subject:(Proto Oncogene Proteins c bcl 2)

University of Missouri – Columbia

1. Balkin, Ethan R., 1978-. Targeted 177 Lu antisense radiotherapy of B-cell non-Hodgkin's lymphoma.

Degree: 2011, University of Missouri – Columbia

URL: https://doi.org/10.32469/10355/14295

► [ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] The B-cell lymphoma/leukemia-2 (bcl-2) proto-oncogene in non-Hodgkin's lymphoma (NHL) is a dominant inhibitor of… (more)

Subjects/Keywords: antisense radiotherapy; B-cell lymphoma-2; peptide nucleic acid; cancer therapy; Lymphomas – Radiotherapy; Antisense nucleic acids – Therapeutic use; Antisense peptides – Therapeutic use; Lutetium – Therapeutic use; Lymphoma, Non-Hodgkin – radiotherapy; Peptide Nucleic Acid – pharmacology; Lutetium – therapeutic use; Molecular Targeted Therapy – methods; Proto-Oncogene Proteins c-bcl-2 – metabolism; Radiotherapy – methods

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

APA (6^th Edition):

Balkin, Ethan R., 1. (2011). Targeted 177 Lu antisense radiotherapy of B-cell non-Hodgkin's lymphoma. (Thesis). University of Missouri – Columbia. Retrieved from https://doi.org/10.32469/10355/14295

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):

Balkin, Ethan R., 1978-. “Targeted 177 Lu antisense radiotherapy of B-cell non-Hodgkin's lymphoma.” 2011. Thesis, University of Missouri – Columbia. Accessed March 07, 2021. https://doi.org/10.32469/10355/14295.

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

MLA Handbook (7^th Edition):

Balkin, Ethan R., 1978-. “Targeted 177 Lu antisense radiotherapy of B-cell non-Hodgkin's lymphoma.” 2011. Web. 07 Mar 2021.

Vancouver:

Balkin, Ethan R. 1. Targeted 177 Lu antisense radiotherapy of B-cell non-Hodgkin's lymphoma. [Internet] [Thesis]. University of Missouri – Columbia; 2011. [cited 2021 Mar 07]. Available from: https://doi.org/10.32469/10355/14295.

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

Council of Science Editors:

Balkin, Ethan R. 1. Targeted 177 Lu antisense radiotherapy of B-cell non-Hodgkin's lymphoma. [Thesis]. University of Missouri – Columbia; 2011. Available from: https://doi.org/10.32469/10355/14295

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

University of Texas Southwestern Medical Center

2. Dospoy, Patrick. Characterizing c-Myc Dependent Lung Cancers.

Degree: 2015, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/4225

► MYC is one of the most commonly deregulated oncogenes in human cancer, including breast, colorectal and lung. While mutations in myc are rare, MYC is… (more)

▼ MYC is one of the most commonly deregulated oncogenes in human cancer, including breast, colorectal and lung. While mutations in myc are rare, MYC is overexpressed and in some cases amplified in these (and other) cancers. Recent reports demonstrate the utility of various drugs in selectively targeting MYC-driven cancers. However, given the lack of consistency across tissue types, particularly lung cancer, a multimodal approach to delineate MYC-dependent lung cancers is required. My goal is to characterize MYC deregulation in lung cancer, investigate the degree of differential dependence on MYC in lung cancer, and to elucidate the mechanism for resistance to MYC inhibition. A large panel of clinically and molecularly annotated NSCLC lines was investigated for MYC mRNA, protein expression, and DNA copy number. In addition, publically available databases were interrogated to characterize the degree of MYC deregulation in lung cancer. Functional tests were performed on a large panel of NSCLC cell lines (n = 83) using four drugs that were recently shown to selectively target MYC-driven cancers. Further, we utilized the dominant negative mini-protein OMOMYC for functional classification. In all cases, drug effects were monitored by colony forming efficiency (CFE) assays. OMOMYC results were confirmed via xenograft experiments. Each of the four MYC inhibitors tested elicited a variable response in a subset of the 83 NSCLC cell lines, though the sensitive subset was not similar between any two drugs (highest correlation coefficient of 0.24). In order to determine which, if any, of the drugs targeted MYC-driven lung cancers, we stably expressed OMOMYC in a subset of the NSCLC cell line panel and performed functional assays. Most of the cell lines were sensitive to OMOMYC (with up to 100 fold reduction in CFE), compared to 3/8 that were totally resistant. The variability in the presence of OMOMYC showed a significant correlation with one of the four MYC inhibitors tested. These results support the idea that this sensitive subset represents a truly MYC-dependent class of lung cancers. Surprisingly, there was no correlation between MYC dependence and either MYC mRNA, protein expression or DNA copy number. OMOMYC levels were normalized in all cell lines tested and quantified using qRT-PCR. Additionally, in all cases, exogenous OMOMYC expression led to down regulation of MYC target genes as measured by both qRT-PCR and microarray. These data could be interpreted to suggest that the observed phenotype was the result of decreased MYC activity. Last, the NSCLC probed with OMOMYC showed a variable response in the Wnt pathway, with some cell lines showing a dramatic activation of the Wnt pathway upon OMOMYC induction. This activation proved to be functionally important, as dual inhibition of β-catenin and MYC proved more effective than either approach alone. To investigate the clinical significance of this approach, a subset of the original panel of NSCLC (n = 15) was screened with the MYC inhibitor 10058-F4, Wnt… Advisors/Committee Members: Scaglioni, Pier Paolo, Shay, Jerry W., White, Michael A., Minna, John D..

Subjects/Keywords: Lung Neoplasms; Peptide Fragments; Proto-Oncogene Proteins c-myc

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

APA (6^th Edition):

Dospoy, P. (2015). Characterizing c-Myc Dependent Lung Cancers. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/4225

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):

Dospoy, Patrick. “Characterizing c-Myc Dependent Lung Cancers.” 2015. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/4225.

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

MLA Handbook (7^th Edition):

Dospoy, Patrick. “Characterizing c-Myc Dependent Lung Cancers.” 2015. Web. 07 Mar 2021.

Vancouver:

Dospoy P. Characterizing c-Myc Dependent Lung Cancers. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2015. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/4225.

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

Council of Science Editors:

Dospoy P. Characterizing c-Myc Dependent Lung Cancers. [Thesis]. University of Texas Southwestern Medical Center; 2015. Available from: http://hdl.handle.net/2152.5/4225

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

University of Texas Southwestern Medical Center

3. Yu, Bingke. Structural and Mechanistic Studies of Two Regulatory Factors in Actin Cytoskeletal Signaling: Vav and VopL.

Degree: 2011, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/960

► Proper control of actin cytoskeletal dynamics is essential for cell survival. The goals of my thesis work have been to characterize the structural and biophysical… (more)

▼ Proper control of actin cytoskeletal dynamics is essential for cell survival. The goals of my thesis work have been to characterize the structural and biophysical properties of two regulatory proteins in actin cytoskeletal rearrangement pathway: Vav and Vibrio outer protein L (VopL). Vav proteins are guanine nucleotide exchange factors for Rho family GTPases. They play key roles in actin regulatory pathways and control diverse cellular processes like T cell maturation and activation, cell migration and phagocytosis. They belong to a group of multi-domain signaling proteins which display complex behaviors because of the collective regulation from multiple domains. Previous work has shown that Vav is autoinhibited in the resting state through the cooperative suppression of N-terminal Calponin domain and Acidic region, with the physical mechanism yet to be determined. Here through structural, energetic and biochemical studies, I demonstrate that the Calponin homology domain of Vav binds to the Pleckstrin homology domain, restrains the inhibitory helix in the Acidic region, and shifts the Dbl homology domain - inhibitory helix equilibrium to a more closed state. This construction enables strong suppression and an efficient activation process. The energetic basis of Vav autoinhibition may turn out to be widespread in multi-domain systems. VopL, a pathogenic effector from Vibrio parahaemalyticus, is an actin nucleation factor that induces stress fibers during bacterial infection. It contains three N-terminal Wiskott-Aldrich Homology 2 (WH2) motifs and a unique VopL C-terminal domain (VCD). It potently promotes actin filament nucleation in vitro. However, the physical basis of VopL mediated nucleation has not been understood. Here I performed structural and biochemical studies to investigate the mechanism of actin filament nucleation by VopL. I found that both the WH2 element and VCD are required for VopL activity. The crystal structure of VCD revealed a U-shaped dimer that is stabilized by a terminal coiled-coil. Dimerization of the WH2 motifs as well as contacts between VCD and actin contribute to the nucleation activity of VopL. My studies suggest the formation of a structurally organized actin cluster involving lateral contacts during nucleation. Stabilization of these lateral contacts may be a common feature of actin filament nucleation by WH2-based factors. Advisors/Committee Members: Rosen, Michael K..

Subjects/Keywords: Proto-Oncogene Proteins c-vav; Models, Molecular; Protein Structure, Tertiary

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

APA (6^th Edition):

Yu, B. (2011). Structural and Mechanistic Studies of Two Regulatory Factors in Actin Cytoskeletal Signaling: Vav and VopL. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/960

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):

Yu, Bingke. “Structural and Mechanistic Studies of Two Regulatory Factors in Actin Cytoskeletal Signaling: Vav and VopL.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/960.

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

MLA Handbook (7^th Edition):

Yu, Bingke. “Structural and Mechanistic Studies of Two Regulatory Factors in Actin Cytoskeletal Signaling: Vav and VopL.” 2011. Web. 07 Mar 2021.

Vancouver:

Yu B. Structural and Mechanistic Studies of Two Regulatory Factors in Actin Cytoskeletal Signaling: Vav and VopL. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/960.

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

Council of Science Editors:

Yu B. Structural and Mechanistic Studies of Two Regulatory Factors in Actin Cytoskeletal Signaling: Vav and VopL. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/960

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

4. Estrozi, Bruna. Avaliação anatomoclínica e molecular do melanoma cutâneo em pacientes jovens (idade 18-30 anos).

Degree: PhD, Patologia, 2015, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5144/tde-01042015-144721/ ;

►

A incidência do melanoma cutâneo em pacientes adultos jovens tem aumentado consideravelmente nos últimos anos. Há, contudo, carência de conhecimentos clinicopatológicos e moleculares sobre os… (more)

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A incidência do melanoma cutâneo em pacientes adultos jovens tem aumentado consideravelmente nos últimos anos. Há, contudo, carência de conhecimentos clinicopatológicos e moleculares sobre os melanomas que ocorrem nessa faixa etária. O presente estudo teve por objetivo avaliar 132 casos de melanoma cutâneo primário em pacientes com idade entre 18 e 30 anos, com ênfase no estudo das características clínicas, histopatológicas e avaliação molecular das mutações nos genes BRAF, NRAS e KIT. Em relação aos achados clínicos e histopatológicos, houve predomínio de indivíduos do sexo feminino (61,4%), sendo o tronco o sítio anatômico mais comumente envolvido (44,3%) e o melanoma extensivo superficial o tipo histológico predominante (79,5%). A mutação V600E no gene BRAF (BRAFV600E) foi analisada em 93 casos, utilizando-se a técnica de RT-PCR. Essa mutação foi identificada em 38,7% (36/93) e, estatisticamente, associada à fase vertical de crescimento (p = 0,01), infiltrado inflamatório discreto (p = 0,02) e presença de mitose intradérmica (p = 0,004). Houve, ainda, forte indício de associação com a presença de ulceração (p = 0,05). Todas essas variáveis apresentaram associação com pior prognóstico do melanoma cutâneo. Observou-se predomínio da mutação BRAFV600E em regiões anatômicas relacionadas à exposição solar intermitente. Nenhum caso de melanoma com fenômeno de regressão apresentou mutação BRAFV600E (p < 0,05). Não houve associação significativa entre BRAFV600E e sexo, tipo histológico, nível de Clark, índice de Breslow, elastose solar, invasão angiolinfática e perineural, satelitose, nevo melanocítico coexistente e sobrevida. A pesquisa de mutações NRAS, pela técnica de RT-PCR, detectou frequência de 3,95% (3/76). As três mutações encontradas foram do tipo 61K e ocorreram em pacientes do sexo masculino e em região de cabeça e pescoço. As mutações BRAFV600E e NRAS, quando presentes, eram mutuamente exclusivas. A frequência de mutações KIT, analisadas por sequenciamento, foi de 11,1% (3/27). As três mutações identificadas estavam localizadas no éxon 9 (G510, G498S e 489I). Houve concomitância de casos com mutação KIT tanto com NRAS, como com BRAFV600E. Devido ao pequeno número de casos com mutação em KIT e NRAS, não foi possível estabelecer correlações clínicas e histopatológicas com esses genes. Este estudo é o primeiro a descrever as mutações G510D e G498S no gene KIT em melanomas cutâneos. No presente estudo, a mutação BRAFV600E, em melanomas cutâneos de adultos jovens, correlacionou-se com características anatomoclínicas de pior prognóstico em relação aos melanomas selvagens para BRAFV600E

The incidence of cutaneous melanoma in young adults has dramatically increased in recent years. However, there is scarce data about the clinicopathological and molecular characteristics on the melanomas occurring at this age group. The present study aimed to evaluate 132 patients aged between 18 and 30 years with primary cutaneous melanoma with emphasis on the study of clinical, histopathological characteristics and molecular…

Advisors/Committee Members: Bacchi, Carlos Eduardo.

Subjects/Keywords: Adulto jovem; Melanoma; Melanoma; Neoplasias cutâneas; Proteínas proto-oncogênicas B-raf; Proteínas proto-oncogênicas c-kit; Proteínas proto-oncogênicas p21(ras); Proto-oncogene proteins B-raf; Proto-oncogene proteins c-kit; Proto-oncogene proteins p21(ras); Skin neoplasms; Younf adult

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

APA (6^th Edition):

Estrozi, B. (2015). Avaliação anatomoclínica e molecular do melanoma cutâneo em pacientes jovens (idade 18-30 anos). (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5144/tde-01042015-144721/ ;

Chicago Manual of Style (16^th Edition):

Estrozi, Bruna. “Avaliação anatomoclínica e molecular do melanoma cutâneo em pacientes jovens (idade 18-30 anos).” 2015. Doctoral Dissertation, University of São Paulo. Accessed March 07, 2021. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-01042015-144721/ ;.

MLA Handbook (7^th Edition):

Estrozi, Bruna. “Avaliação anatomoclínica e molecular do melanoma cutâneo em pacientes jovens (idade 18-30 anos).” 2015. Web. 07 Mar 2021.

Vancouver:

Estrozi B. Avaliação anatomoclínica e molecular do melanoma cutâneo em pacientes jovens (idade 18-30 anos). [Internet] [Doctoral dissertation]. University of São Paulo; 2015. [cited 2021 Mar 07]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5144/tde-01042015-144721/ ;.

Council of Science Editors:

Estrozi B. Avaliação anatomoclínica e molecular do melanoma cutâneo em pacientes jovens (idade 18-30 anos). [Doctoral Dissertation]. University of São Paulo; 2015. Available from: http://www.teses.usp.br/teses/disponiveis/5/5144/tde-01042015-144721/ ;

5. 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 March 07, 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. 07 Mar 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 Mar 07]. 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

University of Oulu

6. Jääskeläinen, M. (Minna). Apoptosis-regulating factors in developing and adult ovaries.

Degree: 2010, University of Oulu

URL: http://urn.fi/urn:isbn:9789514263477

► Abstract Apoptosis plays a crucial part in human ovarian function from fetal development to the end of reproductive potential. Failures in the regulation of ovarian… (more)

▼ Abstract Apoptosis plays a crucial part in human ovarian function from fetal development to the end of reproductive potential. Failures in the regulation of ovarian apoptosis are associated with many pathological conditions such as premature ovarian insufficiency, infertility and cancer. The purpose of the present study was to analyze the factors regulating cell survival in human fetal and adult ovaries. The fetus is exposed to maternal- and placental-derived estrogens and insufficient estrogen action has destructive effects on rodent ovarian development. We detected estrogen receptors and estrogen-converting enzymes in human fetal ovaries after primordial follicle formation, indicating that estrogens participate in human fetal ovarian development, especially after folliculogenesis. The WNT4 gene is crucial for female sexual differentiation, follicle formation and oocyte survival. We detected WNT4 in follicular cells of fetal and adult human ovaries. In addition, Wnt4- knockout mice demonstrated a dramatic loss of oocytes before birth. However, no changes were detected in protein expression patterns of common apoptosis-related proteins. The results support the possible role of WNT4 in human ovarian function and strengthen previous knowledge on the antiapoptotic role of Wnt4. Apoptosis signaling is mediated by extracellular- and mitochondria-associated- pathways, ending in caspase cascade activation and fragmentation of cellular structures. In the present study we analyzed the expression of several apoptosis-related factors and detected TRAIL, TNF, Bcl-XL, Bok and caspase-3 in human ovaries. In addition, TRAIL was found to be a potent and rapid inducer of human granulosa tumor cell (KGN) apoptosis. Lentiviral downregulation of Bok or Bcl-XL protein expression in KGN cells also resulted in significant changes in cell vulnerability to apoptosis. The results show for the first time the spatiotemporal expression patterns of TRAIL, TNF, Bcl-XL, Bok and caspase-3 in human ovaries and suggest an important functional role of TRAIL, Bok and Bcl-XL in regulation of human ovarian apoptosis. The present study offers novel information on the expression and function of cell survival factors in human ovaries. These new findings open possibilities for future clinical research in attempts to understand and treat ovarian diseases caused by imbalanced regulatory pathways of apoptosis. Advisors/Committee Members: Vaskivuo, T. (Tommi), Tapanainen, J. (Juha).

Subjects/Keywords: TNF-related apoptosis-inducing ligand; Wnt proteins; apoptosis; caspase 3; estrogens; granulosa cells; oocytes; ovary; proto-oncogen proteins c-Bcl-2; tumor necrosis factor- alpha

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

APA (6^th Edition):

Jääskeläinen, M. (. (2010). Apoptosis-regulating factors in developing and adult ovaries. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789514263477

Chicago Manual of Style (16^th Edition):

Jääskeläinen, M (Minna). “Apoptosis-regulating factors in developing and adult ovaries.” 2010. Doctoral Dissertation, University of Oulu. Accessed March 07, 2021. http://urn.fi/urn:isbn:9789514263477.

MLA Handbook (7^th Edition):

Jääskeläinen, M (Minna). “Apoptosis-regulating factors in developing and adult ovaries.” 2010. Web. 07 Mar 2021.

Vancouver:

Jääskeläinen M(. Apoptosis-regulating factors in developing and adult ovaries. [Internet] [Doctoral dissertation]. University of Oulu; 2010. [cited 2021 Mar 07]. Available from: http://urn.fi/urn:isbn:9789514263477.

Council of Science Editors:

Jääskeläinen M(. Apoptosis-regulating factors in developing and adult ovaries. [Doctoral Dissertation]. University of Oulu; 2010. Available from: http://urn.fi/urn:isbn:9789514263477

7. Oliveira Filho, João Bosco de. Mutação em NRAS causa uma síndrome autoimune linfoproliferativa humana.

Degree: PhD, Patologia, 2008, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5144/tde-04112008-174252/ ;

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A subfamília p21 RAS de pequenas GTPases, incluindo KRAS, HRAS e NRAS, participa de muitas redes de sinalização, incluindo proliferação celular, organização do citoesqueleto e… (more)

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A subfamília p21 RAS de pequenas GTPases, incluindo KRAS, HRAS e NRAS, participa de muitas redes de sinalização, incluindo proliferação celular, organização do citoesqueleto e apoptose, e é o alvo mais freqüente de mutações ativadoras em câncer. Mutações germinativas em KRAS e HRAS causam graves anormalidades desenvolvimentais levando às síndromes de Noonan, cárdio-facial-cutânea e Costello, porem mutações ativadoras germinativas em NRAS não foram descritas até hoje. A síndrome autoimune linfoproliferativa (ALPS) é o mais comum defeito genético de apoptose linfocitária, cursando com autoimunidade e acúmulo excessivo de linfócitos, particularmente do tipo T + CD4- CD8-. As mutações causadoras de ALPS descritas até hoje afetam a apoptose mediada por Fas, uma das vias extrínsecas de apoptose. Nós demonstramos aqui que os principais achados clínicos de ALPS, bem como uma predisposição para tumores hematológicos, podem ser causados por uma mutação heterozigota ativadora G13D no oncogene NRAS, sem causar prejuízo na apoptose mediada por Fas. O aumento na quantidade intracelular de NRAS ativo, ligado a GTP, induziu a um aumento da sinalização na via RAF/MEK/ERK, o que suprimiu a expressão da proteína pró-apoptótica BIM, e atenuou a apoptose intrínseca mitocondrial. Desta forma, uma mutação germinativa ativadora em NRAS causou um fenótipo clinico diferente do visto em pacientes com mutações em outros membros da família p21 RAS, cursando com um defeito imunológico seletivo, sem distúrbios generalizados do desenvolvimento

The p21 RAS subfamily of small GTPases, including KRAS, HRAS, and NRAS, regulates cell proliferation, cytoskeletal organization and other signaling networks, and is the most frequent target of activating mutations in cancer. Activating germline mutations of KRAS and HRAS cause severe developmental abnormalities leading to Noonan, cardio-facial-cutaneous and Costello syndrome, but activating germline mutations of NRAS have not been reported. Autoimmune lymphoproliferative syndrome (ALPS) is the most common genetic disease of lymphocyte apoptosis and causes autoimmunity as well as excessive lymphocyte accumulation, particularly of CD4-, CD8- ab T cells. Mutations in ALPS typically affect Fas-mediated apoptosis, but certain ALPS individuals have no such mutations. We show here that the salient features of ALPS as well as a predisposition to hematological malignancies can be caused by a heterozygous germline Gly13Asp activating mutation of the NRAS oncogene that does not impair Fas-mediated apoptosis. The increase in active, GTP-bound NRAS augmented RAF/MEK/ERK signaling which markedly decreased the pro-apoptotic protein BIM and attenuated intrinsic, nonreceptor-mediated mitochondrial apoptosis. Thus, germline activating mutations in NRAS differ from other p21 Ras oncoproteins by causing selective immune abnormalities without general developmental defects

Advisors/Committee Members: Duarte, Alberto Jose da Silva.

Subjects/Keywords: Apoptose; Apoptosis; Autoimmunity; Autoimunidade; BCL-2 -like protein 11; BIM; Mitogen activated protein kinase kinases; Proteínas proto-oncogênicas p21 (ras); Proto-oncogene proteins p21 (ras); Quinases de proteína quinase ativadas por mitógeno

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

APA (6^th Edition):

Oliveira Filho, J. B. d. (2008). Mutação em NRAS causa uma síndrome autoimune linfoproliferativa humana. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5144/tde-04112008-174252/ ;

Chicago Manual of Style (16^th Edition):

Oliveira Filho, João Bosco de. “Mutação em NRAS causa uma síndrome autoimune linfoproliferativa humana.” 2008. Doctoral Dissertation, University of São Paulo. Accessed March 07, 2021. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-04112008-174252/ ;.

MLA Handbook (7^th Edition):

Oliveira Filho, João Bosco de. “Mutação em NRAS causa uma síndrome autoimune linfoproliferativa humana.” 2008. Web. 07 Mar 2021.

Vancouver:

Oliveira Filho JBd. Mutação em NRAS causa uma síndrome autoimune linfoproliferativa humana. [Internet] [Doctoral dissertation]. University of São Paulo; 2008. [cited 2021 Mar 07]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5144/tde-04112008-174252/ ;.

Council of Science Editors:

Oliveira Filho JBd. Mutação em NRAS causa uma síndrome autoimune linfoproliferativa humana. [Doctoral Dissertation]. University of São Paulo; 2008. Available from: http://www.teses.usp.br/teses/disponiveis/5/5144/tde-04112008-174252/ ;

8. Liphaus, Bernadete de Lourdes. "Expressão das proteínas Fas e Bcl-2 em células mononucleares de crianças e adolescentes com lúpus eritematoso sistêmico".

Degree: PhD, Pediatria, 2005, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5141/tde-16022006-162336/ ;

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Para verificar a expressão das proteínas Fas e Bcl-2 em linfócitos e suas correlações com a atividade da doença foram avaliados 38 pacientes com lúpus… (more)

Subjects/Keywords: ADOLESCENT; ADOLESCENTE; ANTÍGENOS CD95; ANTIGENS CD95; APOPTOSE; APOPTOSIS; AUTO-IMUNIDADE; AUTOIMMUNITY; CHILD; CITOMETRIA DE FLUXO; CRIANÇA; FLOW CYTOMETRY; ÍNDICE DE GRAVIDADE DE DOENÇA; LÚPUS ERITEMATOSO SISTÊMICO/fisiopatologia; LUPUS ERYTHEMATOSUS SYSTEMIC/physiopathology; PROTEÍNAS PROTO-ONCOGÊNICAS C-BCL-2; PROTO-ONCOGENE PROTEINS c-bcl-2; SEVERITY OF ILLNESS INDEX

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

APA (6^th Edition):

Liphaus, B. d. L. (2005). "Expressão das proteínas Fas e Bcl-2 em células mononucleares de crianças e adolescentes com lúpus eritematoso sistêmico". (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5141/tde-16022006-162336/ ;

Chicago Manual of Style (16^th Edition):

Liphaus, Bernadete de Lourdes. “"Expressão das proteínas Fas e Bcl-2 em células mononucleares de crianças e adolescentes com lúpus eritematoso sistêmico".” 2005. Doctoral Dissertation, University of São Paulo. Accessed March 07, 2021. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-16022006-162336/ ;.

MLA Handbook (7^th Edition):

Liphaus, Bernadete de Lourdes. “"Expressão das proteínas Fas e Bcl-2 em células mononucleares de crianças e adolescentes com lúpus eritematoso sistêmico".” 2005. Web. 07 Mar 2021.

Vancouver:

Liphaus BdL. "Expressão das proteínas Fas e Bcl-2 em células mononucleares de crianças e adolescentes com lúpus eritematoso sistêmico". [Internet] [Doctoral dissertation]. University of São Paulo; 2005. [cited 2021 Mar 07]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5141/tde-16022006-162336/ ;.

Council of Science Editors:

Liphaus BdL. "Expressão das proteínas Fas e Bcl-2 em células mononucleares de crianças e adolescentes com lúpus eritematoso sistêmico". [Doctoral Dissertation]. University of São Paulo; 2005. Available from: http://www.teses.usp.br/teses/disponiveis/5/5141/tde-16022006-162336/ ;

University of Texas Southwestern Medical Center

9. Zhou, Huanyu. Molecular Regulation of Direct Cardiac Reprogramming.

Degree: 2017, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/7208

► A heart attack (also known as myocardial infarction, MI) happens when the flow of blood to the heart is blocked. A massive heart attack can… (more)

▼ A heart attack (also known as myocardial infarction, MI) happens when the flow of blood to the heart is blocked. A massive heart attack can kill billions of cardiomyocytes. The heart has limited regenerative potential because adult mammalian cardiomyocytes cannot proliferate, therefore lost cardiomyocytes cannot be replaced. This causes permanent heart damage and results in decreased contraction properties to a large portion of the heart muscle. Therapeutic treatments for heart attack patients have improved dramatically over the past decades. However, due to the inability to replenish lost cardiomyocytes, heart failure is still the primary cause of death in the world. Cardiac fibroblasts (CFs) constitute ~50% of the cells in the heart and form scar tissue following heart injury. Reprogramming CFs to induced-cardiomyocytes (iCMs) by forced expression of cardiac specific transcription factors holds promise for enhancing cardiac repair by reducing scar tissue while simultaneously generating new cardiomyocytes. However, low efficiency as well as a lack of understanding of molecular mechanism of the reprogramming process have significantly hampered its clinical application. The two goals of my PhD study were 1) to optimize the cardiac reprogramming protocol by increasing the efficiency; and 2) to decipher molecular mechanisms of cardiac reprogramming using the information obtained from the optimization process. To improve the efficiency of reprogramming fibroblasts to iCMs by cardiac transcription factors [Gata4, Hand2, Mef2c, and Tbx5 (GHMT)], we screened 192 protein kinases and discovered that Akt/protein kinase B dramatically accelerates and amplifies this process in three different types of fibroblasts (mouse embryo, adult cardiac, and tail tip). Approximately 50% of the reprogrammed mouse embryo fibroblasts displayed spontaneous beating after 3 weeks of induction by AKT1 plus GHMT (AGHMT). Furthermore, AGHMT evoked a more mature cardiac phenotype for iCMs, as seen by enhanced polynucleation, cellular hypertrophy, gene expression, and metabolic reprogramming. Insulin-like growth factor 1 (IGF1) and phosphoinositol 3-kinase (PI3K) acted upstream of AKT1 whereas the mitochondrial target of rapamycin complex 1 (mTORC1) and forkhead box o3a (Foxo3a) acted downstream of AKT1 to influence fibroblast-to-cardiomyocyte reprogramming. Addition of AGHMT converted 50% of mouse embryo fibroblasts to beating cardiomyocytes. However, only 1% of adult fibroblasts displayed spontaneous beating after three weeks of induction by AGHMT. This indicates that there are "barriers" in adult fibroblasts that hinder cardiac reprogramming. We continued to optimize methods for reprogramming fibroblasts to cardiomyocytes in vitro and in vivo. To identify additional regulators of this reprogramming process, we carried out an unbiased screen of ~1,100 open reading frames (ORFs) encoding transcription factors and cytokines for the ability to enhance reprogramming by AGHMT in adult tail-tip fibroblasts (ATTFs). One of the strongest activators of… Advisors/Committee Members: Zhang, Chun-Li, Hill, Joseph A., Cleaver, Ondine, Olson, Eric N..

Subjects/Keywords: Cellular Reprogramming; Fibroblasts; Myocytes, Cardiac; Proto-Oncogene Proteins c-akt; Transcription, Genetic

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

APA (6^th Edition):

Zhou, H. (2017). Molecular Regulation of Direct Cardiac Reprogramming. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/7208

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):

Zhou, Huanyu. “Molecular Regulation of Direct Cardiac Reprogramming.” 2017. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/7208.

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

MLA Handbook (7^th Edition):

Zhou, Huanyu. “Molecular Regulation of Direct Cardiac Reprogramming.” 2017. Web. 07 Mar 2021.

Vancouver:

Zhou H. Molecular Regulation of Direct Cardiac Reprogramming. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2017. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/7208.

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

Council of Science Editors:

Zhou H. Molecular Regulation of Direct Cardiac Reprogramming. [Thesis]. University of Texas Southwestern Medical Center; 2017. Available from: http://hdl.handle.net/2152.5/7208

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

University of Texas Southwestern Medical Center

10. Ou, Yi-Hung 1977-. Molecular Mechanisms Underlying Innate Immune Kinase TBK1-Driven Oncogenic Transformation.

Degree: 2013, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/ETD-UTSWMED-2013-05-125

► An essential kinase in innate immune signaling, TBK1 couples pathogen surveillance to induction of host defense mechanisms. The pathological activation of TBK1 in cancer can… (more)

▼ An essential kinase in innate immune signaling, TBK1 couples pathogen surveillance to induction of host defense mechanisms. The pathological activation of TBK1 in cancer can overcome programmed cell death cues, enabling cells to survive oncogenic stress. The mechanistic basis of TBK1 prosurvival signaling, however, has been enigmatic. Here we show that TBK1 directly activates AKT by phosphorylation of the canonical activation loop and hydrophobic motif sites independently of PDK1 and mTORC2. A population of AKT is bound to components of the exocyst complex. Upon mitogen stimulation, triggering of the innate immune response, re-exposure to glucose, or oncogene activation, TBK1 is recruited to the exocyst, where it activates AKT. In cells lacking TBK1, insulin activates AKT normally, but AKT activation by these exocyst-dependent mechanisms is impaired. Discovery and characterization of a 6-aminopyrazolopyrimidine derivative, as a selective low nanomolar TBK1 inhibitor, indicates this regulatory arm can be pharmacologically perturbed independently of canonical PI3K/PDK1 signaling. Thus, AKT is a direct TBK1 substrate that connects TBK1 to prosurvival signaling. Additionally, biochemical and cell biological evidence indicates critical roles of TBK1 and its analog IKKε in the amino acid-dependent activation of mTORC1. TBK1 and IKKε are activated by amino acids and both proteins interact with mTORC1. In TBK1 and/or IKKε-deficient cells, mTORC1 activation by amino acids is impaired. Of note, we also discovered a set of TBK1 substrates and interacting proteins participating in amino acid-dependent mTORC1 signaling. In conclusion, our results suggest that TBK1 not only supports physiological and oncogenic activation of AKT, but also plays a central role in the regulation of mTORC1 activation in response to amino acids. In addition, our studies reveal novel mTORC1 components and provide new insights into the regulation of the mTORC1 signaling network. Advisors/Committee Members: Lum, Lawrence, White, Michael A., Cobb, Melanie H., Minna, John D..

Subjects/Keywords: Immunity, Innate; Neoplasms; Protein-Serine-Threonine Kinases; Proto-Oncogene Proteins c-akt

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

APA (6^th Edition):

Ou, Y. 1. (2013). Molecular Mechanisms Underlying Innate Immune Kinase TBK1-Driven Oncogenic Transformation. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/ETD-UTSWMED-2013-05-125

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):

Ou, Yi-Hung 1977-. “Molecular Mechanisms Underlying Innate Immune Kinase TBK1-Driven Oncogenic Transformation.” 2013. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/ETD-UTSWMED-2013-05-125.

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

MLA Handbook (7^th Edition):

Ou, Yi-Hung 1977-. “Molecular Mechanisms Underlying Innate Immune Kinase TBK1-Driven Oncogenic Transformation.” 2013. Web. 07 Mar 2021.

Vancouver:

Ou Y1. Molecular Mechanisms Underlying Innate Immune Kinase TBK1-Driven Oncogenic Transformation. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2013. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/ETD-UTSWMED-2013-05-125.

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

Council of Science Editors:

Ou Y1. Molecular Mechanisms Underlying Innate Immune Kinase TBK1-Driven Oncogenic Transformation. [Thesis]. University of Texas Southwestern Medical Center; 2013. Available from: http://hdl.handle.net/2152.5/ETD-UTSWMED-2013-05-125

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

University of Texas Southwestern Medical Center

11. Bulut, Gamze Betul. Ubiquitination of EpoR and p85 in Ligand Induced EpoR Down-Regulation.

Degree: 2014, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/3581

► Erythropoietin (Epo) is the primary cytokine that drives red blood cell production and signals through its receptor, the EpoR, on erythroid progenitor cells. Epo binding… (more)

▼ Erythropoietin (Epo) is the primary cytokine that drives red blood cell production and signals through its receptor, the EpoR, on erythroid progenitor cells. Epo binding to EpoR activates Janus kinase 2 (JAK2), which phosphorylates cytoplasmic tyrosines of the EpoR. Signaling proteins bind these phosphotyrosines through SH2 domains, leading to the survival and proliferation of erythroid progenitor cells and the differentiation of these progenitors into mature erythrocytes. Therefore, EpoR signaling is essential for red blood cell production. To maintain physiologic numbers of circulating red blood cells EpoR signaling is also subject to negative regulation. Mutations in EpoR or JAK2 that abrogate negative regulation cause erythrocytosis in hematological malignancies. Primary familial and congenital polycythemia (PFCP) is a proliferative disorder characterized by erythrocytosis and hypersensitivity of erythroid progenitors to Epo. Defects in negative regulation of EpoR signaling contribute to the etiology of PFCP. However, the underlying molecular mechanisms are poorly understood. Here we show that ubiquitination of EpoR controls internalization, lysosomal sorting, degradation and signaling of the EpoR. Ubiquitination of EpoR at K256 is necessary and sufficient for efficient Epo-induced receptor internalization, while ubiquitination at K428 promotes trafficking of activated receptors to the lysosomes for degradation. Interestingly, EpoR that cannot be ubiquitinated has reduced mitogenic activities and ability to stimulate the downstream signaling pathways. We propose that ubiquitination of the EpoR critically controls both receptor down-regulation and signaling. Secondly, we identified a novel mechanism mediating Epo-dependent EpoR internalization. Epo induces Cbl-dependent ubiquitination of the p85, which binds to phosphotyrosines on EpoR. Ubiquitination allows p85 to interact with epsin-1, thereby driving EpoR endocytosis. Knockdown of Cbl, expression of its dominant negative forms, or expression of an epsin-1 mutant all compromise Epo-induced EpoR internalization. Mutated EpoRs mimicking those from PFCP patients cannot bind p85, co-localize with epsin-1, nor internalize upon Epo stimulation and exhibit Epo hypersensitivity. Restoring p85 binding to PFCP receptors rescues Epo-induced epsin-1 co-localization, EpoR internalization, and normalizes Epo hypersensitivity. Our results uncover the role of EpoR ubiquitination and a novel Cbl/p85/epsin-1 pathway in EpoR endocytosis and show that defects in this pathway contribute to excessive Epo signaling and erythroid hyperproliferation in PFCP. Advisors/Committee Members: Yin, Helen L., Huang, Lily, Zhang, Chengcheng "Alec", Seemann, Joachim.

Subjects/Keywords: Class Ia Phosphatidylinositol 3-Kinase; Endocytosis; Erythropoietin; Proto-Oncogene Proteins c-cbl; Receptors, Erythropoietin

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

APA (6^th Edition):

Bulut, G. B. (2014). Ubiquitination of EpoR and p85 in Ligand Induced EpoR Down-Regulation. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/3581

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):

Bulut, Gamze Betul. “Ubiquitination of EpoR and p85 in Ligand Induced EpoR Down-Regulation.” 2014. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/3581.

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

MLA Handbook (7^th Edition):

Bulut, Gamze Betul. “Ubiquitination of EpoR and p85 in Ligand Induced EpoR Down-Regulation.” 2014. Web. 07 Mar 2021.

Vancouver:

Bulut GB. Ubiquitination of EpoR and p85 in Ligand Induced EpoR Down-Regulation. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2014. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/3581.

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

Council of Science Editors:

Bulut GB. Ubiquitination of EpoR and p85 in Ligand Induced EpoR Down-Regulation. [Thesis]. University of Texas Southwestern Medical Center; 2014. Available from: http://hdl.handle.net/2152.5/3581

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

Universidade do Rio Grande do Sul

12. Espindola, Marilia Bittencourt. Expressão imunoistoquímica da proteína bcl-2 em metástases de melanoma cutâneo e relação com a sobrevida.

Degree: 2007, Universidade do Rio Grande do Sul

URL: http://hdl.handle.net/10183/11425

► A morte celular programada (apoptose) tem sido implicada no desenvolvimento tumoral e no potencial metastático. O Bcl-2, um proto-oncogene inibidor da apoptose, vem sendo estudado… (more)

Subjects/Keywords: Melanoma; Neoplasias cutâneas; Sobrevida; Metástase neoplásica; Oncogenes; Proteínas proto-oncogênicas c-bcl-2

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

APA (6^th Edition):

Espindola, M. B. (2007). Expressão imunoistoquímica da proteína bcl-2 em metástases de melanoma cutâneo e relação com a sobrevida. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/11425

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):

Espindola, Marilia Bittencourt. “Expressão imunoistoquímica da proteína bcl-2 em metástases de melanoma cutâneo e relação com a sobrevida.” 2007. Thesis, Universidade do Rio Grande do Sul. Accessed March 07, 2021. http://hdl.handle.net/10183/11425.

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

MLA Handbook (7^th Edition):

Espindola, Marilia Bittencourt. “Expressão imunoistoquímica da proteína bcl-2 em metástases de melanoma cutâneo e relação com a sobrevida.” 2007. Web. 07 Mar 2021.

Vancouver:

Espindola MB. Expressão imunoistoquímica da proteína bcl-2 em metástases de melanoma cutâneo e relação com a sobrevida. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2007. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10183/11425.

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

Council of Science Editors:

Espindola MB. Expressão imunoistoquímica da proteína bcl-2 em metástases de melanoma cutâneo e relação com a sobrevida. [Thesis]. Universidade do Rio Grande do Sul; 2007. Available from: http://hdl.handle.net/10183/11425

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

University of Texas Southwestern Medical Center

13. Troutman, Ty Dale. B-Cell Adapter for Phosphoinositide 3-Kinase Is a Signaling Adapter in the Toll-Like Receptor/Interleukin-1 Receptor Superfamily.

Degree: 2014, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/3328

► Toll-like receptor (TLR)/Interleukin-1 receptor (IL1R) superfamily members share signaling components and (with the exception of TLR3) depend on the adapter myeloid differentiation primary response gene… (more)

▼ Toll-like receptor (TLR)/Interleukin-1 receptor (IL1R) superfamily members share signaling components and (with the exception of TLR3) depend on the adapter myeloid differentiation primary response gene 88 (MyD88) for engagement of downstream pathways. Signals from the receptor to the adapter are transmitted through homotypic interaction of TIR (Toll-Interleukin-1 receptor) homology domains found in all TLR/IL1R family members and their adapters. The present work defines a novel TLR/IL1R signaling adapter, termed BCAP (B-cell adapter for PI3K), which was identified based on the presence of a cryptic N-terminal TIR domain. I show here that BCAP (B-cell adapter for PI3K) contains a functional TIR domain enabling its participation in the TLR signaling pathway. Through its TIR domain, BCAP associates with the TLR/IL1R signaling adapter MyD88, as well as the TLR signaling adapter toll-interleukin 1 receptor domain containing adapter protein (TIRAP). Importantly, BCAP plays an obligate role in linking TLRs to activation of phosphoinositide 3-kinase (PI3K) through recruitment of PI3K to the signaling complex and relief of inhibitory influences on PI3K activity. Importantly, BCAP selectively mediates TLR signaling towards the PI3K branch without affecting signaling to NFκB nor MAP kinases. In this capacity, BCAP inhibits secretion of inflammatory cytokines and regulates susceptibility to inflammatory colitis. Because the TLR/IL1R family shares signaling components, BCAP may also function in IL1R family signaling. To test this hypothesis, T cells were chosen as a model cell type responding to IL1R family signals. T helper cells utilize IL18 and IL1 (which engage the IL18R or the IL1R respectively, both IL1R family members) cytokines provided by myeloid cells to achieve optimal Th1 and Th17 effector capacities. I show here that BCAP intrinsically regulates differentiation of naïve T cells towards Th1 and Th17 effector lineages by participation in the IL1R family signaling pathways. Further, BCAP intrinsically regulates both T cell proliferation and survival during priming. The significance of this work lies in the revelation of a TLR signaling adapter serving as a node connecting TLRs to PI3K. Further, the findings here will increase the understanding of key signaling pathways involved in disease and inflammation. Advisors/Committee Members: van Oers, Nicolai S. C., Pasare, Chandrashekhar, Hooper, Lora V., Chen, Zhijian J., Krämer, Helmut.

Subjects/Keywords: Adaptor Proteins, Signal Transducing; B-Lymphocytes; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Signal Transduction; Toll-Like Receptors

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

APA (6^th Edition):

Troutman, T. D. (2014). B-Cell Adapter for Phosphoinositide 3-Kinase Is a Signaling Adapter in the Toll-Like Receptor/Interleukin-1 Receptor Superfamily. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/3328

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):

Troutman, Ty Dale. “B-Cell Adapter for Phosphoinositide 3-Kinase Is a Signaling Adapter in the Toll-Like Receptor/Interleukin-1 Receptor Superfamily.” 2014. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/3328.

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

MLA Handbook (7^th Edition):

Troutman, Ty Dale. “B-Cell Adapter for Phosphoinositide 3-Kinase Is a Signaling Adapter in the Toll-Like Receptor/Interleukin-1 Receptor Superfamily.” 2014. Web. 07 Mar 2021.

Vancouver:

Troutman TD. B-Cell Adapter for Phosphoinositide 3-Kinase Is a Signaling Adapter in the Toll-Like Receptor/Interleukin-1 Receptor Superfamily. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2014. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/3328.

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

Council of Science Editors:

Troutman TD. B-Cell Adapter for Phosphoinositide 3-Kinase Is a Signaling Adapter in the Toll-Like Receptor/Interleukin-1 Receptor Superfamily. [Thesis]. University of Texas Southwestern Medical Center; 2014. Available from: http://hdl.handle.net/2152.5/3328

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

University of Texas Southwestern Medical Center

14. Wu, Nan. Cohesin, the SMC5/6 Complex and SUMO in DNA Repair.

Degree: 2013, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/1259

► DNA double-strand breaks (DSBs) fuel cancer-driving chromosome translocations. Two related structural maintenance of chromosomes (Smc) complexes, cohesin and Smc5/6, promote DSB repair through sister-chromatid homologous… (more)

Subjects/Keywords: Chromatids; Proto-Oncogene Proteins; Recombination, Genetic

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APA (6^th Edition):

Wu, N. (2013). Cohesin, the SMC5/6 Complex and SUMO in DNA Repair. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1259

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):

Wu, Nan. “Cohesin, the SMC5/6 Complex and SUMO in DNA Repair.” 2013. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/1259.

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

MLA Handbook (7^th Edition):

Wu, Nan. “Cohesin, the SMC5/6 Complex and SUMO in DNA Repair.” 2013. Web. 07 Mar 2021.

Vancouver:

Wu N. Cohesin, the SMC5/6 Complex and SUMO in DNA Repair. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2013. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/1259.

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

Council of Science Editors:

Wu N. Cohesin, the SMC5/6 Complex and SUMO in DNA Repair. [Thesis]. University of Texas Southwestern Medical Center; 2013. Available from: http://hdl.handle.net/2152.5/1259

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

University of Florida

15. Guedez, Liliana, 1956-. Differential expression of bcl-2 by hematological tumors anti-apoptosis function and chemotherapy resistance.

Degree: 1995, University of Florida

URL: https://ufdc.ufl.edu/AA00011162

Subjects/Keywords: Apoptosis; Cell cycle; Cell death; Cell growth; Cell lines; Cells; Cytometry; Free radicals; Mice; Tumors; Apoptosis – physiology ( mesh ); Bleomycin – drug effects ( mesh ); Bleomycin – pharmacology ( mesh ); Cytarabine – drug effects ( mesh ); Cytarabine – pharmacology ( mesh ); Drug Resistance, Neoplasm – physiology ( mesh ); Genes, bcl-2 ( mesh ); Hematologic Neoplasms – physiopathology ( mesh ); Proto-Oncogene Proteins c-bcl-2 ( mesh )

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APA (6^th Edition):

Guedez, Liliana, 1. (1995). Differential expression of bcl-2 by hematological tumors anti-apoptosis function and chemotherapy resistance. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00011162

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):

Guedez, Liliana, 1956-. “Differential expression of bcl-2 by hematological tumors anti-apoptosis function and chemotherapy resistance.” 1995. Thesis, University of Florida. Accessed March 07, 2021. https://ufdc.ufl.edu/AA00011162.

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

MLA Handbook (7^th Edition):

Guedez, Liliana, 1956-. “Differential expression of bcl-2 by hematological tumors anti-apoptosis function and chemotherapy resistance.” 1995. Web. 07 Mar 2021.

Vancouver:

Guedez, Liliana 1. Differential expression of bcl-2 by hematological tumors anti-apoptosis function and chemotherapy resistance. [Internet] [Thesis]. University of Florida; 1995. [cited 2021 Mar 07]. Available from: https://ufdc.ufl.edu/AA00011162.

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

Council of Science Editors:

Guedez, Liliana 1. Differential expression of bcl-2 by hematological tumors anti-apoptosis function and chemotherapy resistance. [Thesis]. University of Florida; 1995. Available from: https://ufdc.ufl.edu/AA00011162

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

16. Mendonça, Ullyanov Bezerra Toscano de. Análise de mutações do gene KIT em pacientes com melanoma de mucosa de cabeça e pescoço e relação clínica retrospectiva.

Degree: PhD, Clínica Cirúrgica, 2015, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5132/tde-14122015-114016/ ;

►

Introdução: O melanoma mucoso de cabeça e pescoço (MMCP) é mais agressivo do que o melanoma cutâneo, marcadores prognósticos desta patologia não foram completamente esclarecidos… (more)

▼

Introdução: O melanoma mucoso de cabeça e pescoço (MMCP) é mais agressivo do que o melanoma cutâneo, marcadores prognósticos desta patologia não foram completamente esclarecidos devido a sua raridade. Em recentes estudos, algumas vias moleculares foram descritas na fisiopatologia destes tumores. Entre estas vias, existe a via da MAPK (Mitogen Activated Protein Quinase). Esta via de sinalização está envolvida no controle do crescimento celular, proliferação e migração, com um papel no desenvolvimento e progressão do melanoma. Além disso, a mutação do gene KIT foi identificada em melanomas, indicando a possibilidade de benefícios terapêuticos com o uso dos inibidores de tirosino-quinase. Objetivos: descrever a prevalência e características de mutações ativadoras do gene KIT em 28 pacientes com MMCP tratados no Instituto Nacional do Câncer-INCa; avaliar a relação entre a presença de mutação ativadora do gene KIT e evolução clínica dos pacientes tratados em relação ao estadiamento, sobrevida livre de doença e sobrevida global. Métodos: Estudo retrospectivo de coorte, foram incluídos 28 pacientes com MMCP tratados no INCA, entre 1998 e 2009. Foram analisados: estadiamento, tratamento primário, sobrevida livre de doença (SLD) e sobrevida global (SG). As curvas de sobrevida foram analisados utilizando o método de Kaplan-Meier, com software SPS 11.0. Análise KIT: O DNA foi extraído a partir de tecido incluído e fixado em parafina. O procedimento consiste de múltiplas etapas de desparafinização com xilol. Os restos celulares são precipitados por centrifugação e o DNA, no sobrenadante é utilizado nas reações de PCR (direto ou diluído). A análise mutacional do gene foi realizada utilizando-se a amplificação por PCR seguida pelo sequenciamento genômico. As análises são iniciadas pelo éxon 11, seguidas do éxon 9, 17 e 13. Resultados: Os pacientes eram predominantemente do sexo feminino (57%). A idade de apresentação variou de 27 a 85 anos. A região nasossinusal foi o sítio primário mais frequente (75%). Todos os pacientes foram submetidos a ressecção cirúrgica. Dezessete pacientes receberam radioterapia adjuvante (37%). As recorrências ocorreram em 82% dos pacientes. Presença de mutação de KIT foi encontrada em 7 casos (25%), três no éxon 9, 3 no éxon 11 e 1 no éxon 13. Fatores preditivos de recorrência foram índice mitótico (p = 0,05), invasão vascular (p = 0,043), e a disseminação perineural (p = 0,034). Não houve diferenças significativas na SLD e SG de acordo com a mutação KIT. Conclusão: A presente série incluiu 28 casos tratados. Sete casos (25%) tinham mutações ativadoras KIT. Esta descoberta sugere que existe um grupo de pacientes que poderiam se beneficiar com a terapia-alvo adequado com inibidores de tirosino-quinase

Unlike their cutaneous counterparts, head and neck mucosal malignant melanomas (HNMM) behave much more aggressively and their prognostic markers have not been fully elucidated. In recent studies, some molecular pathways have been found to be involved in the pathogenesis of melanomas. Among these, there…

Advisors/Committee Members: Cernea, Claudio Roberto.

Subjects/Keywords: Buccal mucosa; KIT; KIT; Melanoma; Melanoma; Mucosa bucal; Mucosa nasal; Mutação; Mutation; Nasal mucosa; Proteínas proto-oncogênicas c-kit; Proto-oncogene proteins c-kit

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APA (6^th Edition):

Mendonça, U. B. T. d. (2015). Análise de mutações do gene KIT em pacientes com melanoma de mucosa de cabeça e pescoço e relação clínica retrospectiva. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5132/tde-14122015-114016/ ;

Chicago Manual of Style (16^th Edition):

Mendonça, Ullyanov Bezerra Toscano de. “Análise de mutações do gene KIT em pacientes com melanoma de mucosa de cabeça e pescoço e relação clínica retrospectiva.” 2015. Doctoral Dissertation, University of São Paulo. Accessed March 07, 2021. http://www.teses.usp.br/teses/disponiveis/5/5132/tde-14122015-114016/ ;.

MLA Handbook (7^th Edition):

Mendonça, Ullyanov Bezerra Toscano de. “Análise de mutações do gene KIT em pacientes com melanoma de mucosa de cabeça e pescoço e relação clínica retrospectiva.” 2015. Web. 07 Mar 2021.

Vancouver:

Mendonça UBTd. Análise de mutações do gene KIT em pacientes com melanoma de mucosa de cabeça e pescoço e relação clínica retrospectiva. [Internet] [Doctoral dissertation]. University of São Paulo; 2015. [cited 2021 Mar 07]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5132/tde-14122015-114016/ ;.

Council of Science Editors:

Mendonça UBTd. Análise de mutações do gene KIT em pacientes com melanoma de mucosa de cabeça e pescoço e relação clínica retrospectiva. [Doctoral Dissertation]. University of São Paulo; 2015. Available from: http://www.teses.usp.br/teses/disponiveis/5/5132/tde-14122015-114016/ ;

17. Escamilla-Powers, Julienne Rebeca. Identification of proteins that regulate c-Myc stability and function.

Degree: PhD, 2008, Oregon Health Sciences University

URL: doi:10.6083/M4CR5RB9 ; http://digitalcommons.ohsu.edu/etd/500

Subjects/Keywords: Oncogene Proteins – physiology; Proto-Oncogene Proteins c-myc; Transcriptional Activation; Saccharomyces cerevisiae

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APA (6^th Edition):

Escamilla-Powers, J. R. (2008). Identification of proteins that regulate c-Myc stability and function. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4CR5RB9 ; http://digitalcommons.ohsu.edu/etd/500

Chicago Manual of Style (16^th Edition):

Escamilla-Powers, Julienne Rebeca. “Identification of proteins that regulate c-Myc stability and function.” 2008. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 07, 2021. doi:10.6083/M4CR5RB9 ; http://digitalcommons.ohsu.edu/etd/500.

MLA Handbook (7^th Edition):

Escamilla-Powers, Julienne Rebeca. “Identification of proteins that regulate c-Myc stability and function.” 2008. Web. 07 Mar 2021.

Vancouver:

Escamilla-Powers JR. Identification of proteins that regulate c-Myc stability and function. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 2008. [cited 2021 Mar 07]. Available from: doi:10.6083/M4CR5RB9 ; http://digitalcommons.ohsu.edu/etd/500.

Council of Science Editors:

Escamilla-Powers JR. Identification of proteins that regulate c-Myc stability and function. [Doctoral Dissertation]. Oregon Health Sciences University; 2008. Available from: doi:10.6083/M4CR5RB9 ; http://digitalcommons.ohsu.edu/etd/500

18. Hock, Thomas D. Regulation of the human heme oxygenase-1 gene.

Degree: PhD, 2007, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,126

►

The heme oxygenase-1 (HO-1) gene encodes a microsomal enzyme that catalyzes the conversion of heme to carbon monoxide, Iron, and biliverdin. HO-1 transcription is induced… (more)

Subjects/Keywords: Heme Oxygenase-1 – genetics <; br>; Proto-Oncogene Proteins c-jun – metabolism <; br>; Transcription Factors – metabolism

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APA (6^th Edition):

Hock, T. D. (2007). Regulation of the human heme oxygenase-1 gene. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,126

Chicago Manual of Style (16^th Edition):

Hock, Thomas D. “Regulation of the human heme oxygenase-1 gene.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,126.

MLA Handbook (7^th Edition):

Hock, Thomas D. “Regulation of the human heme oxygenase-1 gene.” 2007. Web. 07 Mar 2021.

Vancouver:

Hock TD. Regulation of the human heme oxygenase-1 gene. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,126.

Council of Science Editors:

Hock TD. Regulation of the human heme oxygenase-1 gene. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,126

19. 竹山, 旭. Expression patterns of CD66a and CD117 in the mouse submandibular gland : CD117 と CD66a による唾液腺上皮細胞の分類.

Degree: 博士（歯学）, 2016, Osaka Dental University / 大阪歯科大学

URL: http://id.nii.ac.jp/1392/00000087/

►

The epithelial tissue of the salivary gland consists of the acinar and ductal parts, the latter of which is further divided into the intercalated, striated… (more)

Subjects/Keywords: Animals; Carcinoembryonic Antigen; Female; Gene Expression Regulation; Mice; Proto-Oncogene Proteins c-kit; Salivary Ducts; Submandibular Gland

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

APA (6^th Edition):

竹山, �. (2016). Expression patterns of CD66a and CD117 in the mouse submandibular gland : CD117 と CD66a による唾液腺上皮細胞の分類. (Thesis). Osaka Dental University / 大阪歯科大学. Retrieved from http://id.nii.ac.jp/1392/00000087/

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):

竹山, 旭. “Expression patterns of CD66a and CD117 in the mouse submandibular gland : CD117 と CD66a による唾液腺上皮細胞の分類.” 2016. Thesis, Osaka Dental University / 大阪歯科大学. Accessed March 07, 2021. http://id.nii.ac.jp/1392/00000087/.

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

MLA Handbook (7^th Edition):

竹山, 旭. “Expression patterns of CD66a and CD117 in the mouse submandibular gland : CD117 と CD66a による唾液腺上皮細胞の分類.” 2016. Web. 07 Mar 2021.

Vancouver:

竹山 �. Expression patterns of CD66a and CD117 in the mouse submandibular gland : CD117 と CD66a による唾液腺上皮細胞の分類. [Internet] [Thesis]. Osaka Dental University / 大阪歯科大学; 2016. [cited 2021 Mar 07]. Available from: http://id.nii.ac.jp/1392/00000087/.

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

Council of Science Editors:

竹山 �. Expression patterns of CD66a and CD117 in the mouse submandibular gland : CD117 と CD66a による唾液腺上皮細胞の分類. [Thesis]. Osaka Dental University / 大阪歯科大学; 2016. Available from: http://id.nii.ac.jp/1392/00000087/

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

20. Carr, Michael I. The Role of MDM2 Phosphorylation in P53 Responses to DNA Damage and Tumor Suppression: A Dissertation.

Degree: Cell Biology, Radiology, 2016, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/847

► The p53 tumor suppressor protein is upregulated in response to DNA damage and other stress signals. The upregulation of p53 involves freeing it from… (more)

▼ The p53 tumor suppressor protein is upregulated in response to DNA damage and other stress signals. The upregulation of p53 involves freeing it from negative regulation imposed by Mdm2 and MdmX (Mdm4). Accumulating evidence indicates that phosphorylation of Mdm proteins by different stress-activated kinases such as ATM or c-Abl significantly impacts p53 functions. We have previously shown that ATM phosphorylation of Mdm2 Ser394 is required for robust p53 stabilization and activation following DNA damage. This dissertation describes in vivo examination of the mechanism by which Mdm2 Ser394 phosphorylation impacts p53 activities and its contribution to suppression of oncogene and DNA damage-induced tumors. We determine that phosphorylation of Mdm2 Ser394 regulates p53 activity by modulating Mdm2 stability and paradoxically delays Myc-driven lymphomagenesis while increasing lymphomagenesis in sub-lethally irradiated mice. c-Abl phosphorylates the residue neighboring Mdm2 Ser394, Mdm2 Tyr393. This dissertation describes the generation of a novel Mdm2Y393F mutant mouse to determine if c-Abl phosphorylation of Mdm2 regulates p53-mediated DNA damage responses or tumor suppression in vivo. Mdm2Y393F mice develop accelerated spontaneous and oncogene-induced tumors, yet display no defects in p53 stabilization and activity following acute genotoxic stress. Furthermore, the effects of these phosphorylation events on p53 regulation are not additive, as Mdm2Y393F/S394A mice and Mdm2S394A mice display similar phenotypes. The studies presented herein further our understanding of the mechanisms by which DNA damage-associated kinases stabilize and activate p53, and influence p53-dependent responses and tumor suppression. A better understanding of the in vivo effects of Mdm2 phosphorylation may facilitate the development of novel therapeutics capable of stimulating p53 anti-tumor activity or alleviating p53- dependent toxicities in non-malignant tissues. Advisors/Committee Members: Stephen Jones, PhD.

Subjects/Keywords: Tumor Suppressor Protein p53; Proto-Oncogene Proteins c-mdm2; DNA Damage; Phosphorylation; Biochemistry; Cancer Biology; Cell Biology

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APA (6^th Edition):

Carr, M. I. (2016). The Role of MDM2 Phosphorylation in P53 Responses to DNA Damage and Tumor Suppression: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/847

Chicago Manual of Style (16^th Edition):

Carr, Michael I. “The Role of MDM2 Phosphorylation in P53 Responses to DNA Damage and Tumor Suppression: A Dissertation.” 2016. Doctoral Dissertation, U of Massachusetts : Med. Accessed March 07, 2021. http://escholarship.umassmed.edu/gsbs_diss/847.

MLA Handbook (7^th Edition):

Carr, Michael I. “The Role of MDM2 Phosphorylation in P53 Responses to DNA Damage and Tumor Suppression: A Dissertation.” 2016. Web. 07 Mar 2021.

Vancouver:

Carr MI. The Role of MDM2 Phosphorylation in P53 Responses to DNA Damage and Tumor Suppression: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2016. [cited 2021 Mar 07]. Available from: http://escholarship.umassmed.edu/gsbs_diss/847.

Council of Science Editors:

Carr MI. The Role of MDM2 Phosphorylation in P53 Responses to DNA Damage and Tumor Suppression: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2016. Available from: http://escholarship.umassmed.edu/gsbs_diss/847

University of Texas Southwestern Medical Center

21. Alibhai, Imran Nizamudin. Regulation of FOSB MRNA Isoforms by Drugs of Abuse.

Degree: 2006, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/586

► ΔFosB, a truncated splice isoform of FosB, is a transcription factor that accumulates within a subset of neurons after chronic administration of drugs of abuse… (more)

▼ ΔFosB, a truncated splice isoform of FosB, is a transcription factor that accumulates within a subset of neurons after chronic administration of drugs of abuse or other chronic stimuli. Due likely to its structure and post-translational modifications, ΔFosB protein is uniquely stable relative to the transiently expressed full-length FosB and all other Fos family proteins. The goal of this study was to determine if the relative expression of the two fosB isoforms is regulated at the mRNA level, thereby further contributing to the accumulation of ΔFosB. First, unlike the protein, the half-life of ΔfosB mRNA is only slightly longer than that of full-length fosB mRNA both in cultured cells in vitro and in the brain in vivo. Additionally, similar to c-fos, both fosB isoforms are induced abundantly in striatum after acute administration of amphetamine and partially desensitize after chronic dosing. Surprisingly, the relative ratio of the fosB to ΔfosB mRNA (normally 16:1 in saline controls) decreases significantly only after acute doses or at doses that elicit the greatest induction of both transcripts. When acute amphetamine doses are incrementally increased, fosB levels are induced to roughly equivalent levels regardless of dose; however, ΔfosB levels increase as the drug dose increases. A similar pattern of fosB and ΔfosB mRNA induction was seen in cell culture. These findings suggest that the splicing of fosB RNA may be regulated by the quantity of unspliced transcript available to the splicing machinery. That is, above a certain threshold of full-length fosB, the remaining primary transcript is alternatively spliced into ΔfosB. This splicing phenomenon is likely regulated by the Polypyrimidine Tract Binding (PTB1) protein. PTB1 protein has been shown to inhibit the U2AF splicing complex and thus prevent alternative splicing of regions in close proximity to where it is bound. It has previously been demonstrated that PTB1 protein binds the fosB transcript in vitro. Here, it is shown that overexpression of PTB1 in PC12 cells alters the ratios of the fosB isoforms by increasing the amount of fosB transcript relative to ΔfosB transcript. Therefore, this study concludes that under basal conditions PTB1 protein binds the majority of the fosB premRNA, thereby inhibiting the generation of the ΔfosB transcript. Only when PTB1 protein is saturated with transcript does the ratio of fosB to ΔfosB decrease significantly, because the unbound pre-mRNA is spliced into ΔfosB. These data provide fundamental information concerning the generation of ΔfosB mRNA and indicate the selective accumulation of ΔFosB protein with chronic drug exposure does not involve its preferential generation by splicing. Advisors/Committee Members: Nestler, Eric J..

Subjects/Keywords: Proto-Oncogene Proteins c-fos; Amphetamine; Drug Abuse

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APA (6^th Edition):

Alibhai, I. N. (2006). Regulation of FOSB MRNA Isoforms by Drugs of Abuse. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/586

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):

Alibhai, Imran Nizamudin. “Regulation of FOSB MRNA Isoforms by Drugs of Abuse.” 2006. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/586.

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

MLA Handbook (7^th Edition):

Alibhai, Imran Nizamudin. “Regulation of FOSB MRNA Isoforms by Drugs of Abuse.” 2006. Web. 07 Mar 2021.

Vancouver:

Alibhai IN. Regulation of FOSB MRNA Isoforms by Drugs of Abuse. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2006. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/586.

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

Council of Science Editors:

Alibhai IN. Regulation of FOSB MRNA Isoforms by Drugs of Abuse. [Thesis]. University of Texas Southwestern Medical Center; 2006. Available from: http://hdl.handle.net/2152.5/586

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

University of Texas Southwestern Medical Center

22. Todorova, Pavlina Krasimirova. Mechanistic Analysis of Radiation-Induced Gliomagenesis.

Degree: 2017, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/7205

► Glioblastomas (GBM) are devastating brain tumors refractory to any available treatment. Exposure to ionizing radiation (IR) is the only known GBM risk factor. The link… (more)

▼ Glioblastomas (GBM) are devastating brain tumors refractory to any available treatment. Exposure to ionizing radiation (IR) is the only known GBM risk factor. The link between low-linear energy transfer (LET) IR and gliomagenesis has been clearly demonstrated by epidemiological studies of human patients receiving diagnostic or therapeutic radiation. Whether such risk exists with particle radiation exposure, which is more densely ionizing, has not been evaluated. Particle radiation is increasingly used in radiotherapy and is also an occupational hazard for astronauts in space. With no human data available, animal models mimicking the process of radiation carcinogenesis are essential for risk assessment. Through a large scale systematic interrogation of multi-allele transgenic mice with brain-restricted deletions of GBM-relevant tumor suppressor genes we identified two complementary genotypes (NesCreInk4ab-/-ArfF/F and NesCrep53+/F;Pten+/F). We irradiated both models intra-cranially with equal doses of a range of charged particles with different LETs. Interestingly, we found an increase in gliomagenesis with LET until a peak frequency was reached with silicon ions (LET of 79.3 KeV/μm) following which tumor frequencies declined with heavier particles with higher LETs. These radiation-induced mouse tumors phenocopy the histopathological features of human GBM, including infiltrative growth, pseudopalisading necrosis, high mitotic index, and positivity for glial (Gfap, Olig2) and stem/progenitor markers (Sox2). Ex-vivo cultures derived from these tumors showed features of glioma stem-like cells underscoring the undifferentiated nature of the parental tumors. Integrated genomic and functional analyses revealed the driving oncogenic changes in tumors from the NesCrep53+/F;Pten+/F model. Regardless of radiation quality, all tumors had genomic deletions of the wild-type alleles of both p53 and Pten. Such concomitant loss signifies the crucial roles that p53 and Pten together play as barriers to radiation-induced transformation. Over-expression of the receptor tyrosine kinase Met following a genomic amplification event harbored by 40% of tumors was similarly observed across all radiation qualities. Met overexpression enhanced the stemness phenotype in the context of p53 loss, and additionally conferred radioresistance. These combinatorial effects illustrate the importance of evaluating GBM drivers as integrated nodes in an oncogenic signaling network. In sum, the identification of two mouse models carrying deletions of independent TSGs has allowed us to establish the universal role of radiation as a genotoxic agent capable of inducing high grade gliomas. These models and the identified key molecular changes accompanying radiation-induced gliomagenesis can be used in the design of therapeutic strategies for patients with secondary glioma who are currently limited in their options. Advisors/Committee Members: Bachoo, Robert, Shay, Jerry W., Scaglioni, Pier Paolo, Burma, Sandeep.

Subjects/Keywords: Brain Neoplasms; Cyclin-Dependent Kinase Inhibitor p15; Cyclin-Dependent Kinase Inhibitor p16; Glioblastoma; Proto-Oncogene Proteins c-met

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APA (6^th Edition):

Todorova, P. K. (2017). Mechanistic Analysis of Radiation-Induced Gliomagenesis. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/7205

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):

Todorova, Pavlina Krasimirova. “Mechanistic Analysis of Radiation-Induced Gliomagenesis.” 2017. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/7205.

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

MLA Handbook (7^th Edition):

Todorova, Pavlina Krasimirova. “Mechanistic Analysis of Radiation-Induced Gliomagenesis.” 2017. Web. 07 Mar 2021.

Vancouver:

Todorova PK. Mechanistic Analysis of Radiation-Induced Gliomagenesis. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2017. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/7205.

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

Council of Science Editors:

Todorova PK. Mechanistic Analysis of Radiation-Induced Gliomagenesis. [Thesis]. University of Texas Southwestern Medical Center; 2017. Available from: http://hdl.handle.net/2152.5/7205

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

University of Texas Southwestern Medical Center

23. Hale, Carly Fenwick. Identification and Characterization of Novel Mechanisms of Functional and Structural Synapse Remodeling: Focus on Vav Guanine Nucleotide Exchange Factors and MEF2 Transcription Factors.

Degree: 2014, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/3588

► Proper development of synaptic connectivity is a dynamic process requiring formation, elimination, maintenance, and plasticity of synapses. During early postnatal development, excess synapses are formed… (more)

▼ Proper development of synaptic connectivity is a dynamic process requiring formation, elimination, maintenance, and plasticity of synapses. During early postnatal development, excess synapses are formed in most neural circuits, which are subsequently pruned during adolescence in a sensory- and activity-dependent mechanism. The brain also exhibits experience-dependent synaptic modifications that may enhance or weaken functional synapse strength. Investigation of numerous neurodevelopmental and psychiatric disorders reveals dysfunctions in synapse formation and function; however, underlying molecular mechanisms remain poorly understood. In Part One of this study, I identify a novel role for Vav guanine nucleotide exchange factors (GEFs) in brain-derived neurotrophic factor (BDNF)-dependent synapse plasticity. BNDF and its receptor, TrkB, are well-established positive modulators of hippocampal long-term potentiation (LTP), and increasing evidence suggests that BDNF/TrkB facilitates LTP in part through the stimulation of Rho GTPases and subsequent F-actin remodeling and dendritic spine structural dynamics. I report that Vav-family GEFs are activated by BDNF/TrkB signaling, and are required for BDNF-induced Rac-GTP formation. Vav GEFs, which are enriched at hippocampal glutamatergic synapses, are necessary for rapid BDNF-induced dendritic spine growth and CA3-CA1 LTP. Furthermore, Vav2/3-deficient mice have impaired contextual fear conditioning, as well as reduced anxiety. Together, findings support a role for Vav-dependent F-actin dynamics in BDNF-stimulated dendritic spine head enlargement and LTP, and normal hippocampal-dependent learning and memory and anxiety in mice. Part Two of this study reports the identification of common MEF2 and FMRP mRNA targets that are required for MEF2-induced synapse elimination. The activity-dependent transcription factor myocyte enhancer factor 2 (MEF2) is a key negative regulator of excitatory synapse number, promoting synapse removal in neurons through a complex program of gene expression. The RNA binding protein and translational regulator fragile X mental retardation protein (FMRP) was recently identified as an essential downstream component of MEF2-induced synapse elimination, suggesting that these autism-linked proteins coordinate transcriptional and translational control of common transcripts to mediate proper synaptic connectivity. Using high throughput sequencing of RNA isolated by cross-linking immunoprecipitation (HITS-CLIP) of FMRP, I find a large overlap of MEF2-induced transcripts and FMRP-associated mRNAs, consistent with their shared roles in synapse elimination. More specifically, protocadherin 17 (Pcdh17) mRNA is induced by MEF2 and exhibits differential binding to FMRP following MEF2 activation. Reducing Pcdh17 alone does not alter basal synapse number, but reducing Pcdh17 levels blocks MEF2-induced dendritic spine elimination of hippocampal neurons. These data suggest that MEF2-induced synapse elimination requires Pcdh17 – a MEF2 target gene and FMRP-associated… Advisors/Committee Members: Huber, Kimberly M., Cowan, Christopher W., Green, Carla B., Kim, Tae-Kyung.

Subjects/Keywords: Cadherins; Fragile X Mental Retardation Protein; MEF2 Transcription Factors; Neuronal Plasticity; Proto-Oncogene Proteins c-vav; Synapses

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

APA (6^th Edition):

Hale, C. F. (2014). Identification and Characterization of Novel Mechanisms of Functional and Structural Synapse Remodeling: Focus on Vav Guanine Nucleotide Exchange Factors and MEF2 Transcription Factors. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/3588

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):

Hale, Carly Fenwick. “Identification and Characterization of Novel Mechanisms of Functional and Structural Synapse Remodeling: Focus on Vav Guanine Nucleotide Exchange Factors and MEF2 Transcription Factors.” 2014. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/3588.

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

MLA Handbook (7^th Edition):

Hale, Carly Fenwick. “Identification and Characterization of Novel Mechanisms of Functional and Structural Synapse Remodeling: Focus on Vav Guanine Nucleotide Exchange Factors and MEF2 Transcription Factors.” 2014. Web. 07 Mar 2021.

Vancouver:

Hale CF. Identification and Characterization of Novel Mechanisms of Functional and Structural Synapse Remodeling: Focus on Vav Guanine Nucleotide Exchange Factors and MEF2 Transcription Factors. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2014. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/3588.

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

Council of Science Editors:

Hale CF. Identification and Characterization of Novel Mechanisms of Functional and Structural Synapse Remodeling: Focus on Vav Guanine Nucleotide Exchange Factors and MEF2 Transcription Factors. [Thesis]. University of Texas Southwestern Medical Center; 2014. Available from: http://hdl.handle.net/2152.5/3588

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

University of Texas Southwestern Medical Center

24. Deb, Dhruba. Oncogene-Induced Signaling Heterogeneity in Lung Cancer.

Degree: 2015, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/4213

► Lung cancer causes the maximum number of cancer related deaths worldwide. In recent years, the cancer genome atlas (TCGA) initiative has identified 138 frequently occurring… (more)

▼ Lung cancer causes the maximum number of cancer related deaths worldwide. In recent years, the cancer genome atlas (TCGA) initiative has identified 138 frequently occurring driver oncogenes and tumor suppressor genes in lung cancer. Currently, only 15 of these genes can be targeted therapeutically. Study of downstream signaling alterations of these oncogenes and tumor suppressor genes may identify novel therapeutic targets. Although studies on genetic heterogeneity in subclonal populations within one tumor using deep sequencing and multiple sectioning have gained popularity recently, the signaling heterogeneity within tumor cells with identical genetic changes remain poorly understood. Hence, I focus on TP53, KRas and C-Myc as they are among the most frequently occurring oncogenic alterations in lung adenocarcinoma. The downstream signaling changes of these genes may be different from one cell to another. Here, I develop high throughput approaches to study alterations of 6 major signaling readouts - phospho-Erk1/2, phospho-Stat3, Smad2/3, β-catenin, P65, and Foxo1 and quantitatively analyze thousands of cells with defined set of genetic changes. I ask - Can I utilize oncogene-induced signaling alterations in single cells to identify novel targetable vulnerabilities? Using single-cell image analysis I show that the genetically transformed HBECs with all 3 oncogenic changes (TP53, KRas and C-Myc) show significant signaling heterogeneity. They exhibit downregulated Smad2/3 signaling in single cells. Next, using a dominant negative construct, I confirm that this phenotype is partially reversible by the removal of C-Myc oncogenic stress. I further observe that the transformed HBECs exhibit upregulated Stat3 signaling in single cells. In addition, the Stat3 inhibitor Stattic causes more cell death in transformed HBECs. Interestingly, our single-cell image analysis suggests that Stat3 upregulation and Smad2/3 downregulation are mutually exclusive. Hence, Stattic will not be able to target the Smad2/3 downregulated cells. To target Smad2/3 downregulated cells, I identify Bcl6, a downstream target of Smad2/3, and I show that Bcl6 is a novel targetable vulnerability in transformed HBECs. I observe that C-Myc and Bcl6 gene expressions are strongly correlated in cell populations as well as in single-cell level. I further show that Bcl6 can be a targetable vulnerability in a subset of c-Myc addicted non-small cell lung cancers. I conclude that single-cell analysis of driver oncogenes and their downstream signaling can identify novel targetable vulnerabilities. Advisors/Committee Members: Garcia, Christine K., White, Michael A., Cobb, Melanie H., Altschuler, Steven J., Wu, Lani, Minna, John D..

Subjects/Keywords: Carcinoma, Squamous Cell; Lung Neoplasms; Proto-Oncogene Proteins c-myc; Smad2 Protein; Transforming Growth Factor beta

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

APA (6^th Edition):

Deb, D. (2015). Oncogene-Induced Signaling Heterogeneity in Lung Cancer. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/4213

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):

Deb, Dhruba. “Oncogene-Induced Signaling Heterogeneity in Lung Cancer.” 2015. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/4213.

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

MLA Handbook (7^th Edition):

Deb, Dhruba. “Oncogene-Induced Signaling Heterogeneity in Lung Cancer.” 2015. Web. 07 Mar 2021.

Vancouver:

Deb D. Oncogene-Induced Signaling Heterogeneity in Lung Cancer. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2015. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/4213.

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

Council of Science Editors:

Deb D. Oncogene-Induced Signaling Heterogeneity in Lung Cancer. [Thesis]. University of Texas Southwestern Medical Center; 2015. Available from: http://hdl.handle.net/2152.5/4213

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

East Carolina University

25. Mohammed Saleem, Yasir Ihsan. MOLECULAR MECHANISM OF ELLAGIC ACID AND UROLITHIN A IN THE SUPPRESSION OF PROSTATE CANCER BY INFLUENCING THE p53-MDM2 PATHWAY.

Degree: PhD, PHD-Pharmacology - Toxicology, 2019, East Carolina University

URL: http://hdl.handle.net/10342/7438

► Carcinoma of the prostate (CaP) is the most common cancer in men and the second leading cause of cancer-related death in men worldwide. Despite the… (more)

▼ Carcinoma of the prostate (CaP) is the most common cancer in men and the second leading cause of cancer-related death in men worldwide. Despite the available treatments for CaP including surgery and Androgen deprivation therapy (ADT), significant number of CaP patients relapse the CaP as the disease becomes hormonal independent. Therefore, it is important to target cell death pathways that function independently of androgen signaling. p53 is a tumor suppressor that mediates apoptosis, cell cycle arrest and DNA repair. The most common negative regulator of p53 is MDM2, which is itself a target gene of p53 to form an autoregulatory negative feedback loop. MDM2 inhibits p53 transcriptional activity through the induction of p53 polyubiquitination and degradation in the proteasome, leading CaP cells to undergo uncontrolled cell growth and cancer progression. Pomegranates, berries, and walnuts contain several bioactive compounds, including the Ellagitannins (ETs). ETs are polyphenolic compounds that are hydrolyzed in the stomach to form Ellagic acid (EA) which is itself metabolized in the gut microbiota to Urolithin A (UA). The purpose of this study was to investigate the influence of EA and UA on the p53-MDM2 signaling pathway in CaP cells. Three models of CaP cell lines were used because each harbor different p53 genotypes: LNCaP (p53+/+), 22RV1(p53-/+) and PC3 (p53-/-). Here we found that, when 22RV1 and LNCaP when treated with EA and UA, the interaction between p53 and MDM2 was disrupted. As a result, both EA and UA caused an increase in p53 protein levels and increased the steady-state concentration of p21, a main downstream target gene of p53 that mediates cell cycle arrest. In addition, EA and UA increased the levels of PUMA and NOXA proteins, both target genes of p53 which confer p53's pro-apoptotic function. Moreover, we confirmed UA inhibits MDM2-mediated polyubiquitination and degradation of p53. Finally, the data show that EA and UA induce apoptosis in PC3 cells (p53-/-), indicating p53 independent role of these compounds. These results suggest that EA and UA may have potential anti-neoplastic activity in CaP cells that may be at least partially attributed to the stabilization and activation of p53. Advisors/Committee Members: Selim, Mustafa I (advisor).

Subjects/Keywords: polyphenols; urolithin a; Prostatic Neoplasms; Tumor Suppressor Protein p53; Ellagic Acid; Heterocyclic Compounds; Proto-Oncogene Proteins c-mdm2; Male

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

APA (6^th Edition):

Mohammed Saleem, Y. I. (2019). MOLECULAR MECHANISM OF ELLAGIC ACID AND UROLITHIN A IN THE SUPPRESSION OF PROSTATE CANCER BY INFLUENCING THE p53-MDM2 PATHWAY. (Doctoral Dissertation). East Carolina University. Retrieved from http://hdl.handle.net/10342/7438

Chicago Manual of Style (16^th Edition):

Mohammed Saleem, Yasir Ihsan. “MOLECULAR MECHANISM OF ELLAGIC ACID AND UROLITHIN A IN THE SUPPRESSION OF PROSTATE CANCER BY INFLUENCING THE p53-MDM2 PATHWAY.” 2019. Doctoral Dissertation, East Carolina University. Accessed March 07, 2021. http://hdl.handle.net/10342/7438.

MLA Handbook (7^th Edition):

Mohammed Saleem, Yasir Ihsan. “MOLECULAR MECHANISM OF ELLAGIC ACID AND UROLITHIN A IN THE SUPPRESSION OF PROSTATE CANCER BY INFLUENCING THE p53-MDM2 PATHWAY.” 2019. Web. 07 Mar 2021.

Vancouver:

Mohammed Saleem YI. MOLECULAR MECHANISM OF ELLAGIC ACID AND UROLITHIN A IN THE SUPPRESSION OF PROSTATE CANCER BY INFLUENCING THE p53-MDM2 PATHWAY. [Internet] [Doctoral dissertation]. East Carolina University; 2019. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10342/7438.

Council of Science Editors:

Mohammed Saleem YI. MOLECULAR MECHANISM OF ELLAGIC ACID AND UROLITHIN A IN THE SUPPRESSION OF PROSTATE CANCER BY INFLUENCING THE p53-MDM2 PATHWAY. [Doctoral Dissertation]. East Carolina University; 2019. Available from: http://hdl.handle.net/10342/7438

26. Besret, Soizic. Ligations chimiques : synthèse d'inhibiteurs extracellulaires de la signalisation HGF/SF-MET : Chemical Ligation Synthesis of extracellular inhibitors of HGF/SF-MET signalling pathway.

Degree: Docteur es, Sciences du médicament, 2011, Université Lille II – Droit et Santé

URL: http://www.theses.fr/2011LIL2S003

►

Les peptides constituent une famille de biomolécules dont l’utilisation dans différents domaines thérapeutiques (cancer, diabète, sida) s’est fortement développée ces dernières années. Le défi pour… (more)

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Les peptides constituent une famille de biomolécules dont l’utilisation dans différents domaines thérapeutiques (cancer, diabète, sida) s’est fortement développée ces dernières années. Le défi pour les chimistes consiste à y accéder grâce à de nouvelles méthodes fiables et efficaces. La première partie de notre travail a d’abord été orientée vers le développement deux méthodes de ligations non natives efficaces et complémentaires de celles existant. La première méthode, appelée ligation thiocarbamate, permet d’obtenir des peptides alkylthiocarbamate avec de très bons rendements, alors que la seconde, appelée ligation azaGly, aboutit à la formation d’un azaGlypeptide. La seconde partie de cette thèse traite de la conception et synthèse de nouveaux peptides susceptibles d’inhiber la signalisation HGF/SF-MET. Le récepteur à activité tyrosine kinase MET et son ligand, l’HGF/SF (Hepatocyte Growth Factor/Scattor Factor), sont des cibles de choix pour une thérapie anti-cancéreuse. La ligation thiocarbamate, précédemment décrite, et la ligation thioéther plus classique ont été utilisées pour préparer une chimiothèque de peptides sulfonatés d’inhiber cette signalisation de façon extracellulaire. La capacité de liaison des composés de la chimiothèque avec le domaine extracellulaire de MET a été évaluée grâce à la technologie biopuces. L’activité biologique (tests MTT, d’activité kinase) des meilleurs produits a été ensuite évaluée.

Use of peptides as biomolecules have been extensively applied to various therapeutic fields (cancer, diabetes, AIDS). The challenge for chemists consists in development of new reliable and efficient strategies. Our work especially focused on the conception of two innovative non native chemical ligations bringing an additionnal asset to the existing state of the art.The first ligation, i.e. thiocarbamate ligation, affords alkylthiocarbamate peptides with remarkable yields. Regarding the second one, the azaGly ligation allows the straightforward synthesis of azaGlypeptides. On the other hand, this thesis deals with the design of new peptides suitable to inhibit the signaling pathway of the tyrosine–kinase MET receptor and its ligand HGF/SF (Hepatocyte Growth factor/Scattor factor). Indeed interfering with MET signaling appears to be a promising therapeutic approach.The thiocarbamate ligation disclosed previously along with a classical thioether ligation have been employed for the chemical library design of sulfonated peptids in order to inhibit extracellular interactions. Binding activities assessment of the chemical libray toward the MET extracellular domain has been achieved using a microarray technology. Biological activities (MTT tests and kinase activity) have also been investigated.

Advisors/Committee Members: Melnyk, Oleg (thesis director), Melnyk, Patricia (thesis director).

Subjects/Keywords: Ligations chimiques; Ligations peptidiques; Aza Glypeptide; Inhibiteurs de MET; Proto Oncogene Proteins c met; Peptide Library

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

APA (6^th Edition):

Besret, S. (2011). Ligations chimiques : synthèse d'inhibiteurs extracellulaires de la signalisation HGF/SF-MET : Chemical Ligation Synthesis of extracellular inhibitors of HGF/SF-MET signalling pathway. (Doctoral Dissertation). Université Lille II – Droit et Santé. Retrieved from http://www.theses.fr/2011LIL2S003

Chicago Manual of Style (16^th Edition):

Besret, Soizic. “Ligations chimiques : synthèse d'inhibiteurs extracellulaires de la signalisation HGF/SF-MET : Chemical Ligation Synthesis of extracellular inhibitors of HGF/SF-MET signalling pathway.” 2011. Doctoral Dissertation, Université Lille II – Droit et Santé. Accessed March 07, 2021. http://www.theses.fr/2011LIL2S003.

MLA Handbook (7^th Edition):

Besret, Soizic. “Ligations chimiques : synthèse d'inhibiteurs extracellulaires de la signalisation HGF/SF-MET : Chemical Ligation Synthesis of extracellular inhibitors of HGF/SF-MET signalling pathway.” 2011. Web. 07 Mar 2021.

Vancouver:

Besret S. Ligations chimiques : synthèse d'inhibiteurs extracellulaires de la signalisation HGF/SF-MET : Chemical Ligation Synthesis of extracellular inhibitors of HGF/SF-MET signalling pathway. [Internet] [Doctoral dissertation]. Université Lille II – Droit et Santé 2011. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2011LIL2S003.

Council of Science Editors:

Besret S. Ligations chimiques : synthèse d'inhibiteurs extracellulaires de la signalisation HGF/SF-MET : Chemical Ligation Synthesis of extracellular inhibitors of HGF/SF-MET signalling pathway. [Doctoral Dissertation]. Université Lille II – Droit et Santé 2011. Available from: http://www.theses.fr/2011LIL2S003

University of Texas Southwestern Medical Center

27. Ahmed, Kamran. Proteomic Discovery of Functionally Important Pathways in Myocardial Ischemia-Reperfusion Injury.

Degree: 2016, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/7069

►

The general metadata – e.g., title, author, abstract, subject headings, etc. – is publicly available, but access to the submitted files is restricted to UT… (more)

▼

The general metadata – e.g., title, author, abstract, subject headings, etc. – is publicly available, but access to the submitted files is restricted to UT Southwestern campus access and/or authorized UT Southwestern users.

BACKGROUND: Coronary heart disease, a source of myocardial ischemia-reperfusion injury (IRI), is the world's leading cause of death and disability. Insulin-like growth factor 1 (IGF1) transgenic (Tg) mouse hearts are protected from IRI, whereas Akt-Tg mouse hearts recover poorly from IRI. Surprisingly, Akt is a downstream component of IGF1 signaling. The Akt-Tg phenotype can be rescued by cardiac gene transfer of activated PI3-kinase (PI3K), another component of the IGF1 pathway, suggesting that PI3K-dependent but Akt-independent pathways are key determinants of IRI. To discern such pathways, we analyzed the proteomic and phosphoproteomic changes in wild-type (WT) mouse hearts subjected to IRI ex vivo, and IGF1-TG and Akt-Tg mouse hearts in order to identify 20 differentially regulated candidates as potential modifiers of IRI, and began testing their functional roles in an in vitro model. OBJECTIVE: We hypothesize that the cardioprotection observed in IGF1 overexpression is a result of PI3K-dependent but Akt-independent signaling pathways. METHODS: WT hearts were collected at 4 time points of ex-vivo Langendorff IRI and analyzed with liquid chromatography-tandem mass spectrometry to determine protein abundance and phosphorylation changes. IGF1-Tg and Akt-Tg hearts were analyzed at baseline. Protein network analysis was performed using Cytoscape software. The functional effects of candidates with abundance or phosphorylation differences ≥2-fold were assessed in rat neonatal ventricular myocytes using in vitro redox-based viability assays and cell proliferation studies. RESULTS: In the WT IRI studies, 6403 proteins and 22833 phosphopeptides were quantified. During IRI, no proteins changed in abundance, 10 phosphopeptides were upregulated, and 330 phosphopeptides were downregulated. In the IGF1-Tg and Akt-Tg hearts, 6700 proteins and 23000 phosphopeptides were quantified. Out of the significantly regulated proteins, in vitro knockdown of rho-associated protein kinase 2 (ROCK2) increased the viability signal by 17% in normoxia and 33% in simulated IRI (p<0.05) and increased EdU incorporation from 28.9% to 40.15% (p<0.00001). Network analysis of Akt-Tg hearts revealed significant downregulation of 24 out of 45 subunits of Complex I of the electron transport chain (p<0.05). CONCLUSION: Dephosphorylation of the cardiac phosphoproteome is the dominant pattern in IRI, which may reflect phosphatase activation or reduced ATP levels inhibiting kinase activity. ROCK2 knockdown increased the viability signal by stimulating proliferation in vitro. Whether ROCK2 is involved in cardiomyogenesis in the adult heart will be addressed in future studies. Akt-Tg hearts may be susceptible to IRI due to a reduced ATP reserve caused by Complex I downregulation.

Advisors/Committee Members: Hill, Joseph A., Rosenzweig, Anthony, Munshi, Nikhil, Sadek, Hesham A..

Subjects/Keywords: Heart; Insulin-Like Growth Factor I; Myocardial Reperfusion Injury; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; rho-Associated Kinases

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

APA (6^th Edition):

Ahmed, K. (2016). Proteomic Discovery of Functionally Important Pathways in Myocardial Ischemia-Reperfusion Injury. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/7069

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):

Ahmed, Kamran. “Proteomic Discovery of Functionally Important Pathways in Myocardial Ischemia-Reperfusion Injury.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021. http://hdl.handle.net/2152.5/7069.

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

MLA Handbook (7^th Edition):

Ahmed, Kamran. “Proteomic Discovery of Functionally Important Pathways in Myocardial Ischemia-Reperfusion Injury.” 2016. Web. 07 Mar 2021.

Vancouver:

Ahmed K. Proteomic Discovery of Functionally Important Pathways in Myocardial Ischemia-Reperfusion Injury. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2152.5/7069.

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

Council of Science Editors:

Ahmed K. Proteomic Discovery of Functionally Important Pathways in Myocardial Ischemia-Reperfusion Injury. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/7069

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

28. Tortelli Júnior, Tharcisio Citrangulo. Avaliação do papel de proibitina no desenvolvimento de resistência à cisplatina em linhagens de melanoma humano.

Degree: Mestrado, Oncologia, 2008, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-12022009-135328/ ;

►

A incidência de melanomas tem crescido mundialmente. Apesar de representar um potencial problema de saúde pública pela sua incidência crescente, melanomas ainda se apresentam como… (more)

▼

A incidência de melanomas tem crescido mundialmente. Apesar de representar um potencial problema de saúde pública pela sua incidência crescente, melanomas ainda se apresentam como tumores de difícil tratamento, especialmente quando diagnosticados em estadios avançados. A taxa de resposta a quimioterapia não ultrapassa 30% de resposta clínica objetiva nestes casos. As bases moleculares da quimiorresistência não são ainda completamente esclarecidas e seu conhecimento será útil para o delineamento de estratégias de quimiossensibilização. Em estudos anteriores, observamos que o tratamento de linhagem de células de melanoma metastático humano com o quimioterápico cisplatina induz o acúmulo de proibitina nas células sobreviventes. Proibitina é uma molécula expressa ubiquamente na maioria das células. Há evidências de que a forma nuclear esteja envolvida com o processo de morte celular e inibição de E2F1 enquanto a forma citoplasmática parece atuar como chaperona mitocondrial, garantindo sua homeostasia. O objetivo deste projeto foi avaliar a compartimentalização subcelular e a expressão de proibitina, após tratamento com 25 M de cisplatina por 24 horas em diferentes linhagens de melanoma metastático humano; e, o efeito de sua subexpressão, usando-se small interference (si) RNA. Nós mostramos que nas linhagens de melanoma humano LB373Mel, SKMel 37 e Mel 85, a proibitina foi encontrada predominantemente no citoplasma, associada, pelo menos em parte, com a mitocôndria. Após tratamento com cisplatina, uma porção da proibitina também foi encontrada no núcleo, como pode ser detectado utilizando-se anticorpo monoclonal (clone II-14-1). Experimentos de knockdown de proibitina por siRNA obtiveram sucesso em duas de três linhagens. Nessas duas linhagens (LB373Mel e Mel 85), o bloqueio do acúmulo de proibitina após tratamento com cisplatina levou à quimiossensibilização. A quimiossensibilização à cisplatina não foi observada na linhagem SKMel 37, que foi capaz de acumular proibitina mesmo quando tratada com siRNA específico para proibitina. A conclusão deste projeto é que a expressão de proibitina é parte da resposta celular que leva a sobrevivência de células de melanoma expostas à cisplatina

The incidence of melanomas has grown world-wide. Besides representing a potential problem of public health for its increasing incidence, melanomas are tumors of difficult treatment, especially when diagnosed in advanced phases. The clinical objective response rate does not exceed 30% in these cases. The molecular bases of chemoresistance are not completely clarified and their understanding will be useful for the delineation of chemosensitization strategies. In previous studies, we observed that the treatment of a human metastatic melanoma cell line with the chemotherapeutic agent cisplatin induced the accumulation of prohibitin in the surviving cells. Prohibitin is ubiquitously expressed molecule in most cells. There is evidence that the nuclear form is involved with the process of cell death and inhibition of E2F1, while the cytoplasmic…

Advisors/Committee Members: Chammas, Roger.

Subjects/Keywords: Cell death; Cisplatin; Cisplatina; Melanoma; Melanoma; Morte celular; Proteínas proto-oncogênicas c-akt; Proto-oncogene proteins; RNA interferente pequeno; RNA small interfering

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

APA (6^th Edition):

Tortelli Júnior, T. C. (2008). Avaliação do papel de proibitina no desenvolvimento de resistência à cisplatina em linhagens de melanoma humano. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5155/tde-12022009-135328/ ;

Chicago Manual of Style (16^th Edition):

Tortelli Júnior, Tharcisio Citrangulo. “Avaliação do papel de proibitina no desenvolvimento de resistência à cisplatina em linhagens de melanoma humano.” 2008. Masters Thesis, University of São Paulo. Accessed March 07, 2021. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-12022009-135328/ ;.

MLA Handbook (7^th Edition):

Tortelli Júnior, Tharcisio Citrangulo. “Avaliação do papel de proibitina no desenvolvimento de resistência à cisplatina em linhagens de melanoma humano.” 2008. Web. 07 Mar 2021.

Vancouver:

Tortelli Júnior TC. Avaliação do papel de proibitina no desenvolvimento de resistência à cisplatina em linhagens de melanoma humano. [Internet] [Masters thesis]. University of São Paulo; 2008. [cited 2021 Mar 07]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-12022009-135328/ ;.

Council of Science Editors:

Tortelli Júnior TC. Avaliação do papel de proibitina no desenvolvimento de resistência à cisplatina em linhagens de melanoma humano. [Masters Thesis]. University of São Paulo; 2008. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-12022009-135328/ ;

29. Willems, Kristen N. Regulation of Humoral Immunity by Pim Kinases: A Dissertation.

Degree: Immunology and Microbiology, Microbiology and Physiological Systems, 2011, U of Massachusetts : Med

URL: https://escholarship.umassmed.edu/gsbs_diss/567

► Pim (Provirus Integration site for Moloney murine leukemia virus) kinases are a family of three serine/threonine kinases involved in cell cycle, survival and metabolism.… (more)

Subjects/Keywords: Proto-Oncogene Proteins c-pim-1; Proto-Oncogene Proteins; Protein-Serine-Threonine Kinases; Immunity; Humoral; Amino Acids, Peptides, and Proteins; Enzymes and Coenzymes; Hemic and Immune Systems; Immunology and Infectious Disease; Viruses

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

APA (6^th Edition):

Willems, K. N. (2011). Regulation of Humoral Immunity by Pim Kinases: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/567

Chicago Manual of Style (16^th Edition):

Willems, Kristen N. “Regulation of Humoral Immunity by Pim Kinases: A Dissertation.” 2011. Doctoral Dissertation, U of Massachusetts : Med. Accessed March 07, 2021. https://escholarship.umassmed.edu/gsbs_diss/567.

MLA Handbook (7^th Edition):

Willems, Kristen N. “Regulation of Humoral Immunity by Pim Kinases: A Dissertation.” 2011. Web. 07 Mar 2021.

Vancouver:

Willems KN. Regulation of Humoral Immunity by Pim Kinases: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2011. [cited 2021 Mar 07]. Available from: https://escholarship.umassmed.edu/gsbs_diss/567.

Council of Science Editors:

Willems KN. Regulation of Humoral Immunity by Pim Kinases: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2011. Available from: https://escholarship.umassmed.edu/gsbs_diss/567

30. Trabucco, Sally E. The SMURF2-YY1-C-MYC Axis in the Germinal Center Reaction and Diffuse Large B Cell Lymphoma: A Dissertation.

Degree: Cell Biology, Pediatrics, 2016, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/864

► Diffuse large B cell lymphoma (DLBCL) is the most common non-Hodgkin’s lymphoma. Patients who fail conventional therapy (~50%) have a poor prognosis and few… (more)

Subjects/Keywords: Diffuse Large B-Cell Lymphoma; YY1 Transcription Factor; Ubiquitin-Protein Ligases; Germinal Center; Proto-Oncogene Proteins c-myc; SMURF2-YY1-C-MYC Axis; Cancer Biology; Cell Biology; Neoplasms

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

APA (6^th Edition):

Trabucco, S. E. (2016). The SMURF2-YY1-C-MYC Axis in the Germinal Center Reaction and Diffuse Large B Cell Lymphoma: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/864

Chicago Manual of Style (16^th Edition):

Trabucco, Sally E. “The SMURF2-YY1-C-MYC Axis in the Germinal Center Reaction and Diffuse Large B Cell Lymphoma: A Dissertation.” 2016. Doctoral Dissertation, U of Massachusetts : Med. Accessed March 07, 2021. http://escholarship.umassmed.edu/gsbs_diss/864.

MLA Handbook (7^th Edition):

Trabucco, Sally E. “The SMURF2-YY1-C-MYC Axis in the Germinal Center Reaction and Diffuse Large B Cell Lymphoma: A Dissertation.” 2016. Web. 07 Mar 2021.

Vancouver:

Trabucco SE. The SMURF2-YY1-C-MYC Axis in the Germinal Center Reaction and Diffuse Large B Cell Lymphoma: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2016. [cited 2021 Mar 07]. Available from: http://escholarship.umassmed.edu/gsbs_diss/864.

Council of Science Editors:

Trabucco SE. The SMURF2-YY1-C-MYC Axis in the Germinal Center Reaction and Diffuse Large B Cell Lymphoma: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2016. Available from: http://escholarship.umassmed.edu/gsbs_diss/864

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