree: PhD, Cell and Developmental Biology, 2016, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/92925

► The mammalian target of rapamycin (mTOR) is a Ser/Thr kinase with remarkable control over cellular status. As a master regulator, mTOR integrates a variety of… (more)

▼ The mammalian target of rapamycin (mTOR) is a Ser/Thr kinase with remarkable control over cellular status. As a master regulator, mTOR integrates a variety of intra- and extra-cellular signals in order to coordinate them with appropriate gene expression, protein synthesis, metabolism, cell migration, autophagy – the list goes on! mTOR signaling, with involvement in so many important cellular processes, can have detrimental physiological effects when dysregulated. Aberrant mTOR signaling is now known to contribute to a great number of the major pathologies we face today. Understanding how mTOR is normally regulated is, therefore, important for informing the development of effective and specific therapeutics for diseases like cancer and diabetes. Significant research efforts over the last two decades have informed our current understanding of the extensive mTOR signaling pathways, but many questions remain. In my dissertation work I have investigated longstanding mysteries of mTOR activation by mitogens and nutrients, with specific focus on the mechanism by which the lipid second messenger, phosphatidic acid, activates mTOR complex 1. The mammalian target of rapamycin complex 1 (mTORC1) is regulated, in part, by the endogenous inhibitor DEPTOR. However, the mechanism of DEPTOR regulation with regard to rapid mTORC1 activation remains unknown. In collaboration with Dr. Mee Sup Yoon, I discovered that DEPTOR is rapidly and temporarily dissociated from mTORC1 upon mitogenic stimulation. We demonstrated that this mitogen stimulated DEPTOR dissociation is blocked by inhibition or depletion of the mTORC1 regulator, phospholipase D (PLD), and is recapitulated with the addition of the PLD product phosphatidic acid (PA). Parallel mass spectrometry analysis independently identified DEPTOR as an mTOR binding partner dissociated by PA. Interestingly, I found that only PA species with unsaturated fatty acid chains, such as those produced by PLD, are capable of displacing DEPTOR and activating mTORC1, with high affinity for the FRB domain of mTOR. Our findings, detailed in Chapter II reveal a mechanism of acute mTORC1 regulation that was previously unidentified and provide a molecular explanation for the exquisite specificity of PA function. In light of PA’s essential role in mTORC1 activation, I found it striking that mTOR proteins containing one of several point mutations have been reported to remain catalytically active in conditions when amino acids, and therefore PA, are absent. The existence of such hyperactive mTOR prompted me to ask whether a point mutation can render mTOR independent of regulation by PA and, if so, by what mechanism? In Chapter III, I describe how by examining the activity of several mTOR proteins each carrying a unique point mutation known to be associated with human cancer, I discovered that individual point mutations can confer varying degrees of PA-independent mTORC1 activity. My finding that an L1460P mutation in mTOR's FAT domain, S2215Y mutation in the kinase N-lobe, and E2419K in the kinase… Advisors/Committee Members: Chen, Jie (advisor), Chen, Jie (Committee Chair), Belmont, Andrew (committee member), Chen, Lin-Feng (committee member), Rivier, David (committee member).

Subjects/Keywords: Mammalian target of rapamycin (mTOR); phosphatidic acid; phospholipase D (PLD); DEP Domain Containing MTOR-Interacting Protein (DEPTOR); hyperactive; cancer

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rosenberger, C. L. (2016). Regulation of mTORC1 by phosphatidic acid: mechanism and structural insight. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/92925

Chicago Manual of Style (16^th Edition):

Rosenberger, Christina Laura. “Regulation of mTORC1 by phosphatidic acid: mechanism and structural insight.” 2016. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed February 28, 2021. http://hdl.handle.net/2142/92925.

MLA Handbook (7^th Edition):

Rosenberger, Christina Laura. “Regulation of mTORC1 by phosphatidic acid: mechanism and structural insight.” 2016. Web. 28 Feb 2021.

Vancouver:

Rosenberger CL. Regulation of mTORC1 by phosphatidic acid: mechanism and structural insight. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2016. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2142/92925.

Council of Science Editors:

Rosenberger CL. Regulation of mTORC1 by phosphatidic acid: mechanism and structural insight. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2016. Available from: http://hdl.handle.net/2142/92925

11. Corvaisier, Matthieu. Implication des co-activateurs transcriptionnels YAP/TAZ dans la régulation entre la croissance et la dormance tumorale des cellules du cancer colorectal : mécanismes moléculaires et perspectives thérapeutiques : Involvement of the transcriptional coactivators YAP/TAZ in the regulation of the switch from tumor growth to dormancy : molecular mechanisms et therapeutical perspectives.

Degree: Docteur es, Biologie cellulaire, 2016, Université Lille II – Droit et Santé

URL: http://www.theses.fr/2016LIL2S028

► Le cancer colorectal est la première pathologie cancéreuse de la sphère digestive, tant en terme de fréquence que de mortalité par an. Chaque année, 41… (more)

▼ Le cancer colorectal est la première pathologie cancéreuse de la sphère digestive, tant en terme de fréquence que de mortalité par an. Chaque année, 41 000 nouveaux cas sont diagnostiqués et 17 000 décès sont dus à ce cancer en France. Deux paramètres cliniques expliquent la mortalité de ce cancer; d'une part le fait qu'un patient sur deux est diagnostiqué au stade métastatique ou va présenter des lésions métastatiques durant l'histoire de sa pathologie, d'autre part le fait que les patients après traitement vont fréquemment présenter une récidive de leur pathologie. L'utilisation de régimes de chimiothérapies avant et après résection métastatique améliore la survie sans récidive à court terme, mais à 2 ans post chirurgie l'avantage apporté est perdu. Ainsi, la compréhension des mécanismes d'échappement à la chimiothérapie et régissant la croissance tumorale est d'intérêt pour tenter de limiter la récidive tumorale. L'objectif de ce travail de thèse a consisté en l'analyse de sous-populations obtenues sous pression de chimiothérapie au 5-Fluorouracile (5FU) dérivées de la lignée cancéreuse colique HT29, ainsi que les mécanismes moléculaires associés. Notre clone le plus chimiorésistant isolé, le modèle cellulaire 5F31, quitte le compartiment prolifératif sous traitement à fortes doses de 5FU, ceci étant associé à une perturbation de la voie de signalisation de la Src kinase c-Yes et de son partenaire, le co-activateur transcriptionnel YAP. Sous traitement, les cellules chimiorésistantes entrent en quiescence, le complexe protéique entre c-Yes et YAP est perdu et la quantité totale et nucléaire de YAP diminue de manière significative (Igoudjil, Touil, Corvaisier et al. 2014 Clinical Cancer Research). Dès lors, la suite des travaux a consisté en l'étude du rôle potentiel de YAP sur la balance quiescence/prolifération sous 5FU. L'inhibition pharmacologique ou l'inhibition transitoire de l'expression de YAP et de son paralogue, la protéine TAZ, dans plusieurs lignées cancéreuses coliques induit l'augmentation de la fraction de cellules quiescentes, associée au ralentissement significatif de la croissance tumorale. A l'inverse, la surexpression d'une forme constitutivement active de YAP demeurant nucléaire sous 5FU maintient les cellules 5F31 en prolifération et sensibilise les cellules à la chimiothérapie. Au niveau des effecteurs protéiques, l'induction de quiescence (par traitement à la chimiothérapie ou inhibition de YAP/TAZ) est associée à la perte d'expression de la Cycline E1 et du facteur de transcription c-Myc. A l'inverse, la surexpression du dominant constitutivement actif de YAP dans les cellules 5F31 conduit à l'expression soutenue de la Cycline E1 sous 5FU, expression nécessitant l'activation du facteur de transcription CREB. L'inhibition de la Cycline E1 permet d'induire la quiescence cellulaire, proposant cette protéine comme l'un des effecteurs des protéines YAP/TAZ dans la régulation entre la quiescence et la prolifération cellulaire (Corvaisier et al, Oncotarget, 2016). En conclusion, nos données… Advisors/Committee Members: Huet, Guillemette (thesis director).

Subjects/Keywords: Cancer colorectal; Traitement médicamenteux; Récidives; YAP; WWTR1; Transcription regulator containing ww domain); Yes associated protein; Colorectal cancer; Metastatic relapse

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Corvaisier, M. (2016). Implication des co-activateurs transcriptionnels YAP/TAZ dans la régulation entre la croissance et la dormance tumorale des cellules du cancer colorectal : mécanismes moléculaires et perspectives thérapeutiques : Involvement of the transcriptional coactivators YAP/TAZ in the regulation of the switch from tumor growth to dormancy : molecular mechanisms et therapeutical perspectives. (Doctoral Dissertation). Université Lille II – Droit et Santé. Retrieved from http://www.theses.fr/2016LIL2S028

Chicago Manual of Style (16^th Edition):

Corvaisier, Matthieu. “Implication des co-activateurs transcriptionnels YAP/TAZ dans la régulation entre la croissance et la dormance tumorale des cellules du cancer colorectal : mécanismes moléculaires et perspectives thérapeutiques : Involvement of the transcriptional coactivators YAP/TAZ in the regulation of the switch from tumor growth to dormancy : molecular mechanisms et therapeutical perspectives.” 2016. Doctoral Dissertation, Université Lille II – Droit et Santé. Accessed February 28, 2021. http://www.theses.fr/2016LIL2S028.

MLA Handbook (7^th Edition):

Corvaisier, Matthieu. “Implication des co-activateurs transcriptionnels YAP/TAZ dans la régulation entre la croissance et la dormance tumorale des cellules du cancer colorectal : mécanismes moléculaires et perspectives thérapeutiques : Involvement of the transcriptional coactivators YAP/TAZ in the regulation of the switch from tumor growth to dormancy : molecular mechanisms et therapeutical perspectives.” 2016. Web. 28 Feb 2021.

Vancouver:

Corvaisier M. Implication des co-activateurs transcriptionnels YAP/TAZ dans la régulation entre la croissance et la dormance tumorale des cellules du cancer colorectal : mécanismes moléculaires et perspectives thérapeutiques : Involvement of the transcriptional coactivators YAP/TAZ in the regulation of the switch from tumor growth to dormancy : molecular mechanisms et therapeutical perspectives. [Internet] [Doctoral dissertation]. Université Lille II – Droit et Santé 2016. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2016LIL2S028.

Council of Science Editors:

Corvaisier M. Implication des co-activateurs transcriptionnels YAP/TAZ dans la régulation entre la croissance et la dormance tumorale des cellules du cancer colorectal : mécanismes moléculaires et perspectives thérapeutiques : Involvement of the transcriptional coactivators YAP/TAZ in the regulation of the switch from tumor growth to dormancy : molecular mechanisms et therapeutical perspectives. [Doctoral Dissertation]. Université Lille II – Droit et Santé 2016. Available from: http://www.theses.fr/2016LIL2S028

Texas Medical Center

12. Espejo, Alexsandra B. Role of phosphorylation in the regulation of PRMT5.

Degree: PhD, 2016, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/711

► PRMT5 is a member of a group of proteins that mediate arginine methylation. It is involved in diverse cellular processes, including cell differentiation, splicing,… (more)

▼ PRMT5 is a member of a group of proteins that mediate arginine methylation. It is involved in diverse cellular processes, including cell differentiation, splicing, transcription elongation and epigenetic silencing, and its expression is dysregulated in many cancers. Due to its pleiotropic functions, PRMT5 is subject to multi-level regulation. Post-translational modification (PTM) of proteins can modulate an array of cellular processes by regulating both protein interactions and protein structural changes. PRMT5 is commonly found associated with other proteins; these interactions seem to control both its catalytic activity and its substrate specificity. Recently, it became clear that PRMT5 is phosphorylated at a number of residues, which prompted us to investigate whether phosphorylation of PRMT5 regulates its subcellular localization and/or substrate choice, by facilitating phospho-dependent protein-protein interactions. To study how phosphorylation affects PRMT5 function, protein microarrays were used to identify novel phosphodependent-interacting proteins. This analysis revealed that phosphorylation mediates the interaction of PRMT5 with several SH2-domain containing proteins, 14-3-3 proteins and the FHA domain of MDC1. These novel phospho-dependent PRMT5 interactions suggest that crosstalk between kinases and arginine methyltransferases may play a pivotal role in modulating the different cellular functions of PRMT5. Additionally, we have found that the C-terminal region of PRMT5 has a recognition motif shared by PDZ domains and 14-3-3 proteins. In order to bind to this motif, 14-3-3 proteins require the C-terminus to be phosphorylated, while PDZ domain recognition is phospho-independent. From these data, a new regulatory mechanism that affects PRMT5 behavior was proposed; the action of kinases and phosphatases on PRMT5 may function as a switch to regulate interactions between 14-3-3 and PDZ domain-containing proteins. We additionally observed this paradigm with a number of proteins, suggesting that this phosphorylation dependent switch, regulating binding to 14-3-3 and PDZ domains, occurs in a wide range of protein-protein interactions. Among the recently discovered PDZ-binding partners, we have found that PRMT5 interacts with NHERF2, a membrane-associated protein that regulates the sodium ion exchanger NHE3. Through this interaction, PRMT5 is placed in close proximity to the membrane and therefore may regulate the influx of ions through selective ion channels. Overall, we hypothesize that the direct interaction of PRMT5 with selected partners mediates the appropriate localization of PRMT5, allowing it to methylate specific substrates. Physiological processes including muscle contraction, cell homeostasis and neurotransmission are controlled by the selective conduction of ions across cell membranes. Ion channels and exchangers are proteins that span cell membranes and form channels or pores, facilitating the movement of ions in and out of cells. Abnormal cellular response to the… Advisors/Committee Members: Mark Bedford, Ph.D., Taiping Chen, Ph.D., Sharon Y.R. Dent, Ph.D..

Subjects/Keywords: PRMT5; phosphorylation; interactions; domain; protein microarray; SH2; PDZ; 14-3-3; FHA; Molecular Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Espejo, A. B. (2016). Role of phosphorylation in the regulation of PRMT5. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/711

Chicago Manual of Style (16^th Edition):

Espejo, Alexsandra B. “Role of phosphorylation in the regulation of PRMT5.” 2016. Doctoral Dissertation, Texas Medical Center. Accessed February 28, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/711.

MLA Handbook (7^th Edition):

Espejo, Alexsandra B. “Role of phosphorylation in the regulation of PRMT5.” 2016. Web. 28 Feb 2021.

Vancouver:

Espejo AB. Role of phosphorylation in the regulation of PRMT5. [Internet] [Doctoral dissertation]. Texas Medical Center; 2016. [cited 2021 Feb 28]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/711.

Council of Science Editors:

Espejo AB. Role of phosphorylation in the regulation of PRMT5. [Doctoral Dissertation]. Texas Medical Center; 2016. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/711

University of Illinois – Chicago

13. Okur, Mustafa N. Intersectin (ITSN) Regulation of Epidermal Growth Factor Receptor (EGFR) Ubiquitylation.

Degree: 2014, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/11279

► Ubiquitylation of receptor tyrosine kinases (RTKs) plays a critical role in regulating their trafficking and lysosomal degradation. Our laboratory identified the multi-domain scaffolding protein intersectin… (more)

Subjects/Keywords: Four-helix Bundle; Alzheimer’s Disease ; Ca2+ binding; Cbl; Coiled-coiled ; Cysteine rich domain; Dbl homology ;

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APA (6^th Edition):

Okur, M. N. (2014). Intersectin (ITSN) Regulation of Epidermal Growth Factor Receptor (EGFR) Ubiquitylation. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/11279

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Okur, Mustafa N. “Intersectin (ITSN) Regulation of Epidermal Growth Factor Receptor (EGFR) Ubiquitylation.” 2014. Thesis, University of Illinois – Chicago. Accessed February 28, 2021. http://hdl.handle.net/10027/11279.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Okur, Mustafa N. “Intersectin (ITSN) Regulation of Epidermal Growth Factor Receptor (EGFR) Ubiquitylation.” 2014. Web. 28 Feb 2021.

Vancouver:

Okur MN. Intersectin (ITSN) Regulation of Epidermal Growth Factor Receptor (EGFR) Ubiquitylation. [Internet] [Thesis]. University of Illinois – Chicago; 2014. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10027/11279.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Okur MN. Intersectin (ITSN) Regulation of Epidermal Growth Factor Receptor (EGFR) Ubiquitylation. [Thesis]. University of Illinois – Chicago; 2014. Available from: http://hdl.handle.net/10027/11279

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Kentucky

14. Chawsheen, Hedy. ROLE OF SULFIREDOXIN INTERACTING PROTEINS IN LUNG CANCER DEVELOPMENT.

Degree: 2016, University of Kentucky

URL: https://uknowledge.uky.edu/toxicology_etds/13

► Sulfiredoxin (Srx) is an antioxidant enzyme that can be induced by oxidative stress. It promotes oncogenic phenotypes of cell proliferation, colony formation, migration, and metastasis… (more)

▼ Sulfiredoxin (Srx) is an antioxidant enzyme that can be induced by oxidative stress. It promotes oncogenic phenotypes of cell proliferation, colony formation, migration, and metastasis in lung, skin and colon cancers. Srx reduces the overoxidation of 2-cysteine peroxiredoxins in cells, in addition to its role of removing glutathione modification from several proteins. In this study, I explored additional physiological functions of Srx in lung cancer through studying its interacting proteins. Protein disulfide isomerase (PDI) family members, thioredoxin domain containing protein 5 (TXNDC5) and protein disulfide isomerase family A member 6 (PDIA6), were detected to interact with Srx. Therefore, I proposed that TXNDC5 and PDIA6 are important for the oncogenic phenotypes of Srx in lung cancer. In chapter one, I presented background information about the role of Srx as an antioxidant enzyme in cancer. I also explained the functional significance of PDIs as oxidoreductase and chaperones in cells. In chapter two, I verified the Srx-TXNDC5/PDIA6 interaction in HEK293T and A549 cells by co-immunoprecipitation and other assays. In TXNDC5 and PDIA6, the N-terminal thioredoxin-like domain (D1) is determined to be the main platform for interaction with Srx. The Srx-TXNDC5 interaction was enhanced by H2O2 treatment in A549 cells. Srx was determined to localize in the endoplasmic reticulum (ER) of A549 cells along with TXNDC5 and PDIA6. This localization was confirmed by both subcellular fractionation and immunofluorescence imaging experiments. In chapter three I focused on studying the physiological function of Srx interacting proteins in the ER. A549 subcellular fractionation results showed that TXNDC5 facilitates Srx retention in the ER. Moreover, TXNDC5 and Srx were found to participate in chaperone activities in lung cancer. Both proteins contributed in the refolding of heat-shock induced protein aggregates. In addition, TXNDC5 and PDIA6 were found to enhance the protein refolding in response to H2O2 treatment. Conversely, Srx appeared to have an inhibitory effect on protein folding under same treatment conditions. Downregulation of Srx, TXNDC5, or PDIA6 significantly reduced cell viability in response to tunicamycin treatment. TXNDC5 knockdown decreased the time required for the splicing of X-box binding protein-1 (XBP-1). In either knockdown Srx or TXNDC5 cells, there was an observable decrease in the expression of GRP78 and the splicing of spliced XBP-1. These results suggest a possible role of Srx in unfolded protein response signaling. TXNDC5 and PDIA6, similar to Srx, contribute to the proliferation, anchorage independent colony formation and migration of lung cancer cells. In this dissertation I concluded that Srx TXNDC5, and PDIA6 proteins participate in oxidative protein folding in lung cancer. Srx and TXNDC5 can modulate unfolded protein response (UPR) sensor activation and growth inhibition. Furthermore, TXNDC5 and PDIA6 can promote tumorigenesis of lung cancer cells. Therefore, the molecular interaction of Srx with…

Subjects/Keywords: Sulfiredoxin; thioredoxin domain containing protein 5; protein disulfide isomerase A isoform 6; interaction; function; Medical Cell Biology; Medical Molecular Biology; Medical Toxicology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chawsheen, H. (2016). ROLE OF SULFIREDOXIN INTERACTING PROTEINS IN LUNG CANCER DEVELOPMENT. (Doctoral Dissertation). University of Kentucky. Retrieved from https://uknowledge.uky.edu/toxicology_etds/13

Chicago Manual of Style (16^th Edition):

Chawsheen, Hedy. “ROLE OF SULFIREDOXIN INTERACTING PROTEINS IN LUNG CANCER DEVELOPMENT.” 2016. Doctoral Dissertation, University of Kentucky. Accessed February 28, 2021. https://uknowledge.uky.edu/toxicology_etds/13.

MLA Handbook (7^th Edition):

Chawsheen, Hedy. “ROLE OF SULFIREDOXIN INTERACTING PROTEINS IN LUNG CANCER DEVELOPMENT.” 2016. Web. 28 Feb 2021.

Vancouver:

Chawsheen H. ROLE OF SULFIREDOXIN INTERACTING PROTEINS IN LUNG CANCER DEVELOPMENT. [Internet] [Doctoral dissertation]. University of Kentucky; 2016. [cited 2021 Feb 28]. Available from: https://uknowledge.uky.edu/toxicology_etds/13.

Council of Science Editors:

Chawsheen H. ROLE OF SULFIREDOXIN INTERACTING PROTEINS IN LUNG CANCER DEVELOPMENT. [Doctoral Dissertation]. University of Kentucky; 2016. Available from: https://uknowledge.uky.edu/toxicology_etds/13

15. Hu, Yu-Jie. Roles of Protein Arginine Methyltransferase 7 and Jumonji Domain-Containing Protein 6 in Adipocyte Differentiation: A Dissertation.

Degree: Cell Biology, Biochemistry and Molecular Pharmacology, 2015, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/797

► Regulation of gene expression comprises a wide range of mechanisms that control the abundance of gene products in response to environmental and developmental changes.… (more)

Subjects/Keywords: Adipocytes; Cell Differentiation; Gene Expression Regulation; Protein-Arginine N-Methyltransferases; Jumonji Domain-Containing Histone Demethylases; Biochemistry; Cell Biology; Cellular and Molecular Physiology; Enzymes and Coenzymes

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hu, Y. (2015). Roles of Protein Arginine Methyltransferase 7 and Jumonji Domain-Containing Protein 6 in Adipocyte Differentiation: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/797

Chicago Manual of Style (16^th Edition):

Hu, Yu-Jie. “Roles of Protein Arginine Methyltransferase 7 and Jumonji Domain-Containing Protein 6 in Adipocyte Differentiation: A Dissertation.” 2015. Doctoral Dissertation, U of Massachusetts : Med. Accessed February 28, 2021. http://escholarship.umassmed.edu/gsbs_diss/797.

MLA Handbook (7^th Edition):

Hu, Yu-Jie. “Roles of Protein Arginine Methyltransferase 7 and Jumonji Domain-Containing Protein 6 in Adipocyte Differentiation: A Dissertation.” 2015. Web. 28 Feb 2021.

Vancouver:

Hu Y. Roles of Protein Arginine Methyltransferase 7 and Jumonji Domain-Containing Protein 6 in Adipocyte Differentiation: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2015. [cited 2021 Feb 28]. Available from: http://escholarship.umassmed.edu/gsbs_diss/797.

Council of Science Editors:

Hu Y. Roles of Protein Arginine Methyltransferase 7 and Jumonji Domain-Containing Protein 6 in Adipocyte Differentiation: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2015. Available from: http://escholarship.umassmed.edu/gsbs_diss/797

Swedish University of Agricultural Sciences

16. Egeblad, Louise. Structural and functional studies of enzymes in nucleotide metabolism.

Degree: 2011, Swedish University of Agricultural Sciences

URL: https://pub.epsilon.slu.se/8107/

► Enzymes in nucleotide metabolism serve as the producers of the building blocks for DNA and RNA. From a medical perspective, nucleotide metabolism, and in particular… (more)

Subjects/Keywords: metabolism; nucleotides; ureaplasma; phosphoribosyltransferase; Nucleotide metabolism; Nucleoside analogs; Ureaplasma parvum; Uridine monophosphate kinase; Phosphoribosyltransferase domain containing protein 1; Nucleoside analog library; Differential static light scattering; Enzyme kinetics; Crystal structure

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Egeblad, L. (2011). Structural and functional studies of enzymes in nucleotide metabolism. (Doctoral Dissertation). Swedish University of Agricultural Sciences. Retrieved from https://pub.epsilon.slu.se/8107/

Chicago Manual of Style (16^th Edition):

Egeblad, Louise. “Structural and functional studies of enzymes in nucleotide metabolism.” 2011. Doctoral Dissertation, Swedish University of Agricultural Sciences. Accessed February 28, 2021. https://pub.epsilon.slu.se/8107/.

MLA Handbook (7^th Edition):

Egeblad, Louise. “Structural and functional studies of enzymes in nucleotide metabolism.” 2011. Web. 28 Feb 2021.

Vancouver:

Egeblad L. Structural and functional studies of enzymes in nucleotide metabolism. [Internet] [Doctoral dissertation]. Swedish University of Agricultural Sciences; 2011. [cited 2021 Feb 28]. Available from: https://pub.epsilon.slu.se/8107/.

Council of Science Editors:

Egeblad L. Structural and functional studies of enzymes in nucleotide metabolism. [Doctoral Dissertation]. Swedish University of Agricultural Sciences; 2011. Available from: https://pub.epsilon.slu.se/8107/

University of Illinois – Urbana-Champaign

17. Shen, Zhen. ORCA/LRWD1, a novel player in the initiation of eukaryotic DNA replication.

Degree: PhD, 4094, 2013, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/42431

► Accurate DNA replication is key to maintaining genome stability in all living species. In eukaryotes, the duplication process starts with the formation of the pre-replicative… (more)

▼ Accurate DNA replication is key to maintaining genome stability in all living species. In eukaryotes, the duplication process starts with the formation of the pre-replicative complex (pre-RC) prior to S phase, followed by the transition to the pre-initiation complex (pre-IC) that is required for DNA synthesis. The conserved canonical model of the pre-RC assembly includes an ordered recruitment of ORC, Cdt1, Cdc6, and the helicase MCMs to replication origins, and is strictly governed by replication licensing system. As the complexity increases dramatically from yeast to human cells, additional replication regulators have been identified in higher eukaryotes. In Chapter I, I review how the canonical pre-RC components were identified; what are the novel players; and our current understanding of how the replication licensing dictates proper DNA synthesis. While how ORC is recruited to specific origins has been studied explicitly in lower organisms, it remains unclear in higher eukaryotes. To understand whether additional factors enable the recruitment of ORC to origins and/or specific chromatin sites in human cells, our lab conducted ORC immunoprecipitations followed by mass spectrometric analysis in order to find novel ORC interactors. In Chapter II, I describe the identification of a highly conserved protein in human cells, leucine-rich repeats and WD40 repeat domain-containing protein 1 (LRWD1) or ORC-associated (ORCA). It interacts with ORC and modulates its chromatin association. ORCA co-localizes with ORC, shows similar cell cycle dynamics, and efficiently recruits ORC to chromatin. Depletion of ORCA in human primary cells and embryonic stem cells results in the loss of ORC association to chromatin, concomitant reduction of MCM binding, and a subsequent accumulation of cells in G1 phase. I therefore propose the model where ORCA-mediated association of ORC to chromatin is critical for pre-RC assembly in G1. In addition to ORC, I describe the interaction of ORCA with replication factor Cdt1 and its inhibitor Geminin in Chapter III. I demonstrate the stoichiometry of these associations via single-molecule pull-down experiments that each molecule of ORCA can bind to one molecule of ORC, one molecule of Cdt1, and two molecules of Geminin. Further, ORCA directly interacts with the N-terminus of Orc2, and this association is essential for ORCA stability. ORCA associates with Orc2 throughout the cell cycle, with Cdt1 during mitosis and G1, and with Geminin in post-G1 cells. Interestingly, overexpression of Geminin results in the loss of interaction between ORCA and Cdt1, suggesting that the increased levels of Geminin in post-G1 cells titrate Cdt1 away from ORCA. Based on these data, I propose that the dynamic association of ORCA with pre-RC components modulates the assembly of its interacting partners on chromatin and plays a key role in replication initiation. ORCA exhibits cell cycle-regulated protein levels that peak in G1; and it can only be stabilized when it is in a complex with Orc2. In Chapter IV, I show that… Advisors/Committee Members: Prasanth, Supriya G. (advisor), Belmont, Andrew S. (Committee Chair), Prasanth, Supriya G. (committee member), Freeman, Brian C. (committee member), Yau, Peter M. (committee member), Cann, Isaac K. (committee member).

Subjects/Keywords: ORC-associated (RCA); origin recognition complex; pre-replicative complex; DNA replication; leucine-rich repeats and WD40 repeat domain-containing protein 1 (LRWD1)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Shen, Z. (2013). ORCA/LRWD1, a novel player in the initiation of eukaryotic DNA replication. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/42431

Chicago Manual of Style (16^th Edition):

Shen, Zhen. “ORCA/LRWD1, a novel player in the initiation of eukaryotic DNA replication.” 2013. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed February 28, 2021. http://hdl.handle.net/2142/42431.

MLA Handbook (7^th Edition):

Shen, Zhen. “ORCA/LRWD1, a novel player in the initiation of eukaryotic DNA replication.” 2013. Web. 28 Feb 2021.

Vancouver:

Shen Z. ORCA/LRWD1, a novel player in the initiation of eukaryotic DNA replication. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2013. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2142/42431.

Council of Science Editors:

Shen Z. ORCA/LRWD1, a novel player in the initiation of eukaryotic DNA replication. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2013. Available from: http://hdl.handle.net/2142/42431

University of Illinois – Urbana-Champaign

18. Sun, Jie. The intramolecular domain interactions and phosphatase activation mechanisms of Shp2.

Degree: PhD, 0325, 2012, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/29512

► Shp2 (Src Homology 2 Domain-containing Protein Tyrosine Phosphatase 2) is a pivotal player in various signaling pathways in response to growth factors. It contains two… (more)

▼ Shp2 (Src Homology 2 Domain-containing Protein Tyrosine Phosphatase 2) is a pivotal player in various signaling pathways in response to growth factors. It contains two SH2 domains (N-SH2 and C-SH2), a phosphatase catalytic domain and a C-terminal tail containing two tyrosyl phosphorylation sites. While the tyrosine phosphorylation of C-terminal tail has been shown to be critical for the proper Shp2 functions, there is a lack of understanding on how the phosphorylation of these two tyrosine sites regulates the conformational changes and functions of Shp2. Here, we developed a FRET-based Shp2 reporter, a single molecule comprised of the full length human Shp2 concatenated in between a FRET pair, ECFP and YPet. In vitro incubation of Shp2 reporter with PDGFRβ induced a significant FRET increase via intramolecular interaction between C-SH2 and phosphotyrosine 580 (pY580). The phosphotyrosine 542 (pY542) has an adverse position despite a favored surrounding amino acid sequence such that it can only bind to C-SH2 in the absence of pY580. In contrast, pY542 dominates the binding of C-SH2 in mouse embryonic fibroblasts (MEFs). This intramolecular binding is essential for the subsequent effective phosphorylation of Y580, which is then sequestered by Grb2 in cells. These results suggested that the cellular environment can tune and switch the interaction of C-SH2 toward pY542. When the sequences containing Y542 and Y580 were engineered to exchange their positions such that the favored sequence containing Y542 is located at the advantageous position of 580 (Y542’), pY542’ constitutively dominates the binding of C-SH2 both in vitro and in MEFs. This rewiring of intramolecular interactions within Shp2 also caused a reprogramming of downstream signaling events, resulting in a more transient ERK phosphorylation. Therefore, our results indicate that the combination of a favorable sequence with an adverse position can create a delicate balance and plasticity of intramolecular interactions, which can determine the downstream cellular signaling/functions, and may represent a general design principle for functional molecular units tunable by environmental inputs. In addition to the intramolecular interactions we discovered, we also investigate the effect of these interactions on Shp2 phosphatase activity. We found that intramolecular binding between C-SH2 and pY580 doesn’t change Shp2 activity while the binding between C-SH2 and pY542 increases Shp2 activity using phosphatase activity assay. Moreover, phosphatase activity assay also showed that N-SH2 domain can also interact intramolecularly with pY542 or pY580 when C-SH2 is mutated and these interactions increase phosphatase activity. Our FRET reporter also enables us to visualize autodephosphorylation process in vitro. The results with the phosphatase inhibitors and inactive phosphatase mutants showed us that phosphatase activity is not necessary for intramolecular interactions. Even though phosphatase domain doesn’t play a direct role in the intramolecular interactions… Advisors/Committee Members: Wang, Yingxiao (advisor), Jakobsson, Eric (committee member), Chen, Jie (committee member), Xiang, Yang (committee member).

Subjects/Keywords: Shp2 (Src Homology 2 Domain-containing Protein Tyrosine Phosphatase 2); FRET reporter; Intramolecular interactions; Phosphatase activation; Fluorescent/ Förster resonance energy transfer (FRET)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sun, J. (2012). The intramolecular domain interactions and phosphatase activation mechanisms of Shp2. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/29512

Chicago Manual of Style (16^th Edition):

Sun, Jie. “The intramolecular domain interactions and phosphatase activation mechanisms of Shp2.” 2012. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed February 28, 2021. http://hdl.handle.net/2142/29512.

MLA Handbook (7^th Edition):

Sun, Jie. “The intramolecular domain interactions and phosphatase activation mechanisms of Shp2.” 2012. Web. 28 Feb 2021.

Vancouver:

Sun J. The intramolecular domain interactions and phosphatase activation mechanisms of Shp2. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2142/29512.

Council of Science Editors:

Sun J. The intramolecular domain interactions and phosphatase activation mechanisms of Shp2. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/29512

Université de Sherbrooke

19. Drapeau, Nicolas. L’expression de SHP-1 induite par l’hyperglycémie inhibe les actions de l’insuline dans les podocytes: Expression of SHP-1 induced by hyperglycemia prevents insulin actions in podocytes.

Degree: 2014, Université de Sherbrooke

URL: http://savoirs.usherbrooke.ca/handle/11143/129

► Résumé : Les podocytes, cellules épithéliales rénales, sont nécessaires au maintien de la structure et de la fonction de filtration des glomérules rénaux. La dédifférenciation… (more)

▼ Résumé : Les podocytes, cellules épithéliales rénales, sont nécessaires au maintien de la structure et de la fonction de filtration des glomérules rénaux. La dédifférenciation et l’apoptose des podocytes sont des évènements précoces de la néphropathie diabétique. Des études ont rapporté que l’insuline est nécessaire à la survie des podocytes puisque la délétion du récepteur à l’insuline dans les podocytes de souris entraîne une pathologie glomérulaire semblable à la néphropathie. D’autres études ont montré que la protéine tyrosine phosphatase Src homology-2 domain-containing phosphatase-1 (SHP-1) inhibe les voies de signalisation de l’insuline au niveau du foie et du muscle en déphosphorylant la sous-unité bêta du récepteur à l’insuline (IRβ) et la kinase Phosphatidylinositide 3-kinase (PI3K). Il a récemment été démontré que l’expression de SHP-1 est élevée dans les cortex rénaux de souris diabétiques. Nous avons donc émis l’hypothèse que l’expression de SHP-1 induite par l’hyperglycémie altère les actions de l’insuline dans les podocytes. Nous avons premièrement utilisé un modèle in vivo de souris diabétiques de type 1 (Ins2+/C96Y; Akita). Comparées aux souris contrôles (Ins2+/+), les souris Akita présentaient une apoptose élevée des podocytes ainsi qu’une perte des pédicelles. La phosphorylation de la protéine kinase B (Akt) et de Extracellular signal-regulated kinase 1/2 (ERK1/2), suite à une injection systémique d’insuline, était également significativement diminuée dans les cortex rénaux des souris Akita. Cette diminution correspondant à une résistance à l’insuline corrélait avec une augmentation de deux fois de l’expression de SHP-1 dans les glomérules. Nous avons ensuite utilisé une lignée immortalisée de podocytes murins en culture et avons observé que l’exposition à des concentrations élevées de glucose (HG; 25 mM) pendant 96 h, entraînait l’augmentation de l’expression de marqueurs apoptotiques et de l’activité enzymatique de caspase-3/7 en comparaison aux concentrations normales de glucose (NG; 5,6 mM). L’exposition en HG a augmenté l’expression de l’ARNm et protéique de SHP-1, en plus de réduire la signalisation de l’insuline dans les podocytes. La surexpression de la forme dominante-négative de SHP-1 dans les podocytes a permis de renverser les effets de HG et de restaurer les actions de l’insuline. Finalement, l’augmentation de l’expression de SHP-1, tant in vivo qu’in vitro, a été directement corrélée à son association avec IRβ et à la diminution de la phosphorylation de IRβ, Akt et ERK1/2 suite à une stimulation à l’insuline. En conclusion, nous avons montré que l’expression élevée de SHP-1 dans les glomérules cause une résistance à l’insuline et la mort des podocytes contribuant ainsi à la néphropathie diabétique. // Abstract : Podocytes are epithelial renal cells required to preserve glomerular structure and filtration. Their dedifferentiation and apoptosis are early events of diabetic nephropathy progression. Previous studies have shown that insulin action is critical for podocyte survival since… Advisors/Committee Members: Geraldes, Pedro Miguel (advisor).

Subjects/Keywords: Signalisation de l’insuline; Protéine tyrosine phosphatase; Récepteur à l’insuline; SHP-1; Néphropathie diabétique; Insulin signaling; Protein tyrosine phosphatase; Insulin receptor-β; Src homology-2 domain-containing phosphatase-1; Diabetic nephropathy

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Drapeau, N. (2014). L’expression de SHP-1 induite par l’hyperglycémie inhibe les actions de l’insuline dans les podocytes: Expression of SHP-1 induced by hyperglycemia prevents insulin actions in podocytes. (Masters Thesis). Université de Sherbrooke. Retrieved from http://savoirs.usherbrooke.ca/handle/11143/129

Chicago Manual of Style (16^th Edition):

Drapeau, Nicolas. “L’expression de SHP-1 induite par l’hyperglycémie inhibe les actions de l’insuline dans les podocytes: Expression of SHP-1 induced by hyperglycemia prevents insulin actions in podocytes.” 2014. Masters Thesis, Université de Sherbrooke. Accessed February 28, 2021. http://savoirs.usherbrooke.ca/handle/11143/129.

MLA Handbook (7^th Edition):

Drapeau, Nicolas. “L’expression de SHP-1 induite par l’hyperglycémie inhibe les actions de l’insuline dans les podocytes: Expression of SHP-1 induced by hyperglycemia prevents insulin actions in podocytes.” 2014. Web. 28 Feb 2021.

Vancouver:

Drapeau N. L’expression de SHP-1 induite par l’hyperglycémie inhibe les actions de l’insuline dans les podocytes: Expression of SHP-1 induced by hyperglycemia prevents insulin actions in podocytes. [Internet] [Masters thesis]. Université de Sherbrooke; 2014. [cited 2021 Feb 28]. Available from: http://savoirs.usherbrooke.ca/handle/11143/129.

Council of Science Editors:

Drapeau N. L’expression de SHP-1 induite par l’hyperglycémie inhibe les actions de l’insuline dans les podocytes: Expression of SHP-1 induced by hyperglycemia prevents insulin actions in podocytes. [Masters Thesis]. Université de Sherbrooke; 2014. Available from: http://savoirs.usherbrooke.ca/handle/11143/129

20. Noda, Yasuha. Fibronectin type III domain-containing protein 5 interacts with APP and decreases amyloid β production in Alzheimer’s disease.

Degree: 2019, Kyoto University

URL: http://hdl.handle.net/2433/236620

Subjects/Keywords: Alzheimer's disease; amyloid β; Fibronectin type III domain-containing protein 5; exercise

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Noda, Y. (2019). Fibronectin type III domain-containing protein 5 interacts with APP and decreases amyloid β production in Alzheimer’s disease. (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/236620

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Noda, Yasuha. “Fibronectin type III domain-containing protein 5 interacts with APP and decreases amyloid β production in Alzheimer’s disease. ” 2019. Thesis, Kyoto University. Accessed February 28, 2021. http://hdl.handle.net/2433/236620.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Noda, Yasuha. “Fibronectin type III domain-containing protein 5 interacts with APP and decreases amyloid β production in Alzheimer’s disease. ” 2019. Web. 28 Feb 2021.

Vancouver:

Noda Y. Fibronectin type III domain-containing protein 5 interacts with APP and decreases amyloid β production in Alzheimer’s disease. [Internet] [Thesis]. Kyoto University; 2019. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2433/236620.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Noda Y. Fibronectin type III domain-containing protein 5 interacts with APP and decreases amyloid β production in Alzheimer’s disease. [Thesis]. Kyoto University; 2019. Available from: http://hdl.handle.net/2433/236620

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Ohio University

21. Ma, Shuang. Preoptic Regulatory Factor 2 Inhibits Proliferation and Enhances Drug Induced Apoptosis in Neural Stem Cells.

Degree: PhD, Biological Sciences (Arts and Sciences), 2009, Ohio University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1236967001

► Neural stem cells (NSCs) exist in both the developing and adult brain. In the developing central nervous system (CNS), NSCs shape the structural and functional… (more)

▼ Neural stem cells (NSCs) exist in both the developing and adult brain. In the developing central nervous system (CNS), NSCs shape the structural and functional layout of the brain. After development, NSCs still contribute to low level neurogenesis in several brain areas including the subventricular zone (SVZ) and hippocampal dentate gyrus (DG). NSCs are important in cancer research and treatment. NSCs are a possible origin of brain-cancer stem cells when the strict control of cell growth is disturbed. They are also important resources for therapeutic transplantation in diverse diseases, including neurodegenerative disorders, brain and spinal cord injuries, stroke and epilepsy. Thus elucidating the growth-regulatory mechanism of NSCs will be helpful for understanding brain development, turmorigenesis and providing a platform for NSCs's clinical application. Preoptic regulatory factor-2 (Porf-2) is a Rho GTPase activator protein (GAP) domain-containing protein found in the CNS. It has been proposed to have a role in gender-related brain development and function. However, the direct effects of Porf-2 on NSCs are not known. The current studies were designed to knock down the expression of Porf-2 in C17.2 cells, a mouse cerebellar NSC line, and investigate the effects of Porf-2 on cell proliferation, apoptosis and differentiation. The mechanisms responsible for the effects of Porf-2 on cell proliferation and apoptosis were also studied. Knockdown of Porf-2 was performed by transducing short hairpin RNA (shRNA) lentivirus into C17.2 cells and confirmed by quantitative RT-PCR and Western blot analysis. Porf-2 knockdown cells exhibited increased proliferative activities and decreased drug induced apoptosis compared to control cells (p<0.05). There was no difference in differentiation directions between Porf-2 knockdown cells and control cells. Mechanistic studies yielded three findings. First, knockdown of Porf-2 lowered the expression level of cyclin kinase inhibitor p21 and expedited G1 to S cell cycle transition. Second, bleomycin, a genotoxic reagent, caused an elevation in p53 transcriptional activity, p21 expression and Bax expression in C17.2 cells. Knockdown of Porf-2 partially blocked the changes caused by bleomycin. Third, staurosporine (STS), a broad-spectrum kinase inhibitor, enhanced the expression of Bax but did not change the transcriptional activity of p53 or expression of p21 in C17.2 cells. Knockdown of Porf-2 had no influence on the enhancement of Bax expression in response to STS treatment. Three conclusions were drawn from these data. First, Porf-2 inhibits NSC proliferation by enhancing p21 expression followed by G1 cell cycle arrest. Second, Porf-2 plays pro-apoptotic roles in response to drug treatment in NSCs through both p53 transcription dependent and independent pathways. Third, Porf-2 shows no influence on NSC differentiation directions. Advisors/Committee Members: Nowak, Felicia V. (Advisor).

Subjects/Keywords: Biology; Porf-2; neural stem cell; RhoGAP domain-containing protein; proliferation; apoptosis; Bax

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ma, S. (2009). Preoptic Regulatory Factor 2 Inhibits Proliferation and Enhances Drug Induced Apoptosis in Neural Stem Cells. (Doctoral Dissertation). Ohio University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1236967001

Chicago Manual of Style (16^th Edition):

Ma, Shuang. “Preoptic Regulatory Factor 2 Inhibits Proliferation and Enhances Drug Induced Apoptosis in Neural Stem Cells.” 2009. Doctoral Dissertation, Ohio University. Accessed February 28, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1236967001.

MLA Handbook (7^th Edition):

Ma, Shuang. “Preoptic Regulatory Factor 2 Inhibits Proliferation and Enhances Drug Induced Apoptosis in Neural Stem Cells.” 2009. Web. 28 Feb 2021.

Vancouver:

Ma S. Preoptic Regulatory Factor 2 Inhibits Proliferation and Enhances Drug Induced Apoptosis in Neural Stem Cells. [Internet] [Doctoral dissertation]. Ohio University; 2009. [cited 2021 Feb 28]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1236967001.

Council of Science Editors:

Ma S. Preoptic Regulatory Factor 2 Inhibits Proliferation and Enhances Drug Induced Apoptosis in Neural Stem Cells. [Doctoral Dissertation]. Ohio University; 2009. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1236967001

University of Michigan

22. Ghosh, Soumi. Probing the Mechanism of Viral Inhibition by the Radical S-adenosyl-L-methionine (SAM) Dependent Enzyme- Viperin.

Degree: PhD, Chemistry, 2020, University of Michigan

URL: http://hdl.handle.net/2027.42/155178

► Viperin (Virus Inhibitory Protein; Endoplasmic Reticulum associated, INterferon inducible) is an endoplasmic reticulum (ER)-associated antiviral responsive protein that is highly up-regulated in eukaryotic cells upon… (more)

▼ Viperin (Virus Inhibitory Protein; Endoplasmic Reticulum associated, INterferon inducible) is an endoplasmic reticulum (ER)-associated antiviral responsive protein that is highly up-regulated in eukaryotic cells upon viral infection. Viperin is a radical S-adenosyl-L-methionine (SAM) enzyme, that catalyses the synthesis of antiviral nucleotide 3’-deoxy-3’, 4’-didehydro-CTP (ddhCTP) exploiting radical SAM chemistry. However, the modulation of its catalytic activity by other intracellular proteins is not well understood and needs further investigation. In this dissertation, I use enzymology-based approaches to investigate how viperin’s enzymatic activity is regulated through its interaction with various cellular and viral proteins that are involved in cellular metabolic and signalling pathways and viral replication. I showed that viperin can reduce the intracellular expression level of the cholesterol biosynthetic enzyme, farnesyl pyrophosphate synthase (FPPS). This, in turn perturbing the intracellular cholesterol synthesis, thereby retarding budding of enveloped viruses from cholesterol-rich lipid rafts of host cell membranes. I also undertook a proteomics study that revealed that viperin interacts with several other endogenous cholesterol biosynthetic enzymes. I also demonstrated that viperin promotes the degradation of viral non-structural protein A (NS5A) from hepatitis C virus through proteasome-mediated degradation in the presence of sterol-regulatory protein VAP-33. In turn, co-expression of viperin with VAP-33 and NS5A reduced the specific activity of viperin by ~ 3-fold. Lastly, this study showed that viperin is activated by innate immune signalling proteins kinase IRAK1 and ubiquitin ligase TRAF6, as it facilitates the ubiquitination of IRAK1 by TRAF6. The results provide valuable insights into the mechanism of action of viperin in regulating these target proteins and its significance as a SAM-dependent enzyme. Advisors/Committee Members: Marsh, E Neil G (committee member), Ragsdale, Stephen W (committee member), Bailey, Ryan Castle (committee member), Bridwell-Rabb, Jennifer Diane (committee member).

Subjects/Keywords: S-adenosylmethionine domain containing protein 2 (RSAD2); anti-viral responsive protein; Radical S-adenosyl-L-methionine enzyme; mammalian cell-based radical SAM enzyme activity; protein-protein interaction in innate immune system; regulation of cellular metabolic and signaling pathways; Chemistry; Science

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ghosh, S. (2020). Probing the Mechanism of Viral Inhibition by the Radical S-adenosyl-L-methionine (SAM) Dependent Enzyme- Viperin. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/155178

Chicago Manual of Style (16^th Edition):

Ghosh, Soumi. “Probing the Mechanism of Viral Inhibition by the Radical S-adenosyl-L-methionine (SAM) Dependent Enzyme- Viperin.” 2020. Doctoral Dissertation, University of Michigan. Accessed February 28, 2021. http://hdl.handle.net/2027.42/155178.

MLA Handbook (7^th Edition):

Ghosh, Soumi. “Probing the Mechanism of Viral Inhibition by the Radical S-adenosyl-L-methionine (SAM) Dependent Enzyme- Viperin.” 2020. Web. 28 Feb 2021.

Vancouver:

Ghosh S. Probing the Mechanism of Viral Inhibition by the Radical S-adenosyl-L-methionine (SAM) Dependent Enzyme- Viperin. [Internet] [Doctoral dissertation]. University of Michigan; 2020. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2027.42/155178.

Council of Science Editors:

Ghosh S. Probing the Mechanism of Viral Inhibition by the Radical S-adenosyl-L-methionine (SAM) Dependent Enzyme- Viperin. [Doctoral Dissertation]. University of Michigan; 2020. Available from: http://hdl.handle.net/2027.42/155178

University of Manchester

23. Edwards, Sarah. Investigating the role of a novel ER molecular chaperone; Creld2 in the physiology and pathophysiology of endochondral bone growth.

Degree: 2015, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:279565

► Cysteine rich with EGF-like domains 2 (Creld2) is a novel endoplasmic reticulum (ER) resident molecular chaperone that has been recently implicated in the ER stress… (more)

▼ Cysteine rich with EGF-like domains 2 (Creld2) is a novel endoplasmic reticulum (ER) resident molecular chaperone that has been recently implicated in the ER stress signalling response (ERSS) and the unfolded protein response (UPR). Global transcriptomic data derived from in vivo mouse models of rare chondrodysplasias; Multiple Epiphyseal Dysplasia (MED Matn3 p.V194D) and Metaphyseal chondrodysplasia type Schmid (MCDS Col10a1 p.N617K), identified a significant upregulation in Creld2 expression in mutant chondrocytes. These chondrodysplasias share a common disease signature consisting of aberrant folding of a matrix component often as a result of inappropriate alignment of intramolecular disulphide bonds. This in turn culminates in toxic protein aggregation, intracellular retention mutant polypeptides and a classical ER stress response. The aim of this study was to further analyse the function of Creld2 in cartilage development and chondrodysplasias in which endochondral bone growth is perturbed. Protein disulphide isomerases (PDIAs) were amongst the most up-regulated genes in the MED and MCDS mouse models, consistent with the prolonged exposure of normally ‘buried’ cysteine residues. This led to the hypothesis that Creld2 was functioning as a novel PDI-like oxidoreductase to assist in the correct folding and maturation of aggregated misfolded polypeptide chains through REDOX regulated thiol disulphide exchange. A series of Creld2-CXXA substrate trapping mutants were generated in order to determine whether Creld2 possessed inherent isomerase activity. Here potential substrates interacting with Creld2 were ‘trapped’ as mixed disulphide intermediates, then isolated by immunoprecipitation and identified by mass spectrometry analysis. It was demonstrated that Creld2 possessed a catalytic active CXXC motif in its N-terminus that enabled the molecular chaperone to participate in REDOX regulated thiol disulphide exchange with at least 20 potential substrates including; laminin (α3,β3,γ2), thrombospondin 1, integrin α3 and type VI collagen. There was also numerous co-chaperones and foldases thought to be part of a specialised protein-protein interactome (PPI) for folding nascent polypeptides translocating the ER lumen. Moreover, co-immunoprecipitation experiments supported a protein-protein interaction between Creld2 and mutant matrilin-3, thereby inferring a potential chondro-protective role in resolving non-native disulphide bonded aggregates in MED. An established biochemical approach was employed to test the hypothesis that all MATN3-MED disease causing mutations have a generic cellular response to the β-sheet V194D mutation, consisting of intracellular retention, protein aggregation and ER stress induction. Several missense mutations were selected for analyses which encompassed a spectrum of disease severity and included examples of both β-sheet and α helical mutations. It was possible to define a reliable and reproducible assay for categorising MATN3 missense mutations into pathological or benign based on these basic… Advisors/Committee Members: BRIGGS, MICHAEL MD, Briggs, Michael, Boot-Handford, Raymond.

Subjects/Keywords: Multiple Epiphyseal Dysplasia; Cartilage Development; Creld2; Matrilin-3; Collagen VI; von Willebrand Factor A domain; Endochondral Ossification; Protein disulphide isomerase

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Edwards, S. (2015). Investigating the role of a novel ER molecular chaperone; Creld2 in the physiology and pathophysiology of endochondral bone growth. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:279565

Chicago Manual of Style (16^th Edition):

Edwards, Sarah. “Investigating the role of a novel ER molecular chaperone; Creld2 in the physiology and pathophysiology of endochondral bone growth.” 2015. Doctoral Dissertation, University of Manchester. Accessed February 28, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:279565.

MLA Handbook (7^th Edition):

Edwards, Sarah. “Investigating the role of a novel ER molecular chaperone; Creld2 in the physiology and pathophysiology of endochondral bone growth.” 2015. Web. 28 Feb 2021.

Vancouver:

Edwards S. Investigating the role of a novel ER molecular chaperone; Creld2 in the physiology and pathophysiology of endochondral bone growth. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2021 Feb 28]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:279565.

Council of Science Editors:

Edwards S. Investigating the role of a novel ER molecular chaperone; Creld2 in the physiology and pathophysiology of endochondral bone growth. [Doctoral Dissertation]. University of Manchester; 2015. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:279565

University of Manchester

24. Edwards, Sarah. Investigating the role of a novel ER molecular chaperone : Creld2 in the physiology and pathophysiology of endochondral bone growth.

Degree: PhD, 2015, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-role-of-a-novel-er-molecular-chaperone-creld2-in-the-physiology-and-pathophysiology-of-endochondral-bone-growth(6fd49909-beec-42d1-a546-8b2411616e59).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.756800

► Cysteine rich with EGF-like domains 2 (Creld2) is a novel endoplasmic reticulum (ER) resident molecular chaperone that has been recently implicated in the ER stress… (more)

▼ Cysteine rich with EGF-like domains 2 (Creld2) is a novel endoplasmic reticulum (ER) resident molecular chaperone that has been recently implicated in the ER stress signalling response (ERSS) and the unfolded protein response (UPR). Global transcriptomic data derived from in vivo mouse models of rare chondrodysplasias; Multiple Epiphyseal Dysplasia (MED Matn3 p.V194D) and Metaphyseal chondrodysplasia type Schmid (MCDS Col10a1 p.N617K), identified a significant upregulation in Creld2 expression in mutant chondrocytes. These chondrodysplasias share a common disease signature consisting of aberrant folding of a matrix component often as a result of inappropriate alignment of intramolecular disulphide bonds. This in turn culminates in toxic protein aggregation, intracellular retention mutant polypeptides and a classical ER stress response. The aim of this study was to further analyse the function of Creld2 in cartilage development and chondrodysplasias in which endochondral bone growth is perturbed. Protein disulphide isomerases (PDIAs) were amongst the most up-regulated genes in the MED and MCDS mouse models, consistent with the prolonged exposure of normally 'buried' cysteine residues. This led to the hypothesis that Creld2 was functioning as a novel PDI-like oxidoreductase to assist in the correct folding and maturation of aggregated misfolded polypeptide chains through REDOX regulated thiol disulphide exchange. A series of Creld2-CXXA substrate trapping mutants were generated in order to determine whether Creld2 possessed inherent isomerase activity. Here potential substrates interacting with Creld2 were 'trapped' as mixed disulphide intermediates, then isolated by immunoprecipitation and identified by mass spectrometry analysis. It was demonstrated that Creld2 possessed a catalytic active CXXC motif in its N-terminus that enabled the molecular chaperone to participate in REDOX regulated thiol disulphide exchange with at least 20 potential substrates including; laminin (alpha3,β3,γ2), thrombospondin 1, integrin alpha3 and type VI collagen. There was also numerous co-chaperones and foldases thought to be part of a specialised protein-protein interactome (PPI) for folding nascent polypeptides translocating the ER lumen. Moreover, co-immunoprecipitation experiments supported a protein-protein interaction between Creld2 and mutant matrilin-3, thereby inferring a potential chondro-protective role in resolving non-native disulphide bonded aggregates in MED. An established biochemical approach was employed to test the hypothesis that all MATN3-MED disease causing mutations have a generic cellular response to the β-sheet V194D mutation, consisting of intracellular retention, protein aggregation and ER stress induction. Several missense mutations were selected for analyses which encompassed a spectrum of disease severity and included examples of both β-sheet and alpha helical mutations. It was possible to define a reliable and reproducible assay for categorising MATN3 missense mutations into pathological or benign based on…

Subjects/Keywords: 571.6; von Willebrand Factor A domain; Endochondral Ossification; Collagen VI; Protein disulphide isomerase; Creld2; Cartilage Development; Multiple Epiphyseal Dysplasia; Matrilin-3

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Edwards, S. (2015). Investigating the role of a novel ER molecular chaperone : Creld2 in the physiology and pathophysiology of endochondral bone growth. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-role-of-a-novel-er-molecular-chaperone-creld2-in-the-physiology-and-pathophysiology-of-endochondral-bone-growth(6fd49909-beec-42d1-a546-8b2411616e59).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.756800

Chicago Manual of Style (16^th Edition):

Edwards, Sarah. “Investigating the role of a novel ER molecular chaperone : Creld2 in the physiology and pathophysiology of endochondral bone growth.” 2015. Doctoral Dissertation, University of Manchester. Accessed February 28, 2021. https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-role-of-a-novel-er-molecular-chaperone-creld2-in-the-physiology-and-pathophysiology-of-endochondral-bone-growth(6fd49909-beec-42d1-a546-8b2411616e59).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.756800.

MLA Handbook (7^th Edition):

Edwards, Sarah. “Investigating the role of a novel ER molecular chaperone : Creld2 in the physiology and pathophysiology of endochondral bone growth.” 2015. Web. 28 Feb 2021.

Vancouver:

Edwards S. Investigating the role of a novel ER molecular chaperone : Creld2 in the physiology and pathophysiology of endochondral bone growth. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2021 Feb 28]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-role-of-a-novel-er-molecular-chaperone-creld2-in-the-physiology-and-pathophysiology-of-endochondral-bone-growth(6fd49909-beec-42d1-a546-8b2411616e59).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.756800.

Council of Science Editors:

Edwards S. Investigating the role of a novel ER molecular chaperone : Creld2 in the physiology and pathophysiology of endochondral bone growth. [Doctoral Dissertation]. University of Manchester; 2015. Available from: https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-role-of-a-novel-er-molecular-chaperone-creld2-in-the-physiology-and-pathophysiology-of-endochondral-bone-growth(6fd49909-beec-42d1-a546-8b2411616e59).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.756800

Université de Sherbrooke

25. Lessard-Beaudoin, Mélissa. Implication de deux nouveaux partenaires d'interaction de la Caspase-6, DAXX et STK3, dans le vieillissement et la maladie de Huntington.

Degree: 2018, Université de Sherbrooke

URL: http://hdl.handle.net/11143/11831

► La neurodégénérescence fait partie intégrante de la maladie de Huntington (MH) dont les premiers symptômes moteurs et cognitifs apparaissent vers l’âge de 30 à 40… (more)

▼ La neurodégénérescence fait partie intégrante de la maladie de Huntington (MH) dont les premiers symptômes moteurs et cognitifs apparaissent vers l’âge de 30 à 40 ans. Cette maladie incurable est causée par une mutation dans le gène codant pour la protéine huntingtin (htt). L’activation de la caspase-6 (casp6) est observée au stade présymptomatique chez l’humain et les modèles murins MH faisant de la casp6 un joueur majeur dans la neurodégénérescence précoce associé à la MH. De plus, le clivage de htt mutant par la casp6 produit un fragment N-terminal neurotoxique essentielle au développement de la MH. Des résultats préliminaires ont permis de révéler l’interaction et le clivage des protéines proapoptotiques Serine/Threonine Kinase 3 (STK3), Death-Domain Associated Protein (DAXX) par la casp6. Des effets proapoptotiques sont associés à leurs fragments et leur production par les caspases pourrait influencer la neurodégénérescence observée dans diverses maladies neurodégénératives et dans le vieillissement normal. Nos résultats dans les souris C57Bl/6 démontrent que l’expression de DAXX varie fortement avec l’âge selon l’organe analysé. Ses divers fragments ne suivent pas la même tendance d’un organe à l’autre suggérant des fonctions différentielles à travers l’organisme et une importante régulation de ses fonctions par des modifications post-traductionnelles. Chez les modèles murins de la MH, les souris YAC128, nous avons constaté une augmentation des fragments à 65 et 70 kDa dans le cortex et une diminution de DAXX entier et du fragment à 70 kDa dans le cervelet soulignant la possibilité de fonctions spécifiques selon les régions cérébrales. Nous avons aussi démontré pour la première fois le clivage de STK3 par la caspase-7 et la production différentielle de fragments par les caspase-3, 6 et 7. L’expression protéique de STK3 augmente globalement à travers l’organisme avec l’âge et dans le cervelet des souris YAC128. Par contre, une diminution de l’expression de STK3 est observée dans le cortex des individus atteints de la MH et des souris YAC128. Finalement, par l’induction de différents stress cellulaires, nous avons constaté la présence d’un mécanisme adaptatif des neurones modèles de la MH impliquant STK3. En conclusion, l’expression de DAXX et STK3 varie avec l’âge à travers l’organisme et est altérée dans la maladie de Huntington. Plus particulièrement, STK3semble être impliqué dans un mécanisme protégeant les neurones de la mort cellulaire dans la MH. Advisors/Committee Members: Graham, Rona (advisor).

Subjects/Keywords: Caspase; Death-domain associated protein 6 (DAXX); Sérine-Thréonine kinase 3 (STK3); Vieillissement; Maladie de Huntington; YAC 128

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lessard-Beaudoin, M. (2018). Implication de deux nouveaux partenaires d'interaction de la Caspase-6, DAXX et STK3, dans le vieillissement et la maladie de Huntington. (Masters Thesis). Université de Sherbrooke. Retrieved from http://hdl.handle.net/11143/11831

Chicago Manual of Style (16^th Edition):

Lessard-Beaudoin, Mélissa. “Implication de deux nouveaux partenaires d'interaction de la Caspase-6, DAXX et STK3, dans le vieillissement et la maladie de Huntington.” 2018. Masters Thesis, Université de Sherbrooke. Accessed February 28, 2021. http://hdl.handle.net/11143/11831.

MLA Handbook (7^th Edition):

Lessard-Beaudoin, Mélissa. “Implication de deux nouveaux partenaires d'interaction de la Caspase-6, DAXX et STK3, dans le vieillissement et la maladie de Huntington.” 2018. Web. 28 Feb 2021.

Vancouver:

Lessard-Beaudoin M. Implication de deux nouveaux partenaires d'interaction de la Caspase-6, DAXX et STK3, dans le vieillissement et la maladie de Huntington. [Internet] [Masters thesis]. Université de Sherbrooke; 2018. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/11143/11831.

Council of Science Editors:

Lessard-Beaudoin M. Implication de deux nouveaux partenaires d'interaction de la Caspase-6, DAXX et STK3, dans le vieillissement et la maladie de Huntington. [Masters Thesis]. Université de Sherbrooke; 2018. Available from: http://hdl.handle.net/11143/11831

Washington University in St. Louis

26. Essuman, Kow. The Enzymatic Function of the TIR domain: From Axon Degeneration to Innate Immunity.

Degree: PhD, Biology & Biomedical Sciences (Molecular Genetics & Genomics), 2020, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/art_sci_etds/2183

► The Toll/Interleukin-1 Receptor (TIR) domain is an evolutionarily ancient protein domain conserved from bacteria to eukaryotes, and is an essential signaling component of innate immunity… (more)

▼ The Toll/Interleukin-1 Receptor (TIR) domain is an evolutionarily ancient protein domain conserved from bacteria to eukaryotes, and is an essential signaling component of innate immunity pathways. In animal innate immunity, TIR domains have primarily been described for their scaffolding function in assembling protein complexes in host defense. In plant immunity, TIR domains are key components of the intracellular Nucleotide Binding Leucine rich repeat (NLR) immune receptors that confer resistance to pathogens. These NLR receptors trigger cell death and an immune response upon activation, but their mechanism has remained elusive. In bacteria, TIR domain proteins have been suggested to function as secreted virulence factors against eukaryotic hosts. My dissertation work begins with the study of a TIR domain containing protein, SARM1 (Sterile Alpha and TIR motif containing 1) that is expressed in neurons, and is activated upon axonal injury. SARM1 activation triggers depletion of the essential metabolic cofactor Nicotinamide Adenine Dinucleotide (NAD+), results in energetic failure in the axon, and ultimately axonal death. Since TIR domains were primarily known to function as scaffolds in immune signaling pathways, I embarked on a search for the NAD+ depleting enzyme that was activated by the SARM1 TIR domain, or was binding to the SARM1 TIR scaffold. These studies aimed not only to advance our understanding of the mechanism of axon degeneration, but sought to identify a therapeutic target for diseases characterized by axon degeneration. In my pursuit of this aim, I surprisingly found that rather than activating a secondary NAD+ depleting enzyme, the SARM1 TIR domain itself functioned as the enzyme that depleted axons of NAD+ and caused axonal death. Since TIR domains were not known to possess enzymatic activity, the discovery of the TIR NADase activity in SARM1 placed SARM1 as the founding member of a potentially new class of enzymes. Soon after, I found that the TIR domain enzymatic activity was an ancient enzymatic property, conserved even in bacterial and archaeal TIR domains. Finally, my work has provided significant insights into the biology of plant NLR receptors. We show that TIR domain containing NLR receptors transduce pathogen recognition into cell death via a conserved NAD+ cleavage activity. These findings establish TIR domain proteins as a new family of enzymes, and carries significant implications for innate immunity, and the treatment of diverse neurodegenerative diseases. Advisors/Committee Members: Jeffrey Milbrandt, Marco Colonna, Aaron DiAntonio, Daniel Link, Albert Kim.

Subjects/Keywords: axon degeneration, immunity, NAD+, NLR, SARM1, TIR domain; Allergy and Immunology; Biochemistry; Immunology and Infectious Disease; Medical Immunology; Neuroscience and Neurobiology

Record Details Similar Records Cite « Share

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Essuman, K. (2020). The Enzymatic Function of the TIR domain: From Axon Degeneration to Innate Immunity. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/2183

Chicago Manual of Style (16^th Edition):

Essuman, Kow. “The Enzymatic Function of the TIR domain: From Axon Degeneration to Innate Immunity.” 2020. Doctoral Dissertation, Washington University in St. Louis. Accessed February 28, 2021. https://openscholarship.wustl.edu/art_sci_etds/2183.

MLA Handbook (7^th Edition):

Essuman, Kow. “The Enzymatic Function of the TIR domain: From Axon Degeneration to Innate Immunity.” 2020. Web. 28 Feb 2021.

Vancouver:

Essuman K. The Enzymatic Function of the TIR domain: From Axon Degeneration to Innate Immunity. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2020. [cited 2021 Feb 28]. Available from: https://openscholarship.wustl.edu/art_sci_etds/2183.

Council of Science Editors:

Essuman K. The Enzymatic Function of the TIR domain: From Axon Degeneration to Innate Immunity. [Doctoral Dissertation]. Washington University in St. Louis; 2020. Available from: https://openscholarship.wustl.edu/art_sci_etds/2183

Mississippi State University

27. Reddy, Swetha Mamidi. CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS LACKING A JUMONJI DOMAIN CONTAINING HISTONE DEMETHYLASE AND A SET DOMAIN CONTAINING HISTONE METHYL TRANSFERASE.

Degree: PhD, Biochemistry and Molecular Biology, 2010, Mississippi State University

URL: http://sun.library.msstate.edu/ETD-db/theses/available/etd-07092010-173356/ ;

► Condensation of chromatin and alteration of chemical groups in the proteins around which the DNA is wrapped play major role in regulation of transcription.… (more)

▼ Condensation of chromatin and alteration of chemical groups in the proteins around which the DNA is wrapped play major role in regulation of transcription. Histones are basic proteins rich in arginine and lysine residues which form the nucleosomal core. Histone modifications like acetylation, methylation, phosphorylation, etc. have broadened the horizon for researchers to study epigenetics more in detail. Histone methyl transferases and histone demethyl transferases are enzymes which add or remove methyl groups on histone lysine and arginine residues respectively. In this study a jumonji domain containing putative histone demethyltransferase has been shown to be responsible in controlling flowering phenotype in Arabidopsis thaliana. The knocked out mutants for this gene (JMJ14) showed an early flowering phenotype along with elevated levels of FT transcript (Flowering locus T, gene responsible for controlling the flowering time in Arabidopsis thaliana). We show that methylation was altered on H3K36 in the FT gene in the mutants using ChIP (chromatin immunoprecipitation experiments). The possible role of SDG8 gene, a histone methyl transferase in ABA signaling was also studied during the research. A SET domain containing Sdg8 (group 8 methyltransferase) mutant was found to be responsible for ABA signaled altered root growth in Arabidopsis thaliana. The cell number and cell size in roots decreased in both meristematic and elongation zones leading to decrease in root size in sdg8 mutants and number of root hairs increased when treated with Abscisic acid, a plant hormone. In this part of study, as part of an interaction between epigenetics and gene regulation, it was observed that a putative histone demethylase gene, JMJ14 was responsible for regulating the flowering time by controlling the expression of FT and SDG8 played a role in altered root growth in response to ABA in Arabidopsis thaliana. Further studies on these genes could lead to generation of commercial crops with phenotypes that would increase the plant productivity and be beneficial agronomically. Advisors/Committee Members: Jiaxu Li (chair).

Subjects/Keywords: JUMONJI DOMAIN CONTAINING HISTONE DEMETHYLASE

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Reddy, S. M. (2010). CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS LACKING A JUMONJI DOMAIN CONTAINING HISTONE DEMETHYLASE AND A SET DOMAIN CONTAINING HISTONE METHYL TRANSFERASE. (Doctoral Dissertation). Mississippi State University. Retrieved from http://sun.library.msstate.edu/ETD-db/theses/available/etd-07092010-173356/ ;

Chicago Manual of Style (16^th Edition):

Reddy, Swetha Mamidi. “CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS LACKING A JUMONJI DOMAIN CONTAINING HISTONE DEMETHYLASE AND A SET DOMAIN CONTAINING HISTONE METHYL TRANSFERASE.” 2010. Doctoral Dissertation, Mississippi State University. Accessed February 28, 2021. http://sun.library.msstate.edu/ETD-db/theses/available/etd-07092010-173356/ ;.

MLA Handbook (7^th Edition):

Reddy, Swetha Mamidi. “CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS LACKING A JUMONJI DOMAIN CONTAINING HISTONE DEMETHYLASE AND A SET DOMAIN CONTAINING HISTONE METHYL TRANSFERASE.” 2010. Web. 28 Feb 2021.

Vancouver:

Reddy SM. CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS LACKING A JUMONJI DOMAIN CONTAINING HISTONE DEMETHYLASE AND A SET DOMAIN CONTAINING HISTONE METHYL TRANSFERASE. [Internet] [Doctoral dissertation]. Mississippi State University; 2010. [cited 2021 Feb 28]. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-07092010-173356/ ;.

Council of Science Editors:

Reddy SM. CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS LACKING A JUMONJI DOMAIN CONTAINING HISTONE DEMETHYLASE AND A SET DOMAIN CONTAINING HISTONE METHYL TRANSFERASE. [Doctoral Dissertation]. Mississippi State University; 2010. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-07092010-173356/ ;

28. keerthi gottipati. Correlated long-distance dynamics modulate monoclonal antibody binding resistance in flaviviral envelope pretein domain-3: A molecular dynamics simulations study.

Degree: MS, Human Biological Chemistry and Genetics, 2008, The University of Texas Medical Branch

URL: http://hdl.handle.net/2152.3/277

► Numerous monoclonal antibody (MAb) binding resistant mutations have been localized to the envelope protein domain-3 (ED3) of flaviviruses. Previously it was shown that regions constituting… (more)

Subjects/Keywords: protein-dynamics; MD-simulations; long-distance communication; flavivirus; envelope protein; domain-3

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

gottipati, k. (2008). Correlated long-distance dynamics modulate monoclonal antibody binding resistance in flaviviral envelope pretein domain-3: A molecular dynamics simulations study. (Masters Thesis). The University of Texas Medical Branch. Retrieved from http://hdl.handle.net/2152.3/277

Chicago Manual of Style (16^th Edition):

gottipati, keerthi. “Correlated long-distance dynamics modulate monoclonal antibody binding resistance in flaviviral envelope pretein domain-3: A molecular dynamics simulations study.” 2008. Masters Thesis, The University of Texas Medical Branch. Accessed February 28, 2021. http://hdl.handle.net/2152.3/277.

MLA Handbook (7^th Edition):

gottipati, keerthi. “Correlated long-distance dynamics modulate monoclonal antibody binding resistance in flaviviral envelope pretein domain-3: A molecular dynamics simulations study.” 2008. Web. 28 Feb 2021.

Vancouver:

gottipati k. Correlated long-distance dynamics modulate monoclonal antibody binding resistance in flaviviral envelope pretein domain-3: A molecular dynamics simulations study. [Internet] [Masters thesis]. The University of Texas Medical Branch; 2008. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2152.3/277.

Council of Science Editors:

gottipati k. Correlated long-distance dynamics modulate monoclonal antibody binding resistance in flaviviral envelope pretein domain-3: A molecular dynamics simulations study. [Masters Thesis]. The University of Texas Medical Branch; 2008. Available from: http://hdl.handle.net/2152.3/277

Universidade do Rio Grande do Sul

29. Viscardi, Lucas Henriques. História evolutiva da subfamília FOXP : análise evolutiva molecular e estrutural em tetrápodes.

Degree: 2015, Universidade do Rio Grande do Sul

URL: http://hdl.handle.net/10183/150633

►

A família gênica Forkhead P {FOXP) tem sido alvo de muitos estudos envolvendo evolução do cérebro e comportamento animal. Destacam-se particularmente as investigações com o… (more)

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A família gênica Forkhead P {FOXP) tem sido alvo de muitos estudos envolvendo evolução do cérebro e comportamento animal. Destacam-se particularmente as investigações com o gene FOXP2, que indicam que mudanças neste gene estariam associadas com a evolução da vocalização em algumas espécies de mamíferos, incluindo o Homo sapiens. Recentemente, estudos de desordem intrínseca de proteínas (IDPs) tem ganhado ênfase no contexto evolut ivo, visto que uma correlação posit iva entre regiões de desordem e altas taxas evolutivas tem sido observada. Através de um conjunto de abordagens que inclui predizer o conteúdo de desordem e os motivos lineares de interação, bem como as taxas evolutivas, buscamos desvendar a historia evolutiva dos genes da subfamília FOXP. Concentramos nossas análises sobre regiões desordenadas das proteínas FOXPl, FOXP2, FOXP3 e FOXP4 encontradas em 77 espécies de tetrápodes. Tais regiões proteicas são normalmente negligenciadas em estudos dessa natureza, pois se localizam fora de seus tra dicionais domínios conservados, normalmente associados à função principal da proteína. Sít ios apontados estando sob seleção positiva e relaxamento da restrição seletiva mostraram-se hotspots importantes para mudanças que podem impactar na capacidade de interação das proteínas. Encontramos que os maiores valores de w são mais prevalentes em regiões desordenadas que em ordenadas. Ainda, alto e similar valor de desordem (70%) foi encontrado nas 77 proteínas ortólogas de FOXPl , FOXP2, e FOXP4, indicando a manutenção de um "padrão geral" sobre um longo tempo evolutivo. Portanto, a variabilidade tanto de aminoácidos quanto de motivos lineares dentro das regiões de desordem foi marcante. A proteína FOXP3 apresentou menor nível de desordem (30%), mas signif icante sinal de seleção positiva em alguns sítios. Composição idênt ica de resíduo de aminoácido e/ou motivos lineares em espécies filogeneticamente distantes, indica clara convergência molecular, provavelmente associada a pressões seletivas similares. Sucessivamente, nossos achados mostraram uma clara diferença na composição de motivos lineares entre mamíferos e não mamíferos, dando suporte para a importância dos estudos de evolução da interatividade proteica para as compreensões de características taxa-específicas.

Forkhead Family P (FOXP) has been target of many studies about brain and behavior evo lution among species. FOXP2 receives special attention in academic society, due associations with vocalízation evolution in mammals, including Homo sapiens. Recently, intrinsically disorder proteins studies have gained emphasis in the evolutionary context, as positive correlation between disorder regions and higher evolutionary rate has been observed. Through a set of approaches, including disorder and linear motif predictions, as well as estimate evolutionary rates, we aimed to unveil the evolutionary history of FOXP subfamily genes. We focused our ana lysis over disordered regions of FOXPl, FOXP2, FOXP3 and FOXP4 proteins retrieved in 77 tetrapods. Such protein regions…

Advisors/Committee Members: Bau, Claiton Henrique Dotto.

Subjects/Keywords: lntrinsica lly disordered protein; Evolução molecular; Molecular evolution; Tetrapodes; Linear motifs; Forkhead domain; FOXP gene family

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Viscardi, L. H. (2015). História evolutiva da subfamília FOXP : análise evolutiva molecular e estrutural em tetrápodes. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/150633

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Viscardi, Lucas Henriques. “História evolutiva da subfamília FOXP : análise evolutiva molecular e estrutural em tetrápodes.” 2015. Thesis, Universidade do Rio Grande do Sul. Accessed February 28, 2021. http://hdl.handle.net/10183/150633.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Viscardi, Lucas Henriques. “História evolutiva da subfamília FOXP : análise evolutiva molecular e estrutural em tetrápodes.” 2015. Web. 28 Feb 2021.

Vancouver:

Viscardi LH. História evolutiva da subfamília FOXP : análise evolutiva molecular e estrutural em tetrápodes. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2015. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10183/150633.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Viscardi LH. História evolutiva da subfamília FOXP : análise evolutiva molecular e estrutural em tetrápodes. [Thesis]. Universidade do Rio Grande do Sul; 2015. Available from: http://hdl.handle.net/10183/150633

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Kyoto University / 京都大学

30. Kakimoto, Yu. Sorbin and SH3 Domain-containing Protein 2 Is Released from Infarcted Heart in Very Early Phase: Proteomic Analysis of Cardiac Tissues from Patients : SORBS2は超急性期の梗塞心筋から逸脱する : 患者心臓組織を用いたプロテオーム解析.

Degree: 博士(医学), 2014, Kyoto University / 京都大学

URL: http://hdl.handle.net/2433/188650 ; http://dx.doi.org/10.14989/doctor.k18138

新制・課程博士

甲第18138号

医博第3858号

Subjects/Keywords: Acute Myocardial Infarction; Proteomics; Sorbin and SH3 Domain-containing Protein 2; Postmortem Diagnosis; Human Tissue

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kakimoto, Y. (2014). Sorbin and SH3 Domain-containing Protein 2 Is Released from Infarcted Heart in Very Early Phase: Proteomic Analysis of Cardiac Tissues from Patients : SORBS2は超急性期の梗塞心筋から逸脱する : 患者心臓組織を用いたプロテオーム解析. (Thesis). Kyoto University / 京都大学. Retrieved from http://hdl.handle.net/2433/188650 ; http://dx.doi.org/10.14989/doctor.k18138

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kakimoto, Yu. “Sorbin and SH3 Domain-containing Protein 2 Is Released from Infarcted Heart in Very Early Phase: Proteomic Analysis of Cardiac Tissues from Patients : SORBS2は超急性期の梗塞心筋から逸脱する : 患者心臓組織を用いたプロテオーム解析.” 2014. Thesis, Kyoto University / 京都大学. Accessed February 28, 2021. http://hdl.handle.net/2433/188650 ; http://dx.doi.org/10.14989/doctor.k18138.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kakimoto, Yu. “Sorbin and SH3 Domain-containing Protein 2 Is Released from Infarcted Heart in Very Early Phase: Proteomic Analysis of Cardiac Tissues from Patients : SORBS2は超急性期の梗塞心筋から逸脱する : 患者心臓組織を用いたプロテオーム解析.” 2014. Web. 28 Feb 2021.

Vancouver:

Kakimoto Y. Sorbin and SH3 Domain-containing Protein 2 Is Released from Infarcted Heart in Very Early Phase: Proteomic Analysis of Cardiac Tissues from Patients : SORBS2は超急性期の梗塞心筋から逸脱する : 患者心臓組織を用いたプロテオーム解析. [Internet] [Thesis]. Kyoto University / 京都大学; 2014. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2433/188650 ; http://dx.doi.org/10.14989/doctor.k18138.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kakimoto Y. Sorbin and SH3 Domain-containing Protein 2 Is Released from Infarcted Heart in Very Early Phase: Proteomic Analysis of Cardiac Tissues from Patients : SORBS2は超急性期の梗塞心筋から逸脱する : 患者心臓組織を用いたプロテオーム解析. [Thesis]. Kyoto University / 京都大学; 2014. Available from: http://hdl.handle.net/2433/188650 ; http://dx.doi.org/10.14989/doctor.k18138

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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