subject:(heat shock protein 70)

University of New South Wales

1. Huo, Yuantao. Design, synthesis, and evaluation of pentapeptides that inhibit the function of heat shock protein 70.

Degree: Chemistry, 2018, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/61939 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:57828/SOURCE02?view=true

► Protein-protein interactions (PPIs) regulate the cell’s protein-folding machinery, which relies on a multiprotein complex formed with heat shock protein 70 (Hsp70). Hsp70 is a molecular… (more)

▼ Protein-protein interactions (PPIs) regulate the cell’s protein-folding machinery, which relies on a multiprotein complex formed with heat shock protein 70 (Hsp70). Hsp70 is a molecular chaperone responsible for partially folding nascent peptides and refolding misfolded proteins, whereupon it transfers the partially folded proteins to Hsp90. The transfer process is mediated by the co-chaperone heat shock organising protein (HOP). HOP binds to Hsp70 via its tetratricopeptide repeat 1 (TPR1) domain. Hence, the PPI between HOP and Hsp70 is critical for the Hsp70’s function. This interaction is particularly important in cancer cells, where Hsp70 is overexpressed to fold the rapidly produced proteins and facilitate cancer growth.This thesis describes the de-novo design, synthesis and biological evaluation of molecules aimed to regulate the interaction between Hsp70 and HOP. Peptides were designed based on the sequence HOP’s TPR1 domain. The aim was to mimics the HOP interaction with Hsp70 and inhibits Hsp70’s function by modulating Hsp70-HOP interaction. The author synthesized seven molecules in this series. Using solid phase peptide synthesis, the seven peptides were purified by HPLC and verified by LCMS, 1H NMR and 2D NMR. These compounds were then tested in a binding assay and a functional luciferase refolding assay. A structurally unique Hsp70 inhibitor, C1, was identified as lead molecule, which is the first molecule to directly regulate PPI and inhibit protein folding events.The author then synthesized tagged version of C1 and tested in a protein pulldown assay against Hsp70 to assess its ability to bind to Hsp70. To identify the domain binding site, a pulldown assay was run using the C1-Tag against Hsp70’s substrate binding domain (SBD). The author demonstrated that C1 bound to Hsp70 at the SBD. Finally, a structure-activity relationship study on C1 was carried out by producing molecules to perform alanine. C1 is a pentapeptide, and each amino acid residue was substituted for alanine in the backbone. Of the five derivatives produced, the author synthesized three. This project is demonstrating a proof of a successful approach for designing new small molecules that will modulate protein-protein interactions and interfere in large dynamic protein complexes. Advisors/Committee Members: McAlpine, Shelli R., Chemistry, Faculty of Science, UNSW.

Subjects/Keywords: Protein-protein interactions (PPIs); Heat shock protein 70 (Hsp70); Inhibitor

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APA (6^th Edition):

Huo, Y. (2018). Design, synthesis, and evaluation of pentapeptides that inhibit the function of heat shock protein 70. (Masters Thesis). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/61939 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:57828/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Huo, Yuantao. “Design, synthesis, and evaluation of pentapeptides that inhibit the function of heat shock protein 70.” 2018. Masters Thesis, University of New South Wales. Accessed March 09, 2021. http://handle.unsw.edu.au/1959.4/61939 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:57828/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Huo, Yuantao. “Design, synthesis, and evaluation of pentapeptides that inhibit the function of heat shock protein 70.” 2018. Web. 09 Mar 2021.

Vancouver:

Huo Y. Design, synthesis, and evaluation of pentapeptides that inhibit the function of heat shock protein 70. [Internet] [Masters thesis]. University of New South Wales; 2018. [cited 2021 Mar 09]. Available from: http://handle.unsw.edu.au/1959.4/61939 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:57828/SOURCE02?view=true.

Council of Science Editors:

Huo Y. Design, synthesis, and evaluation of pentapeptides that inhibit the function of heat shock protein 70. [Masters Thesis]. University of New South Wales; 2018. Available from: http://handle.unsw.edu.au/1959.4/61939 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:57828/SOURCE02?view=true

2. Makri, Angeliki. Ο ρόλος των πρωτεϊνών θερμικού σοκ (HSPS) στην εμβρυοεμφύτευση σε φυσιολογικές και παθολογικές κυήσεις.

Degree: 2019, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/45203

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Problem To study the balance of circulating Heat shock protein Hsp60 and Hsp70 in preterm deliveryMethod of study A two-stage approach was used. At first… (more)

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Problem To study the balance of circulating Heat shock protein Hsp60 and Hsp70 in preterm deliveryMethod of study A two-stage approach was used. At first stage we run retrospective analysis of prospective collected clinical data and at a second stage we studied an animal model of preterm delivery (PTD). Blood samples were collected for prenatal screening in 3,629 women. Samples from 23 women with miscarriage before gestational week 21 and 53 well-matched comparators for age, body mass index, parity and previous miscarriage with full-term pregnancy were depicted. Women with risk factors were excluded. Hsp60 and Hsp70 were measured by an enzyme immunosorbent assay. PTD was induced after injection of low dose of bacterial lipopolysaccharide; mice were sacrificed for the measurement of Hsp60 and Hsp70 in blood and tissues. The study endpoint was the association of the Hsp60 to Hsp70 ratio to miscarriage.Results A ratio greater than 6 could distinguish between women who will miscarry from women with term pregnancies with sensitivity 60%, specificity 81.8%, positive predictive value 81.8% and negative predictive value 60% (OR: 6.750, p= 0.025). Mice of the LPS-group PTD had this ratio significantly increased in maternal serum, placentas and embryos compared to the sham-operation group. Gene expression of Hsp60/70 remained in tissues unaltered.Conclusions An Hsp60/Hsp70 ratio equal to or more than 6 until gestational week 12 is accompanied with great likelihood for miscarriage. A similar ratio applies in an animal model of PTD induced by low-dose LPS.Keywords: Miscarriage, Heat shock protein 60, Heat shock protein 70

Η μελέτη της ισορροπίας των πρωτεϊνών Θερμικής καταπληξίας 60 και 70 (Hsp60 και Hsp70) στην κυκλοφορία του αίματος, κατά τον πρόωρο τοκετόΜέθοδος της μελέτης: Χρησιμοποιήθηκε προσέγγιση δύο σταδίων. Στο πρώτο στάδιο πραγματοποιήσαμε μία ανασκοπική ανάλυση κλινικών προοπτικών δεδομένων και στο δεύτερο στάδιο μελετήσαμε ένα ζωικό μοντέλο πρόωρου τοκετού. Συλλέχθηκαν δείγματα αίματος για προγεννητικό έλεγχο από 3,629 γυναίκες. Δείγματα από 23 γυναίκες που απέβαλαν πριν την 21 εβδομάδα κύησης και από 53 γυναίκες με φυσιολογικό τοκετό, της ομάδας ελέγχου, επιλέχθηκαν σύμφωνα με την ηλικία, το ΔΜΣ, ισοτιμία και προηγούμενες αποβολές. Γυναίκες με παράγοντες κινδύνου αποκλείστηκαν. Οι πρωτεΐνες θερμικής καταπληξίας 60 και 70 (Hsp60 και Hsp70) μετρήθηκαν με δοκιμασία ενζύμου ανοσοαπορροφητικότητας. Προκλήθηκε πρόωρος τοκετός μετά από ένεση μικρής δόσης βακτηριακού λιποσακχαρίτη. Τα ποντίκια θυσιάστηκαν για την μέτρηση των πρωτεϊνών θερμικής καταπληξίας 60 και 70 (Hsp60 και Hsp70) στο αίμα και τους ιστούς. Το τελικό σημείο της μελέτης ήταν η συσχέτιση του πηλίκου των πρωτεϊνών θερμικής καταπληξίας 60 kai 70 (Hsp60 και Hsp70) με την αποβολή.Αποτελέσματα: Πηλίκο μεγαλύτερο του 6 παρείχε τη δυνατότητα διάκρισης μεταξύ των γυναικών που μπορεί να έχουν αποβολή από τις γυναίκες με φυσιολογικό τοκετό, με ευαισθησία 60%, ειδικότητα 81,8%, θετική προβλεπτική αξία 81,8% και αρνητική προβλεπτική αξία 60% (OR: 6.750, p= 0.025).…

Subjects/Keywords: Αποβολή; Πρωτεΐνη θερμικής καταπληξίας 60; Πρωτεΐνη θερμικής καταπληξίας 70 ; Miscarriage; Heat shock protein 60; Heat shock protein 70

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

APA (6^th Edition):

Makri, A. (2019). Ο ρόλος των πρωτεϊνών θερμικού σοκ (HSPS) στην εμβρυοεμφύτευση σε φυσιολογικές και παθολογικές κυήσεις. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/45203

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):

Makri, Angeliki. “Ο ρόλος των πρωτεϊνών θερμικού σοκ (HSPS) στην εμβρυοεμφύτευση σε φυσιολογικές και παθολογικές κυήσεις.” 2019. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed March 09, 2021. http://hdl.handle.net/10442/hedi/45203.

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

MLA Handbook (7^th Edition):

Makri, Angeliki. “Ο ρόλος των πρωτεϊνών θερμικού σοκ (HSPS) στην εμβρυοεμφύτευση σε φυσιολογικές και παθολογικές κυήσεις.” 2019. Web. 09 Mar 2021.

Vancouver:

Makri A. Ο ρόλος των πρωτεϊνών θερμικού σοκ (HSPS) στην εμβρυοεμφύτευση σε φυσιολογικές και παθολογικές κυήσεις. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/10442/hedi/45203.

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

Council of Science Editors:

Makri A. Ο ρόλος των πρωτεϊνών θερμικού σοκ (HSPS) στην εμβρυοεμφύτευση σε φυσιολογικές και παθολογικές κυήσεις. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. Available from: http://hdl.handle.net/10442/hedi/45203

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

Vanderbilt University

3. Lizama, Britney Nola. Novel Functions of C-terminus of HSC70-Interacting Protein (CHIP) in Mitophagy and Neuroprotection.

Degree: PhD, Neuroscience, 2018, Vanderbilt University

URL: http://hdl.handle.net/1803/13149

► C-terminus of HSC70-interacting protein (CHIP, STUB1) is a ubiquitously expressed cytosolic E3-ubiquitin ligase. CHIP-deficient mice exhibit cardiovascular stress and motor dysfunction prior to premature death.… (more)

▼ C-terminus of HSC70-interacting protein (CHIP, STUB1) is a ubiquitously expressed cytosolic E3-ubiquitin ligase. CHIP-deficient mice exhibit cardiovascular stress and motor dysfunction prior to premature death. This phenotype is more consistent with animal models in which master regulators of autophagy are affected rather than with the mild phenotype of classic E3-ubiquitin ligase mutants. The cellular and biochemical events that contribute to neurodegeneration and premature aging in CHIP KO models remain poorly understood. Electron and fluorescent microscopy demonstrates that CHIP deficiency is associated with greater numbers of mitochondria, but these organelles are swollen and misshapen. Acute bioenergetic stress triggers CHIP induction and re-localization to mitochondria where it plays a role in the removal of damaged organelles. This mitochondrial clearance is required for protection following low-level bioenergetic stress in neurons. CHIP expression overlaps with stabilization of the redox stress sensor PTEN-inducible kinase 1 (PINK1) and is associated with increased LC3-mediated mitophagy. Introducing human promoter-driven vectors with mutations in either the E3 ligase or TPR domains of CHIP in primary neurons derived from CHIP-null animals enhances CHIP accumulation at mitochondria. Exposure to autophagy inhibitors suggests the increase in mitochondrial CHIP is likely due to diminished clearance of these CHIP-tagged organelles. Proteomic analysis of WT and CHIP KO mouse brains from both sexes reveals proteins essential for maintaining energetic, redox and mitochondrial homeostasis undergo significant changes in expression dependent upon genotype. Together these data support the use of CHIP deficient animals as a predictive model of age-related degeneration with selective neuronal proteotoxicity and mitochondrial failure. Advisors/Committee Members: Joshua P. Fessel (committee member), Fiona E. Harrison (committee member), BethAnn McLaughlin (committee member), Kevin D. Niswender (Committee Chair).

Subjects/Keywords: ischemic preconditioning; heat shock protein 70; STUB1; mitochondria

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

APA (6^th Edition):

Lizama, B. N. (2018). Novel Functions of C-terminus of HSC70-Interacting Protein (CHIP) in Mitophagy and Neuroprotection. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13149

Chicago Manual of Style (16^th Edition):

Lizama, Britney Nola. “Novel Functions of C-terminus of HSC70-Interacting Protein (CHIP) in Mitophagy and Neuroprotection.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed March 09, 2021. http://hdl.handle.net/1803/13149.

MLA Handbook (7^th Edition):

Lizama, Britney Nola. “Novel Functions of C-terminus of HSC70-Interacting Protein (CHIP) in Mitophagy and Neuroprotection.” 2018. Web. 09 Mar 2021.

Vancouver:

Lizama BN. Novel Functions of C-terminus of HSC70-Interacting Protein (CHIP) in Mitophagy and Neuroprotection. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/1803/13149.

Council of Science Editors:

Lizama BN. Novel Functions of C-terminus of HSC70-Interacting Protein (CHIP) in Mitophagy and Neuroprotection. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://hdl.handle.net/1803/13149

University of Waterloo

4. Faught, Leslie Erin. Modulation of Extracellular Heat Shock Protein 70 Levels in Rainbow Trout.

Degree: 2013, University of Waterloo

URL: http://hdl.handle.net/10012/7319

► At the cellular level, the stress response involves the synthesis of a highly conserved family of heat shock proteins (Hsps). These proteins are essential for… (more)

▼ At the cellular level, the stress response involves the synthesis of a highly conserved family of heat shock proteins (Hsps). These proteins are essential for maintenance of cellular homeostasis, both in times of stress and in normal cell functioning. Some of the most abundant forms of Hsps in the cell are members of the 70 kDa family. Intracellular heat shock protein 70 (Hsp70) expression in response to proteotoxicity is a highly conserved cellular stress response, but little is known about the role of extracellular Hsp70 (eHsp70) in fish. In order to begin characterizing eHsp70 in fish, the hypothesis that an acute stressor will elevate plasma Hsp70 levels in rainbow trout (Oncorhynchus mykiss) was tested. Subsequent in vitro studies examined whether eHsp70 level was modulated by cortisol and if this involved the action of the glucocorticoid receptor (GR), a ligand-activated transcription factor. The effect of cortisol on the eHsp70 response is important to consider because this steroid is elevated as a result of stressor exposure to allow for short-term allocation of energy stores to cope with stress. Cortisol is the primary corticosteroid in fish and exerts its main effects by binding to either GR or mineralocorticoid receptors (MR). Furthermore, eHsp70 has been previously implicated as having important immunoregulatory roles in mammalian models, but nothing has yet been reported in fish. To this end, a hypothesis tested here was that eHsp70 levels will increase after exposure to the bacterial endotoxin lipopolysaccharide (LPS), and that this response is modulated by cortisol. Finally, research on the effects of exogenous Hsp70 has not been reported in lower vertebrates; however, the relevance of this protein in intercellular signaling, especially in regards to immune regulation, is gaining increasing importance in mammalian models. Therefore, an experiment to determine whether Hsp70 would elicit upregulation of key immunoregulatory cytokines was also conducted. To accurately measure the low levels of Hsp70 in the plasma, a competitive antibody-capture enzyme-linked immunosorbent assay (ELISA) was developed. In the in vivo study, fish exposed to an acute heat shock (1h at 10°C above ambient temperature) exhibited a significant elevation in red blood cell Hsp70 levels over a 24 h period. There was also a significant increase in plasma Hsp70 levels at 4 h, but not at 24 h post-heat shock. To more specifically determine how cortisol affected the release of Hsp70, in vitro studies using primary cultures of hepatocytes demonstrated that cortisol significantly decreased eHsp70 levels in the medium at 24 h when compared with untreated controls, and this response was abolished in the presence of a GR antagonist, mifepristone (RU486). This result for the first time established a link between cortisol signaling and eHsp70 release in any animal model. When hepatocytes were exposed to LPS in vitro, eHsp70 levels were significantly lower in the LPS (30 µg/ml) group; however, heat shock abolished this effect at 24 h.…

Subjects/Keywords: extracellular heat shock protein 70; cellular stress response; cortisol; ELISA

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

APA (6^th Edition):

Faught, L. E. (2013). Modulation of Extracellular Heat Shock Protein 70 Levels in Rainbow Trout. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/7319

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):

Faught, Leslie Erin. “Modulation of Extracellular Heat Shock Protein 70 Levels in Rainbow Trout.” 2013. Thesis, University of Waterloo. Accessed March 09, 2021. http://hdl.handle.net/10012/7319.

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

MLA Handbook (7^th Edition):

Faught, Leslie Erin. “Modulation of Extracellular Heat Shock Protein 70 Levels in Rainbow Trout.” 2013. Web. 09 Mar 2021.

Vancouver:

Faught LE. Modulation of Extracellular Heat Shock Protein 70 Levels in Rainbow Trout. [Internet] [Thesis]. University of Waterloo; 2013. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/10012/7319.

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

Council of Science Editors:

Faught LE. Modulation of Extracellular Heat Shock Protein 70 Levels in Rainbow Trout. [Thesis]. University of Waterloo; 2013. Available from: http://hdl.handle.net/10012/7319

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

University of Minnesota

5. MacKenzie, Tiffany Noelle. Role of microRNAs in mediating pancreatic cancer response to triptolide.

Degree: PhD, Pharmacology, 2013, University of Minnesota

URL: http://purl.umn.edu/151156

► Pancreatic ductal adenocarcinoma (PDAC), one of the deadliest malignancies, is resistant to current chemotherapies. We previously showed that triptolide inhibits PDAC cell growth in vitro… (more)

Subjects/Keywords: Heat shock protein 70; Microarray; miR-142-3p; miRNA

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

APA (6^th Edition):

MacKenzie, T. N. (2013). Role of microRNAs in mediating pancreatic cancer response to triptolide. (Doctoral Dissertation). University of Minnesota. Retrieved from http://purl.umn.edu/151156

Chicago Manual of Style (16^th Edition):

MacKenzie, Tiffany Noelle. “Role of microRNAs in mediating pancreatic cancer response to triptolide.” 2013. Doctoral Dissertation, University of Minnesota. Accessed March 09, 2021. http://purl.umn.edu/151156.

MLA Handbook (7^th Edition):

MacKenzie, Tiffany Noelle. “Role of microRNAs in mediating pancreatic cancer response to triptolide.” 2013. Web. 09 Mar 2021.

Vancouver:

MacKenzie TN. Role of microRNAs in mediating pancreatic cancer response to triptolide. [Internet] [Doctoral dissertation]. University of Minnesota; 2013. [cited 2021 Mar 09]. Available from: http://purl.umn.edu/151156.

Council of Science Editors:

MacKenzie TN. Role of microRNAs in mediating pancreatic cancer response to triptolide. [Doctoral Dissertation]. University of Minnesota; 2013. Available from: http://purl.umn.edu/151156

University of Western Ontario

6. Dey, Adwitia. The Effect of Aerobic Exercise Training on Cerebrovascular HSP70, HSP90, INOS and ENOS Expression in Type 1 Diabetes.

Degree: 2013, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/1612

► The purpose of this study was to determine the effect of exercise training alone and in a model of Type 1 Diabetes Mellitus (T1DM), on… (more)

Subjects/Keywords: cerebral vessels; exercise; type 1 diabetes mellitus; Heat shock protein 70; heat shock protein 90; inducible nitric oxide synthase; Exercise Physiology

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

APA (6^th Edition):

Dey, A. (2013). The Effect of Aerobic Exercise Training on Cerebrovascular HSP70, HSP90, INOS and ENOS Expression in Type 1 Diabetes. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/1612

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):

Dey, Adwitia. “The Effect of Aerobic Exercise Training on Cerebrovascular HSP70, HSP90, INOS and ENOS Expression in Type 1 Diabetes.” 2013. Thesis, University of Western Ontario. Accessed March 09, 2021. https://ir.lib.uwo.ca/etd/1612.

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

MLA Handbook (7^th Edition):

Dey, Adwitia. “The Effect of Aerobic Exercise Training on Cerebrovascular HSP70, HSP90, INOS and ENOS Expression in Type 1 Diabetes.” 2013. Web. 09 Mar 2021.

Vancouver:

Dey A. The Effect of Aerobic Exercise Training on Cerebrovascular HSP70, HSP90, INOS and ENOS Expression in Type 1 Diabetes. [Internet] [Thesis]. University of Western Ontario; 2013. [cited 2021 Mar 09]. Available from: https://ir.lib.uwo.ca/etd/1612.

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

Council of Science Editors:

Dey A. The Effect of Aerobic Exercise Training on Cerebrovascular HSP70, HSP90, INOS and ENOS Expression in Type 1 Diabetes. [Thesis]. University of Western Ontario; 2013. Available from: https://ir.lib.uwo.ca/etd/1612

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

7. Λέκκας, Παναγιώτης. Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες.

Degree: 2014, University of Patras

URL: http://hdl.handle.net/10889/8684

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O ψευδάργυρος -Zn ελέγχει τον μεταβολισμό των λιπιδίων και γλυκόζης μέσω Ζn-μεταγραφικών παραγόντων. Δίαιτες υψηλών λιπαρών οδηγούν στην ενδοκυτταρική συσσώρευση ελευθέρων ριζών, μειώνουν την μεταγραφική… (more)

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O ψευδάργυρος -Zn ελέγχει τον μεταβολισμό των λιπιδίων και γλυκόζης μέσω Ζn-μεταγραφικών παραγόντων. Δίαιτες υψηλών λιπαρών οδηγούν στην ενδοκυτταρική συσσώρευση ελευθέρων ριζών, μειώνουν την μεταγραφική έκφραση των εκκαθαριστών τους και την ενεργότητα αντιοξειδωτικών ενζύμων και οδηγούν σε μεταβολικό σύνδρομο. Οι πρωτεϊνες του θερμικού shock (Heat shock proteins-HSP) παίζουν σημαντικό ρόλο στην αντίσταση στο κυτταρικό stress ως προσαρμογή ,μετά από έκθεση, σε διάφορα ερεθίσματα. ΣΚΟΠΟΣ : Μελέτη της επίδρασης του διατροφικού Ζn και των Hsp70,στην μεταβονομική των λιπιδίων αίματος και ήπατος ποντικών ΥΛΙΚΟ-ΜΕΘΟΔΟΙ :Ενήλικα αρσενικά ποντίκια: 1. Wild type (Wt) Hybrid (F1/F1) C57Bl/6 x CBA και 2. Transgenic (Tg) human HSP70 overexpressing mice, από ηλικίας ενός μηνός εντάχθηκαν στις παρακάτω διατροφές ,επί 10 εβδομάδες. Διατροφή Αριθμός Wt Αριθμός Tg Chow Diet (30 Zn) 6 10 High Fat Diet (3 Zn) 13 12 High Fat Diet (30 Zn) 9 8 High Fat Diet (300 Zn) 12 12 Σύνθεση των τριών διαιτών υψηλών λιπαρών -HFD: 3mg, 30mg, 300mg Zn /kg τροφής (mucedoola s.r.l Ιtaly-55% Cal από λιπαρά στοιχεία), Chow : δίαιτα ελέγχου Βιοχημικές αναλύσεις: Cholesterol ,Triglycerides ,HDL-cholesterol, Glucose ,Insulin Μετρήσεις μετάλλων και αντιοξειδωτικών παραγόντων: SOD (ερυθρά αιμοσφαίρια ) TAC (ορός αίματος) Zn , Cu (ερυθρά αιμοσφαίρια και ιστός ήπατος) Μεταβονομική ανάλυση και αξιολόγηση λιπιδίων :Εκχύλιση ορού αίματος και ηπατικού ιστού για λήψη Φάσματος 1H-NMR ΣΥΜΠΕΡΑΣΜΑΤΑ 1. Η HF δίαιτα αύξησε σημαντικά ,το τελικό βάρος και τον ρυθμό αύξησης βάρους ,τη χοληστερόλη -CL και την λιποπρωτεϊνη υψηλής πυκνότητας-ΗDL ,την ινσουλίνη –Ins, στα WT & Tg και μείωσε την ολική αντιοξειδωτική ικανότητα-TAC στο πλάσμα και την δραστηριότητα της σουπεροξείδιο-δισμουτάσης-SOD στα ερυθροκύταρα των WΤ και Tg 2. Ο επαρκής διατροφικός Zn (30mg/kgτροφής) φαίνεται να αποτελεί κρίσιμο παράγοντα διαμόρφωσης προστατευτικού ηπατολιπιδαιμικού προφίλ, ποντικών σε υπερλιπιδική δίαιτα. Η αύξηση ή μείωση του Zn σε HFDς φαίνεται να μειώνει την TAC του πλάσματος σε WΤ και Tg ενώ η δραστικότητα της SOD φαίνεται ανάλογη των επιπέδων του Zn Η ανεπάρκεια ή περίσσεια Zn αυξάνει τα αθηρογόνα SFA και μειώνει τα αντι-αθηρογόνα λιπίδια, PC, DU, LA DIAL ,UFA στις HDL, nonHDL και το ήπαρ, στα WΤHFD και στα ΤgHFD 3. Οι HSP70 : Τα διαγονιδιακά ζώα που φέρουν το γονίδιο hHsp70, φαίνεται ότι είτε σε έλλειψη είτε σε περίσσεια Ζn, που συνήθως συνοδεύoνται από μεταβολικό σύνδρομο, κατορθώνουν να διατηρούν καλλίτερους δείκτες λιπιδικού προφίλ σε σχέση με τα WT ζώα. Τα Τg εμφάνισαν σημαντικά χαμηλότερη CL ,TG , HDL σε σύγκριση με τα WT ενώ η HSP70 αύξησε σημαντικά την ενεργότητα της ολικής SOD στα ερυθρά αιμοσφαίρια. Η HSP70 μείωσε τα αθηρογόνα SFA και αύξησε τα αντιαθηρογόνα λιπίδια DIAL, DU, LA, UFA, SM στις HDL, nonHDL , και στο ήπαρ ποντικών που εκτέθηκαν σε HFD και σε όλες τις συγκεντρώσεις Zn.

Zinc –Zn controls lipid and glucose metabolism via Zn-transcription factors. High fat diets –HFDs…

Advisors/Committee Members: Καλφακάκου, Βασιλική, Lekkas, Panagiotis, Αγγελίδης, Χαράλαμπος, Βεζυράκη, Πάτρα, Ευαγγέλου, Άγγελος, Κιόρτσης, Δημήτριος, Καλφακάκου, Βασιλική,, Μπαϊρακτάρη, Ελένη, Παπαδοπούλου, Χρυσάνθη.

Subjects/Keywords: Ψευδάργυρος; Δίαιτα υψηλών λιπαρών; Μεταβονομική λιπιδίων; Πρωτεΐνη θερμικού shock -70; 572.64; Zinc (Zn); High fat diet (HFD); Lipid metabolomics; Heat shock protein-70 (HSP-70)

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APA (6^th Edition):

Λέκκας, �. (2014). Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες. (Doctoral Dissertation). University of Patras. Retrieved from http://hdl.handle.net/10889/8684

Chicago Manual of Style (16^th Edition):

Λέκκας, Παναγιώτης. “Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες.” 2014. Doctoral Dissertation, University of Patras. Accessed March 09, 2021. http://hdl.handle.net/10889/8684.

MLA Handbook (7^th Edition):

Λέκκας, Παναγιώτης. “Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες.” 2014. Web. 09 Mar 2021.

Vancouver:

Λέκκας �. Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες. [Internet] [Doctoral dissertation]. University of Patras; 2014. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/10889/8684.

Council of Science Editors:

Λέκκας �. Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες. [Doctoral Dissertation]. University of Patras; 2014. Available from: http://hdl.handle.net/10889/8684

8. LEKKAS, PANAGIOTIS. Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες.

Degree: 2014, University of Patras; Πανεπιστήμιο Πατρών

URL: http://hdl.handle.net/10442/hedi/40115

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INTRODUCTION: Zinc –Zn controls lipid and glucose metabolism via Zn-transcription factors. High fat diets –HFDs lead to intracellular free radicals accumulation, decrease the transcriptional expression… (more)

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INTRODUCTION: Zinc –Zn controls lipid and glucose metabolism via Zn-transcription factors. High fat diets –HFDs lead to intracellular free radicals accumulation, decrease the transcriptional expression of their scavengers and anti-oxidative enzymes’ activity leading finally to metabolic syndrome. Heat shock proteins-HSPs play a significant role in cellular resistance response , as an adaptation mechanism, after exposure to various stimuli.SCOPE: To study the effects of nutritional Zn and HSP70s on the metabonomics of serum and liver lipids in miceMATERIALS-METHODS: Male mice: 1. Wild type (Wt) Hybrid (F1/F1) C57Bl/6 x CBA και 2. Transgenic (Tg) human HSP70 overexpressing mice, one month old, were subjected for 10 weeks to the following diets :DietNumber of Wt Number of Tg Chow Diet (30 Zn) 6 10 High Fat Diet (3 Zn) 13 12 High Fat Diet (30 Zn) 9 8 High Fat Diet (300 Zn) 12 12 Composition of the three HF Diets: 3mg, 30mg, 300mg Zn /kg τροφής (mucedoola s.r.l Ιtaly-55% Cal from greasy ingredients),Chow :control dietBiochemical analyses: Cholesterol ,Triglycerides ,HDL-cholesterol, Glucose ,Insulin Metals and antioxidative factors levels: SOD (red blood cells )TAC (blood serum) Zn , Cu (red blood cells and liver tissue)Lipids metabonomics : Blood serum and liver tissue extracts for 1H-NMR spectrum analysis and evaluationCONCLUSIONS1. HFDiet significantly increased the rate of mice body weight gaining, as well as, cholesterol-CL, high density lipoproteins-HDL, insulin, in WT and Tg mice and decreased plasma total antioxidant capacity-TAC and red blood cell super oxide dismutase –SOD activity , in WT and Tg mice2.Suficient nutritional Zn (30 mg/kg food) prevails as a crucial modulator of a protective hepato-lipidaemic profil of mice in high fat diet.Zinc deficiency or excessiveness , in HFDiets , decreases plasma TAC in WT and Tg mice, while SOD activity shows proportional to Zn levels. Zinc deficiency or excessiveness increases the atherogenic SFA and decreases the anti –atherogenic lipids : PC, DU, LA DIAL ,UFA, in HDL, nonHDL and liver, in WΤ-HFD and Τg-HFD mice3. HSP70s : Transgenic mice over-expressing hHsp70 gene and exposed either to Zn deficiency or Zn excessiveness , both driving usually to metabolic syndrome , reveal significantly better lipid profile indicators, comparing to WT mice.Tg mice revealed significantly lower CL , TG , HDL levels compared to WT, while HSP70 in Τg mice significantly increased total SOD activity in red blood cells.HSP70 also decreased the atherogenic SFAs and increased the anti-atherogenic lipids DIAL, DU, LA, UFA, SM in HDL, nonHDL and in the liver of mice exposed to HFDiets and all Zn concentrations.

ΕΙΣΑΓΩΓΗ: O ψευδάργυρος -Zn ελέγχει τον μεταβολισμό των λιπιδίων και γλυκόζης μέσω Ζn-μεταγραφικών παραγόντων. Δίαιτες υψηλών λιπαρών οδηγούν στην ενδοκυτταρική συσσώρευση ελευθέρων ριζών, μειώνουν την μεταγραφική έκφραση των εκκαθαριστών τους και την ενεργότητα αντιοξειδωτικών ενζύμων και οδηγούν σε…

Subjects/Keywords: Ψευδάργυρος (Zn); Δίαιτα υψηλων λιπαρών; Μεταβονομική λιπιδίων; Πρωτεΐνη θερμικού shock -70; Zinc (Zn); Zn; High fat diet ( HFD); Lipid metabolomics; Heat shock protein-70 (HSP-70)

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

APA (6^th Edition):

LEKKAS, P. (2014). Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες. (Thesis). University of Patras; Πανεπιστήμιο Πατρών. Retrieved from http://hdl.handle.net/10442/hedi/40115

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):

LEKKAS, PANAGIOTIS. “Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες.” 2014. Thesis, University of Patras; Πανεπιστήμιο Πατρών. Accessed March 09, 2021. http://hdl.handle.net/10442/hedi/40115.

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

MLA Handbook (7^th Edition):

LEKKAS, PANAGIOTIS. “Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες.” 2014. Web. 09 Mar 2021.

Vancouver:

LEKKAS P. Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες. [Internet] [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2014. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/10442/hedi/40115.

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

Council of Science Editors:

LEKKAS P. Παρασκευή και πιστοποίηση ζωοτροφής για πειραματική μελέτη των επιδράσεων των μετάλλων στις λιπιδαιμίες. [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2014. Available from: http://hdl.handle.net/10442/hedi/40115

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

University of Michigan

9. Davis, Amanda. Pharmacology of Hsp70 Activation.

Degree: PhD, Pharmacology, 2020, University of Michigan

URL: http://hdl.handle.net/2027.42/155148

► The heat shock protein 90 and 70 (Hsp90 and Hsp70) chaperone system maintains protein quality control for over one hundred client proteins, including many implicated… (more)

▼ The heat shock protein 90 and 70 (Hsp90 and Hsp70) chaperone system maintains protein quality control for over one hundred client proteins, including many implicated in neurodegenerative disorders, by surveilling substrate binding clefts and selectively targeting damaged proteins for degradation. Hsp90 stabilizes client proteins in their native state and prevents degradation, whereas Hsp70 facilitates ubiquitination by E3 ligases and promotes proteasomal degradation. Traditionally the chaperone system has been targeted with Hsp90 inhibitors, and while many Hsp90 inhibitors have entered clinical trials for cancer they have failed to progress due in part to toxicity. Activation of Hsp70 has recently emerged as an alternative approach, with numerous genetic studies demonstrating that activation of Hsp70-dependent ubiquitination increases the degradation of disease-causing client proteins in cellular and animal models. Studies on the pharmacological activation of Hsp70 have been limited by the small number of compounds known to activate Hsp70-dependent ubiquitination. Thus, an innovative workflow was developed to discover novel small molecule activators of Hsp70. A high-throughput Hsp70 thermal shift assay and Hsp90 counter screen were utilized to identify compounds that bind and thermostabilize Hsp70. To test the functional effect of Hsp70 thermostabilizers in vitro, a purified protein system for Hsp70-dependent ubiquitination of neuronal nitric oxide synthase (nNOS) and a highly sensitive ELISA for the measurement of nNOS ubiquitination were established. With the use of this workflow we successfully identified one novel small molecule activator of Hsp70-dependent ubiquitination. Moreover, in the course of these studies we discovered pharmacological activation of Hsp70 can selectively increase the ubiquitination of damaged nNOS over nNOS in its native state. The small molecule identified by this workflow increases the structural diversity of compounds known to activate Hsp70-dependent ubiquitination and may provide a valuable tool to advance the study of pharmacological activation of Hsp70 as a therapeutic strategy. Advisors/Committee Members: Osawa, Yoichi (committee member), Lieberman, Andrew P (committee member), Alt, Andrew Jason (committee member), Groppi, Vincent (committee member), Pratt, William B (committee member).

Subjects/Keywords: nitric oxide synthase; heat shock protein 70; Pharmacy and Pharmacology; Health Sciences

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

APA (6^th Edition):

Davis, A. (2020). Pharmacology of Hsp70 Activation. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/155148

Chicago Manual of Style (16^th Edition):

Davis, Amanda. “Pharmacology of Hsp70 Activation.” 2020. Doctoral Dissertation, University of Michigan. Accessed March 09, 2021. http://hdl.handle.net/2027.42/155148.

MLA Handbook (7^th Edition):

Davis, Amanda. “Pharmacology of Hsp70 Activation.” 2020. Web. 09 Mar 2021.

Vancouver:

Davis A. Pharmacology of Hsp70 Activation. [Internet] [Doctoral dissertation]. University of Michigan; 2020. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/2027.42/155148.

Council of Science Editors:

Davis A. Pharmacology of Hsp70 Activation. [Doctoral Dissertation]. University of Michigan; 2020. Available from: http://hdl.handle.net/2027.42/155148

Texas A&M University

10. Francis Stuart, Samantha D. The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus.

Degree: MS, Toxicology, 2014, Texas A&M University

URL: http://hdl.handle.net/1969.1/152822

► Cadmium (Cd) is a toxic heavy metal with no known physiological function in higher order animals. Previous studies in primary cultures of neonatal rat choroid… (more)

▼ Cadmium (Cd) is a toxic heavy metal with no known physiological function in higher order animals. Previous studies in primary cultures of neonatal rat choroid plexus (CP) epithelial cells indicated Cd induced oxidative stress and stimulated apical choline transport, and suggested zinc (Zn) supplementation might abate both oxidative stress and modulation of transport. The objective of this thesis was to elucidate how Zn, a nutritive mineral normally accumulated by CP, attenuated oxidative stress. I hypothesize that Zn, which can function as a pro-antioxidant, abates Cd-induced oxidative stress either by induction of metallothionein-1 (MT-1) or enhancement of glutathione (GSH) biochemistry. Thus, in primary cultures of neonatal rat CP epithelial cells, I characterized the effects of sub-micromolar Cd and efficacy of Zn supplementation to attenuate Cd-induced cellular and oxidative stress without or with manipulation of GSH synthesis. To characterize the Cd-induced stress response, CP epithelial cells were treated with 0 or 500 nM CdCl_(2) in serum-free medium (SFM) for 12 h; samples were collected at 3, 6, 9, and 12 h. Induction of heme oxygenase-1 (HO-1), heat-shock protein 70 (HSP70), and metallothionein-1 (MT-1) in Cd-treated cells was compared to time-matched controls by immunoblot and qRT-PCR analyses. Cd induced the catalytic and modifier subunits of glutamate-cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis. To elucidate the effects Zn supplementation in Cd-treated cells depleted of GSH, cells were supplemented for 48 h with 0 or 25 μM ZnCl_(2) alone or with 100 μM buthionine sulfoximine (BSO), an inhibitor of GCL, before treatment with 0 or 500 nM CdCl_(2) ± 100 μM BSO ± 10μM ZnCl_(2) in SFM for 12 h. By luminescence assay, intracellular GSH and oxidized glutathione (GSSG) concentrations were measured. Cd increased intracellular GSH and GSSG, but markedly decreased GSH:GSSG ratio. Inhibition of GSH synthesis exacerbated Cd-induced stress. However, Zn supplementation attenuated the stress response irrespective of BSO treatment, as per decreased induction of HSP70. These data indicate that CP adapts to low-dose Cd by up-regulation of stress proteins and GSH synthesis. Zinc supplementation also may attenuate Cd-induced cellular and oxidative stress, but cytoprotection is independent of GSH status. Advisors/Committee Members: Villalobos, Alice R.A. (advisor), Abbott, Louise (committee member), Tian, Yanan (committee member).

Subjects/Keywords: choroid plexus; cadmium; zinc; oxidative stress; glutathione; metallothionein; heat-shock protein 70; hemeoxygenase

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

APA (6^th Edition):

Francis Stuart, S. D. (2014). The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/152822

Chicago Manual of Style (16^th Edition):

Francis Stuart, Samantha D. “The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus.” 2014. Masters Thesis, Texas A&M University. Accessed March 09, 2021. http://hdl.handle.net/1969.1/152822.

MLA Handbook (7^th Edition):

Francis Stuart, Samantha D. “The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus.” 2014. Web. 09 Mar 2021.

Vancouver:

Francis Stuart SD. The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus. [Internet] [Masters thesis]. Texas A&M University; 2014. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/1969.1/152822.

Council of Science Editors:

Francis Stuart SD. The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus. [Masters Thesis]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/152822

11. 김, 호연. The expression of Heat Shock Protein 70 in the placental tissue with preeclampsia.

Degree: 2008, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/1831 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000007246

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OBJECTIVE: Placental ischemia caused by abnormal trophoblastic invasion to spiral arteries, immunologic intolerance and inflammatory change explain etiology of preeclampsia. As a consequence, inflammatory cells… (more)

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OBJECTIVE: Placental ischemia caused by abnormal trophoblastic invasion to spiral arteries, immunologic intolerance and inflammatory change explain etiology of preeclampsia. As a consequence, inflammatory cells are released and they induce oxidative stress contributing to endothelial dysfunction and endothelial cell injury. Also apoptosis is closely related to preeclampsia in recent finding that placental ischemia contributes to increased apoptotic activity. Heat shock protein 70 (Hsp70) is a stress-induced protein and this protein can be a specific marker for this ischemic and apoptotic circumstance, preeclampsia. Therefore we compared immunohistochemical expression of Hsp70 in normotensive and preeclampsia pregnancies. METHODS: Placenta tissue were obtained from twenty four women complicated by mild and severe preeclampsia, twelve each and from twelve normotensive women right after delivery. Cryosection was immunostained with 1:50 Hsp70 first antibody and the expression of Hsp70 was observed in syncytiotrophoblast, cytotrophoblast, intravillous endothelial cells, extravillous trophoblast in basal layer and decidual cell. And according to the intensity of immunostaining, we compared these three groups. Western blot analysis was performed and the quantification and comparison of Hsp70 were done in placental tissue among the three group of patients. RESULTS: All groups demonstrated positive immunostaining for Hsp70 in cytoplasm of placental cells. But the intensity of immunostaining showed no statistical differences among three groups. The result of Western blot analysis resulted in no differences. CONCLUSION: In other words, the expression of Hsp70 in preeclampsia and normotensive pregnancies demonstrated no differences. This cannot define the oxidative stress as the pathophysiology of preeclampsia and proapoptotic activity in preeclampsia correlated with Hsp70. Since preeclampsia is complicated disease, combination of other Hsp and mediators as cytokines can be used in the future study for better understanding of preeclampsia.

목적: 자간전증은 영양세포의 나선혈관으로의 부적절한 침윤으로 태반 조직의 허헐을 초래하는 면역반응의 부전과 염증 반응에 의한다고 알려져 있다. 이와 같은 염증 매개 인자들이 산화적 스트레스를 유발하여 혈관 내피 세포 손상을 일으킨다. 또한 태반 혈류감소에 따른 허혈에 의해 세포고사가 증가된다는 세포고사와 연관이 있는 병태생리가 최근 규명되고 있다. 이와 밀접한 관계가 있는 스트레스 단백질인 Heat hock protein 70 (Hsp70)을 이용하여 정상 임신과 자간전증의 태반 조직에서의 발현에 있어 차이의 여부를 알아보고자 한다. 연구대상 및 방법: 아주대학교 병원 산부인과에서 제왕절개술로 분만한 산모들 중 태아발육부전을 동반하지 않은 경증 및 중증 자간전증 산모 각각12명과 자간전증을 동반하지 않은 정상 산모 12명을 대상으로 하여 분만 후 태반 조직을 채취하였다. 동결조직에 1:50 Heat shock protein 70 일차 항체를 사용하여 면역조직화학적 염색을 하였고 합포체영양막, 세포영양막, 태반기저부의 융모외영약막, 태반기저부 혈관의 내피세포, 탈락막에서 Hsp70의 발현 정도를 관찰하였으며 강도에 따라 세 환자군을 비교하였다. Western blot 분석을 하여 정상 임신과 전자간증 태반에서의 Hsp70 정량을 비교하였다. 결과: 세 환자군의 모든 태반 세포에서 면역 조직화학적 염색에 의해 Hsp70의 발현을 보였다. 그러나 세 군에 있어서 Hsp70의 발현 강도는 통계학적으로 유의하게 차이가 없었다. Western blot분석 결과에서도 세 환자군의 Hsp70 band의 강도에서 차이가 없었다. 결론: 따라서 경증과 중증의 자간전증 태반에서 Hsp70의 발현은 정상 임신과 차이를 보이지 않았다. 이는 Hsp70만으로는 자간전증의 병태생리인 산화적 스트레스를 설명할 수 없으며 세포고사와의 관계 규명을 할 수 없으며 다른 Hsp나 매개 인자들과 복합적으로 작용할 것으로 보여 추가적인 연구가 필요할 것으로 사료된다.

"국문요약 = ⅰ 차례 = ⅱ …

Advisors/Committee Members: 대학원 의학과, 200624169, 김, 호연.

Subjects/Keywords: preeclampsia; heat shock protein 70; placenta

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

APA (6^th Edition):

김, �. (2008). The expression of Heat Shock Protein 70 in the placental tissue with preeclampsia. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/1831 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000007246

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):

김, 호연. “The expression of Heat Shock Protein 70 in the placental tissue with preeclampsia.” 2008. Thesis, Ajou University. Accessed March 09, 2021. http://repository.ajou.ac.kr/handle/201003/1831 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000007246.

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

MLA Handbook (7^th Edition):

김, 호연. “The expression of Heat Shock Protein 70 in the placental tissue with preeclampsia.” 2008. Web. 09 Mar 2021.

Vancouver:

김 �. The expression of Heat Shock Protein 70 in the placental tissue with preeclampsia. [Internet] [Thesis]. Ajou University; 2008. [cited 2021 Mar 09]. Available from: http://repository.ajou.ac.kr/handle/201003/1831 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000007246.

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

Council of Science Editors:

김 �. The expression of Heat Shock Protein 70 in the placental tissue with preeclampsia. [Thesis]. Ajou University; 2008. Available from: http://repository.ajou.ac.kr/handle/201003/1831 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000007246

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

Rice University

12. Kilpatrick, Kiri. Reprogramming the proteostasis network to prevent the accumulation of alpha-synuclein aggregates.

Degree: PhD, Engineering, 2014, Rice University

URL: http://hdl.handle.net/1911/77191

► Protein misfolding and aggregation characterizes the development of a number of neurodegenerative diseases, such as Parkinson’s, Alzheimer’s and Huntington’s disease. The hallmark of Parkinson’s disease… (more)

▼ Protein misfolding and aggregation characterizes the development of a number of neurodegenerative diseases, such as Parkinson’s, Alzheimer’s and Huntington’s disease. The hallmark of Parkinson’s disease is the formation of proteinaceous inclusions, which consist primarily of α-synuclein (α-syn), a natively unstructured protein with propensity to misfold and aggregate. Cells have evolved sophisticated systems of protein quality control to prevent accumulation of non-native proteins and maintain protein homeostasis. However, the load of misfolded α-syn typically exceeds the capacity of the quality control system. Aberrant accumulation of misfolded α-syn leads to proteotoxic stress, eventually resulting in neurodegeneration. The objective of this project is to investigate chemical and genetic approaches to modulate the protein quality control system and reduce the accumulation of aberrant α-syn species. Studying α-syn aggregation in cells presents a number of challenges mainly due to the limited availability of tools to quantitatively distinguish between different α-syn conformational species within the cellular environment. To address this need, we engineered an in vitro model system based on neuroglioma cells that accumulate α-syn aggregates and developed a set of analytical tools based on the use of aggregation responsive probes to quantify α-syn aggregation in cells. To test whether modulating the protein quality control system affects the accumulation of α-syn aggregates, we investigated a series of complementary approaches aimed at i) enhancing the innate cellular chaperone machinery, which promotes folding and prevents aggregation, and ii) upregulating the autophagy pathway, which mediates clearance of aggregated proteins. We demonstrated that chemical modulation of Hsp70, a ubiquitously expressed molecular chaperone, affects the accumulation of α-syn aggregates. Particularly, the Hsp70 upregulator carbenoxolone was found to reduce α-syn aggregation and prevent α-syn-induced cytotoxicity via activation of the heat shock response. We also found that activation of the transcription factor EB (TFEB), a master regulator of the autophagy-lysosomal pathway, results in enhanced autophagic clearance of α-syn aggregates. We demonstrated that cell treatment with 2-hydroxypropyl-β-cyclodextrin reduces the accumulation of aggregated α-syn specifically by upregulating TFEB-mediated autophagic clearance. These findings lay the foundation for the development of pharmacological strategies to reduce the accumulation of misfolded and aggregated α-syn for the treatment of Parkinson’s disease. Advisors/Committee Members: Segatori, Laura (advisor), Gonzalez, Ramon (committee member), Silberg, Jonathan J. (committee member), Nagrath, Deepak (committee member).

Subjects/Keywords: Alpha-synuclein; Aggregation; Parkinson's disease; 70-kDa heat shock protein; Transcription factor EB

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

APA (6^th Edition):

Kilpatrick, K. (2014). Reprogramming the proteostasis network to prevent the accumulation of alpha-synuclein aggregates. (Doctoral Dissertation). Rice University. Retrieved from http://hdl.handle.net/1911/77191

Chicago Manual of Style (16^th Edition):

Kilpatrick, Kiri. “Reprogramming the proteostasis network to prevent the accumulation of alpha-synuclein aggregates.” 2014. Doctoral Dissertation, Rice University. Accessed March 09, 2021. http://hdl.handle.net/1911/77191.

MLA Handbook (7^th Edition):

Kilpatrick, Kiri. “Reprogramming the proteostasis network to prevent the accumulation of alpha-synuclein aggregates.” 2014. Web. 09 Mar 2021.

Vancouver:

Kilpatrick K. Reprogramming the proteostasis network to prevent the accumulation of alpha-synuclein aggregates. [Internet] [Doctoral dissertation]. Rice University; 2014. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/1911/77191.

Council of Science Editors:

Kilpatrick K. Reprogramming the proteostasis network to prevent the accumulation of alpha-synuclein aggregates. [Doctoral Dissertation]. Rice University; 2014. Available from: http://hdl.handle.net/1911/77191

University of Michigan

13. Assimon, Victoria A. Strategies for Modulating the Diverse Activities of Heat Shock Protein 70.

Degree: PhD, Chemical Biology, 2015, University of Michigan

URL: http://hdl.handle.net/2027.42/116624

► Heat shock protein 70 (Hsp70) is an essential regulator of protein homeostasis. Dysfunction of protein homeostasis is directly linked to many diseases, including cancer and… (more)

Subjects/Keywords: Heat shock protein 70; protein-protein interactions; co-chaperones; allostery; drug-resistant bacteria; protein homeostasis; Biological Chemistry; Science

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

APA (6^th Edition):

Assimon, V. A. (2015). Strategies for Modulating the Diverse Activities of Heat Shock Protein 70. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/116624

Chicago Manual of Style (16^th Edition):

Assimon, Victoria A. “Strategies for Modulating the Diverse Activities of Heat Shock Protein 70.” 2015. Doctoral Dissertation, University of Michigan. Accessed March 09, 2021. http://hdl.handle.net/2027.42/116624.

MLA Handbook (7^th Edition):

Assimon, Victoria A. “Strategies for Modulating the Diverse Activities of Heat Shock Protein 70.” 2015. Web. 09 Mar 2021.

Vancouver:

Assimon VA. Strategies for Modulating the Diverse Activities of Heat Shock Protein 70. [Internet] [Doctoral dissertation]. University of Michigan; 2015. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/2027.42/116624.

Council of Science Editors:

Assimon VA. Strategies for Modulating the Diverse Activities of Heat Shock Protein 70. [Doctoral Dissertation]. University of Michigan; 2015. Available from: http://hdl.handle.net/2027.42/116624

University of Kansas

14. Zhang, Xinyue. Modulating Molecular Chaperones to Treat Demyelinating Neuropathies.

Degree: PhD, Pharmacology & Toxicology, 2018, University of Kansas

URL: http://hdl.handle.net/1808/27832

► Peripheral neuropathies can be classified into two categories, demyelinating or axonal neuropathy. Demyelinating neuropathies are characterized by damaged myelin but intact axons. Recent evidence suggests… (more)

▼ Peripheral neuropathies can be classified into two categories, demyelinating or axonal neuropathy. Demyelinating neuropathies are characterized by damaged myelin but intact axons. Recent evidence suggests that the leucine zipper transcription factor c-jun is at the center of driving demyelination. c-Jun is required for Schwann cells (SCs) to dedifferentiate after injury, and up-regulation of c-jun has been reported in human neuropathies. It remains to be tested whether c-jun would be a valid target for treating demyelinating neuropathies. Previously, our published work has shown that modulating the expression of heat shock protein 70 (Hsp70) using a novel small molecule drug called KU-32 attenuated the expression of c-jun and the extent of demyelination in SC-dorsal root ganglia (DRG) co-cultures in an Hsp70 dependent manner. To extend these data, this work examined the in vivo effects of modulating molecular chaperones using the next generation novologue KU-596 in two mouse models of demyelinating neuropathies. MPZ-Raf mice are a conditional transgenic mouse line that exhibits a demyelinating neuropathy due to the SC-specific induction of mitogen-activated protein kinase (MAPK) and c-jun induction after tamoxifen (TMX) injections in adult mice. Five days of TMX treatment induced a severe motor deficits starting from day 8 and treating the MPZ-Raf mice with 20 mg/kg of KU-596 every other day reduced c-jun levels in the sciatic nerves. The decrease in c-jun correlated with an improvement in the myelination status of the nerves and motor function. In line with previous findings, the effects of KU-596 were Hsp70-dependent, as MPZ-RAF × Hsp70 knockout (KO) mice did not show improvement following drug treatment. This study provides proof of principal that modulating molecular chaperones would be beneficial in treating demyelinating neuropathies. However, as this model is less relevant to an actual disease, we complemented our study using a model of human X-linked Charcot-Marie-Tooth disease (CMT1X). CMT1X is caused by the mutation of gap junction beta 1 gene (GJB1) that encodes the gap junction protein connexin 32 (Cx32). Recent evidence suggests an elevated c-jun expression is associated with the disease. Since c-jun could promote demyelination, targeting c-jun using KU-596 could provide a potential therapeutic strategy to treat CMT1X. The pathology of Cx32 deficient (Cx32def) mice occurs in two stages where young mice develop a pre-demyelinating axonopathy, which progresses to a more severe demyelinating neuropathy in older mice. We show that in young mice that exhibit a pre-demyelinating axonopathy, one-month of KU-596 treatment decreased c-jun expression and improved motor nerve conduction velocity (MNCV) and compound muscle action potential (CMAP). In older Cx32def mice that developed a demyelinating neuropathy, 3 months of KU-596 treatment decreased c-jun expression and improved grip strength, MNCV and CMAP. Hsp70 is required for drug efficacy as neither young nor old Cx32def × Hsp70 KO mice showed improvement… Advisors/Committee Members: Dobrowsky, Rick T. (advisor), Lundquist, Erik A. (cmtemember), Shi, Honglian (cmtemember), Wright, Douglas E. (cmtemember), Zhao, Liqin (cmtemember).

Subjects/Keywords: Pharmacology; c-jun; Demyelination; Heat shock protein 70 (Hsp70); Heat shock protein 90 (Hsp90); neuropathy; X-linked Charcot-Marie-Tooth disease (CMT1X)

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

APA (6^th Edition):

Zhang, X. (2018). Modulating Molecular Chaperones to Treat Demyelinating Neuropathies. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/27832

Chicago Manual of Style (16^th Edition):

Zhang, Xinyue. “Modulating Molecular Chaperones to Treat Demyelinating Neuropathies.” 2018. Doctoral Dissertation, University of Kansas. Accessed March 09, 2021. http://hdl.handle.net/1808/27832.

MLA Handbook (7^th Edition):

Zhang, Xinyue. “Modulating Molecular Chaperones to Treat Demyelinating Neuropathies.” 2018. Web. 09 Mar 2021.

Vancouver:

Zhang X. Modulating Molecular Chaperones to Treat Demyelinating Neuropathies. [Internet] [Doctoral dissertation]. University of Kansas; 2018. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/1808/27832.

Council of Science Editors:

Zhang X. Modulating Molecular Chaperones to Treat Demyelinating Neuropathies. [Doctoral Dissertation]. University of Kansas; 2018. Available from: http://hdl.handle.net/1808/27832

North Carolina State University

15. Rivera, Rafael Edgardo. The Effect of Selenium on Heat Shock Protein 70 Expression in Turkey Embryos.

Degree: MS, Poultry Science, 2004, North Carolina State University

URL: http://www.lib.ncsu.edu/resolver/1840.16/2417

► The optimum incubation environment to obtain the best poult quality has always been an important issue in the turkey industry. Heat shock protein 70 (hsp70)… (more)

▼ The optimum incubation environment to obtain the best poult quality has always been an important issue in the turkey industry. Heat shock protein 70 (hsp70) has been associated with the acquisition of thermal tolerance and tolerance to other stressors. Hsp70 functions as a molecular chaperone, assisting in protein refolding after stress-induced denaturation. Selenium is an essential trace mineral and must be incorporated into the enzyme glutathione peroxidase (GPx). GPx functions in the GSH/GSSG-px antioxidant system. It protects cells from damage due to oxidative stress. This study was conducted to examine a potential relationship between dietary supplementation of selenium to turkey hens and the expression of hsp70 in turkey embryos. A total of 52 Nicholas turkey breeder hens were fed either a breeder diet with no supplemental selenium or one supplemented with 0.3ppm organic selenium in yeast (Sel-Plex®, Alltech Inc., Nicholasville, KY). The hens were fed the experimental diets for a minimum of two weeks before the eggs were collected. The eggs were incubated at 37.5°C for 21 days, and the embryos then were heat stressed at 40°C for 2 hr. Liver samples were collected immediately after the termination of the heating episode. The liver samples were analyzed for hsp70 using an immunoblotting procedure. Selenium activity was analyzed by determination of GPx activity. There were no significant differences (P>0.05) between treatment effects on hsp70 expression and GPx activity in embryonic liver samples. A second experiment was done using commercial breeder flocks. 100 eggs were collected from a non Se-supplemented flock and 90 eggs were collected from a flock, fed 0.3 ppm of organic selenium in yeast (Sel-Plex®, Alltech Inc., Nicholasville, KY). The eggs were incubated for 21 days at 37.5°C and at day 22 half of the eggs were stressed at 40°C and the other half was kept at normal incubation temperatures. The stressed eggs were returned to normal incubator temperatures to recover for 3h. Livers were collected and analyzed as described above. They were compared with the results of the first experiments to see the results. Before stress, hsp70levels were minimal while GPx were at maximal levels with significant GPx levels between treatments. During stress (Experiment 1), there was a non-significant (P>0.05) induction of hsp70 and a significant (P<0.05) decrease of GPx with no significant differences between treatments. After stress hsp70 levels were significantly (P<0.05) higher in the non Se-supplemented samples while the Se-supplemented sample were at pre-stress levels. GPx activity in non Se-supplemented samples did not improve after stress while Se-supplemented samples were significantly (P<0.05) increasing activity after stress. Hsp70 function is an energy dependent reaction, which protects newly synthesized proteins during and after heat stress. The cell needs to stop normal protein production and divert its energy sources to keep itself alive. Se supplementation helped increase GPx… Advisors/Committee Members: Frank Edens, Committee Member (advisor), Vern Christensen, Committee Chair (advisor), Jesse Grimes, Committee Member (advisor), Michael Wineland, Committee Member (advisor).

Subjects/Keywords: Glutathione peroxidase; Selenium; hsp70; heat shock protein 70

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APA (6^th Edition):

Rivera, R. E. (2004). The Effect of Selenium on Heat Shock Protein 70 Expression in Turkey Embryos. (Thesis). North Carolina State University. Retrieved from http://www.lib.ncsu.edu/resolver/1840.16/2417

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):

Rivera, Rafael Edgardo. “The Effect of Selenium on Heat Shock Protein 70 Expression in Turkey Embryos.” 2004. Thesis, North Carolina State University. Accessed March 09, 2021. http://www.lib.ncsu.edu/resolver/1840.16/2417.

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

MLA Handbook (7^th Edition):

Rivera, Rafael Edgardo. “The Effect of Selenium on Heat Shock Protein 70 Expression in Turkey Embryos.” 2004. Web. 09 Mar 2021.

Vancouver:

Rivera RE. The Effect of Selenium on Heat Shock Protein 70 Expression in Turkey Embryos. [Internet] [Thesis]. North Carolina State University; 2004. [cited 2021 Mar 09]. Available from: http://www.lib.ncsu.edu/resolver/1840.16/2417.

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

Council of Science Editors:

Rivera RE. The Effect of Selenium on Heat Shock Protein 70 Expression in Turkey Embryos. [Thesis]. North Carolina State University; 2004. Available from: http://www.lib.ncsu.edu/resolver/1840.16/2417

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

Virginia Commonwealth University

16. Brunn, Jonathan. Investigation of Possible Novel Peptide Inhibitors to BAG-1 Based On Peptidyl-Biomimetics.

Degree: MS, Engineering, 2012, Virginia Commonwealth University

URL: https://doi.org/10.25772/MQHX-7C69 ; https://scholarscompass.vcu.edu/etd/2942

► In this Master’s Thesis Research the results can be summarized from two major tasks: (1) In our first task, we utilized our two protein system… (more)

Subjects/Keywords: peptide; inhibitor; BAG-1; HSP-70; heat shock protein; bcl-2 associated anthanogene; peptidly-biomimetics; peptidly; biomimetics; Engineering

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APA (6^th Edition):

Brunn, J. (2012). Investigation of Possible Novel Peptide Inhibitors to BAG-1 Based On Peptidyl-Biomimetics. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/MQHX-7C69 ; https://scholarscompass.vcu.edu/etd/2942

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):

Brunn, Jonathan. “Investigation of Possible Novel Peptide Inhibitors to BAG-1 Based On Peptidyl-Biomimetics.” 2012. Thesis, Virginia Commonwealth University. Accessed March 09, 2021. https://doi.org/10.25772/MQHX-7C69 ; https://scholarscompass.vcu.edu/etd/2942.

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

MLA Handbook (7^th Edition):

Brunn, Jonathan. “Investigation of Possible Novel Peptide Inhibitors to BAG-1 Based On Peptidyl-Biomimetics.” 2012. Web. 09 Mar 2021.

Vancouver:

Brunn J. Investigation of Possible Novel Peptide Inhibitors to BAG-1 Based On Peptidyl-Biomimetics. [Internet] [Thesis]. Virginia Commonwealth University; 2012. [cited 2021 Mar 09]. Available from: https://doi.org/10.25772/MQHX-7C69 ; https://scholarscompass.vcu.edu/etd/2942.

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

Council of Science Editors:

Brunn J. Investigation of Possible Novel Peptide Inhibitors to BAG-1 Based On Peptidyl-Biomimetics. [Thesis]. Virginia Commonwealth University; 2012. Available from: https://doi.org/10.25772/MQHX-7C69 ; https://scholarscompass.vcu.edu/etd/2942

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

University of Victoria

17. Montgomery, Amy. Combining induced pluripotent stem cells and fibrin matrices for spinal cord injury repair.

Degree: Department of Mechanical Engineering, 2014, University of Victoria

URL: http://hdl.handle.net/1828/5272

► Spinal cord injuries result in permanent loss of motor function, leaving those affected with long term physical and financial burdens. Strategies for spinal cord injury… (more)

Subjects/Keywords: induced pluripotent stem cells; spinal cord injury; fibrin; neural differentiation; heat shock protein 70; tissue engineering; biomaterials

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APA (6^th Edition):

Montgomery, A. (2014). Combining induced pluripotent stem cells and fibrin matrices for spinal cord injury repair. (Masters Thesis). University of Victoria. Retrieved from http://hdl.handle.net/1828/5272

Chicago Manual of Style (16^th Edition):

Montgomery, Amy. “Combining induced pluripotent stem cells and fibrin matrices for spinal cord injury repair.” 2014. Masters Thesis, University of Victoria. Accessed March 09, 2021. http://hdl.handle.net/1828/5272.

MLA Handbook (7^th Edition):

Montgomery, Amy. “Combining induced pluripotent stem cells and fibrin matrices for spinal cord injury repair.” 2014. Web. 09 Mar 2021.

Vancouver:

Montgomery A. Combining induced pluripotent stem cells and fibrin matrices for spinal cord injury repair. [Internet] [Masters thesis]. University of Victoria; 2014. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/1828/5272.

Council of Science Editors:

Montgomery A. Combining induced pluripotent stem cells and fibrin matrices for spinal cord injury repair. [Masters Thesis]. University of Victoria; 2014. Available from: http://hdl.handle.net/1828/5272

18. Saby, Manon. Identification de gènes candidats pour l'anémie de Blackfan-Diamond et caractérisation phénotypique : Identification of candidate genes for Blackfan-Diamond anemia and phenotypic characterization.

Degree: Docteur es, Sciences de la vie et de la santé. Biologie cellulaire et moléculaire, physiologie, physiopathologie, 2019, Université de Paris (2019-....)

URL: http://www.theses.fr/2019UNIP7128

► L’anémie de Blackfan-Diamond (ABD) est une érythroblastopénie congénitale rare secondaire à un blocage de la maturation des cellules érythroïdes entre les stades BFU-e (EPO indépendant)… (more)

▼ L’anémie de Blackfan-Diamond (ABD) est une érythroblastopénie congénitale rare secondaire à un blocage de la maturation des cellules érythroïdes entre les stades BFU-e (EPO indépendant) et CFU-e (EPO dépendant). La maladie se manifeste par une anémie arégénérative, le plus souvent macrocytaire. Dans 50% des cas, à l’anémie s’associe un syndrome malformatif affectant l’aire céphalique et les extrémités et incluant un retard de croissance. Bien que très hétérogène tant phénotypiquement que génotypiquement, l'ABD est due à des mutations toujours hétérozygotes dans des gènes de protéines ribosomiques (RP) pour 80% des cas. Le premier gène identifié comme impliqué dans l’ABD est le gène de la RPS19 (RPS19), faisant de l’ABD la première ribosomopathie décrite. A ce jour, 20 gènes de RP ont été identifiés. L'haplo-insuffisance en RP entraîne un défaut de maturation des ARN ribosomiques (ARNr) générant un stress nucléolaire, qui lui-même conduit à la stabilisation de la protéine p53. La p53 stabilisée induit l’apoptose et l'arrêt du cycle cellulaire qui sont responsables en grande partie de l’érythroblastopénie. Plus rarement, l’ABD peut être la conséquence de mutations présentes sur le gène GATA-1 (facteur de transcription majeur de l’érythropoïèse), le gène TSR2 (interagissant avec la protéine RPS26 et intervenant dans la biogenèse des ribosomes) ou encore le gène EPO (cytokine clé de l’érythropoïèse). Cependant, 20% des patients atteints d’ABD ne sont toujours pas génotypiquement diagnostiqués : de nouveaux gènes candidats sont encore à découvrir chez ces patients. Dans cette perspective, l’objectif de ma thèse a donc été de caractériser le rôle fonctionnel de nouveaux gènes candidats afin de confirmer leur lien avec l’ABD. Nous avons procédé à un séquençage d’exomes chez 25 familles ce qui a permis d’identifier 8 gènes candidats. Nous présentons ici quatre de ces gènes dont deux gènes codant pour un chaperon ribosomique : HSPA14 et HEATR3, un gène codant pour une RP : RPL9 et un gène codant un facteur de croissance : CECR1.Les protéines chaperons du ribosome représentent un nouveau groupe de gènes pouvant être associé à la maladie. Mes travaux de thèse ont permis d’étudier la prolifération, la division, l’amplification, la différenciation et la viabilité des cellules primaires érythroïdes issues des patients porteurs de variations alléliques dans ces gènes. Ces expériences ont permis de mettre en évidence un défaut de prolifération érythroïde chez l’ensemble des patients testés accompagné d’une diminution de l’amplification et de la division cellulaire ainsi qu’un retard de différenciation. Ces résultats sont objectivés par la persistance des marqueurs d’immaturité CD34 et IL-3R ainsi que d’un retard d’apparition des marqueurs terminaux tels que la BAND3 ou l’alpha4-intégrine. L’étude transcriptionnelle et protéique met en évidence une stabilisation de p53, conduisant à une activation de ces cibles p21 et de bax. Le travail est finalisé pour HEATR3 (manuscrit en préparation) et en cours de finalisation pour… Advisors/Committee Members: Da Costa, Lydie (thesis director).

Subjects/Keywords: Ribosomopathie; Érythroblastopénie; Biogenèse des ribosomes; Diamond-Blackfan anemia; Ribosomopathy; Erythroblastopenia; Ribosomal chaperone; Heat shock protein 70 (HSP70); Ribosome biogenesis; Erythropoiesis

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

APA (6^th Edition):

Saby, M. (2019). Identification de gènes candidats pour l'anémie de Blackfan-Diamond et caractérisation phénotypique : Identification of candidate genes for Blackfan-Diamond anemia and phenotypic characterization. (Doctoral Dissertation). Université de Paris (2019-....). Retrieved from http://www.theses.fr/2019UNIP7128

Chicago Manual of Style (16^th Edition):

Saby, Manon. “Identification de gènes candidats pour l'anémie de Blackfan-Diamond et caractérisation phénotypique : Identification of candidate genes for Blackfan-Diamond anemia and phenotypic characterization.” 2019. Doctoral Dissertation, Université de Paris (2019-....). Accessed March 09, 2021. http://www.theses.fr/2019UNIP7128.

MLA Handbook (7^th Edition):

Saby, Manon. “Identification de gènes candidats pour l'anémie de Blackfan-Diamond et caractérisation phénotypique : Identification of candidate genes for Blackfan-Diamond anemia and phenotypic characterization.” 2019. Web. 09 Mar 2021.

Vancouver:

Saby M. Identification de gènes candidats pour l'anémie de Blackfan-Diamond et caractérisation phénotypique : Identification of candidate genes for Blackfan-Diamond anemia and phenotypic characterization. [Internet] [Doctoral dissertation]. Université de Paris (2019-....); 2019. [cited 2021 Mar 09]. Available from: http://www.theses.fr/2019UNIP7128.

Council of Science Editors:

Saby M. Identification de gènes candidats pour l'anémie de Blackfan-Diamond et caractérisation phénotypique : Identification of candidate genes for Blackfan-Diamond anemia and phenotypic characterization. [Doctoral Dissertation]. Université de Paris (2019-....); 2019. Available from: http://www.theses.fr/2019UNIP7128

Indian Institute of Science

19. Namsa, Nima Dondu. Studies On Phosphorylation And Oligomerization Of Rotavirus Nonstructural Protein 5 (NSP5) And Cellular Pathways That Regulate Virus Replication.

Degree: PhD, Faculty of Science, 2016, Indian Institute of Science

URL: http://etd.iisc.ac.in/handle/2005/2526

► Rotavirus is one of the leading etiological agents of gastroenteritis in young of many species including humans worldwide and is responsible for about 600,000 infant… (more)

▼ Rotavirus is one of the leading etiological agents of gastroenteritis in young of many species including humans worldwide and is responsible for about 600,000 infant deaths per annum. Rotavirus belongs to the Reoviridae family, and its genome is composed of 11 double-stranded RNA segments that encode six structural proteins and six nonstructural proteins. Rotavirus replication is fully cytoplasmic and occurs within highly specialized regions called viroplasms. NSP2 and NSP5 have been shown to be essential for viroplasm formation and, when co-expressed in uninfected cells, to form viroplasm¬like structures. A recent study suggest a key role for NSP5 in architectural assembly of viroplasms and in recruitment of viroplasmic proteins, containing four structural (VP1, VP2, VP3 and VP6) and two nonstructural (NSP2 and NSP5) proteins. NSP5, the translation product of gene segment 11 has a predicted molecular eight of 21 kDa. NSP5 has been reported to exist in multiple isoforms ranging in size from 28-and 32-35 kDa from a 26-kDa precursor has been attributed to O-glycosylation and hyperphosphorylation. To study different properties of the protein, recombinant NSP5 containing an N-terminal hisidine tag was expressed in bacteria and purified by affinity chromatography. A significant observation was the similarity in phosphorylation property of the bacterially expressed and that expressed in mammalian cells. While the untagged recombinant protein failed to undergo phosphorylation in vitro, addition of His tag or deletions at the N-terminus promoted phosphorylation of the protein in vitro, which is very similar to the reported properties exhibited by the corresponding proteins expressed in mammalian cells. Phosphorylation of NSP5 in vitro is independent of the cell type from which the extract is derived suggesting that the kinases that phosphorylate NSP5 are distributed in all cell types. Among the C-terminal deletion mutants studied, NH-∆C5 and NH-∆C10 were phosphorylated better than full-length NSP5, but NH-∆C25 and NH¬∆C35 showed substantial reduction in the level of phosphorylation compared to full-length NSP5. These results indicate that the C-terminal 30 residues spanning the predicted α-helical domain of NSP5 are critical for its phosphorylation in vitro which is in correspondence with previous findings that C-terminal 21 amino acids of NSP5 direct its insolubility, hyperphosphorylation, and VLS formation. The results revealed that though the tagged full-length and some of the mutants could be phosphorylated in vitro, they are not suitable substrates for hyperphosphorylation unlike the similar proteins expressed in mammalian cells or infected cells. Analysis by western blot and mass spectrometry revealed that the bacterially expressed NH-NSP5 is indeed phosphorylated. It appears that prior phosphorylation in bacteria renders the protein conformationally not amendable for hyperphosphorylation by cellular kinases in vitro. Mutation of the highly conserved proline marginally enhanced its phosphorylation in vitro but the… Advisors/Committee Members: Rao, C Durga (advisor).

Subjects/Keywords: Rotaviruses; Rotaviral Nonstructural Proteins; Nonstructural Protein; Viral Proteins; Heat Shock Protein 70 (Hsp70); Viral Replication; Rotaviral Replication; Rotavirus Nonstructural Protein 5 (NSP5); Heat Shock Protein and Rotaviral Protein Interaction; Rotavirus; Rotaviral Structural Proteins; Rotaviral Proteins; Nonstructural Protein 5; VP1; VP4; Virology

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

APA (6^th Edition):

Namsa, N. D. (2016). Studies On Phosphorylation And Oligomerization Of Rotavirus Nonstructural Protein 5 (NSP5) And Cellular Pathways That Regulate Virus Replication. (Doctoral Dissertation). Indian Institute of Science. Retrieved from http://etd.iisc.ac.in/handle/2005/2526

Chicago Manual of Style (16^th Edition):

Namsa, Nima Dondu. “Studies On Phosphorylation And Oligomerization Of Rotavirus Nonstructural Protein 5 (NSP5) And Cellular Pathways That Regulate Virus Replication.” 2016. Doctoral Dissertation, Indian Institute of Science. Accessed March 09, 2021. http://etd.iisc.ac.in/handle/2005/2526.

MLA Handbook (7^th Edition):

Namsa, Nima Dondu. “Studies On Phosphorylation And Oligomerization Of Rotavirus Nonstructural Protein 5 (NSP5) And Cellular Pathways That Regulate Virus Replication.” 2016. Web. 09 Mar 2021.

Vancouver:

Namsa ND. Studies On Phosphorylation And Oligomerization Of Rotavirus Nonstructural Protein 5 (NSP5) And Cellular Pathways That Regulate Virus Replication. [Internet] [Doctoral dissertation]. Indian Institute of Science; 2016. [cited 2021 Mar 09]. Available from: http://etd.iisc.ac.in/handle/2005/2526.

Council of Science Editors:

Namsa ND. Studies On Phosphorylation And Oligomerization Of Rotavirus Nonstructural Protein 5 (NSP5) And Cellular Pathways That Regulate Virus Replication. [Doctoral Dissertation]. Indian Institute of Science; 2016. Available from: http://etd.iisc.ac.in/handle/2005/2526

Indian Institute of Science

20. Samaddar, Madhuja. Understanding in vivo Significance of Allosteric Regulation in mtHsp70s : Revealing its Implications in Parkinson's Disease Progression.

Degree: PhD, Faculty of Science, 2018, Indian Institute of Science

URL: http://etd.iisc.ac.in/handle/2005/3034

► Mitochondria are essential eukaryotic organelles, acting as the sites for numerous crucial metabolic and signalling pathways. The biogenesis of mitochondria requires efficient targeting of several… (more)

▼ Mitochondria are essential eukaryotic organelles, acting as the sites for numerous crucial metabolic and signalling pathways. The biogenesis of mitochondria requires efficient targeting of several hundreds of proteins from the cytosol, to their varied functional locations within the organelle. The translocation of localized proteins across the inner membrane, and their subsequent folding is achieved by the ATP-dependent function of mitochondrial Hsp70 (mtHsp70). It is a bonafide member of the Hsp70 chaperone family, which are involved in a multitude of functions, together aimed at protein quality control and maintenance of cellular homeostasis. These varied functions of Hsp70 proteins require binding to exposed hydrophobic patches in substrate polypeptides thus preventing non-productive associations. The interaction with substrates occurs through the substrate-binding domain (SBD) and is regulated by the ATPase activity of the nucleotide-binding domain (NBD), through a series of conformational changes. Conversely, substrate binding to the SBD also stimulates ATP hydrolysis, and thereby the core activities of the two domains are regulated by mutual allosteric signalling. This mechanism of bidirectional inter-domain communication is indispensable for Hsp70 function, which is characterized by cycles of substrate binding and release, coupled to cycles of ATP binding and hydrolysis. The process of allosteric regulation in Hsp70 proteins has been comprehensively investigated, especially in the bacterial homolog, DnaK. However, the in vivo functional significance of inter-domain communication in the eukaryotic mtHsp70 system and the mechanism of its regulation remain unexplored. Furthermore, the complex physiological implications of impairment in allosteric communication and their correlation with diverse disease conditions, including Myelodysplastic syndrome (MDS), and Parkinson’s disease (PD), are yet to be elucidated. Based on this brief introduction, the primary research objectives set out in the present thesis were to: 1. uncover the regulation of ligand-modulated allosteric communication between the two domains of mtHsp70; and its in vivo significance in the context of protein import into the organelle. (Chapter 2) 2. understand the role of mtHsp70 in progression of Parkinson’s disease; and to study the modulation of α-synuclein toxicity by the protein quality control function of the mtHsp70 chaperone network. (Chapters 3 and 4) We have employed a battery of genetic and biochemical approaches to investigate the above questions using the Saccharomyces cerevisiae mtHsp70 protein, Ssc1; an essential protein that is involved in a plethora of critical functions in this eukaryotic model system. Objective 1: Structural studies, primarily in bacterial DnaK, have yielded mechanistic insights into its interactions with ligands and cochaperones, as well as conformational transitions in different ligand-bound states. In recent years, the availability of crystal structures of full-length DnaK and detailed information… Advisors/Committee Members: D'Silva, Patrick (advisor).

Subjects/Keywords: Eukaryotic Organelle; Mitochonodria; Parkinson's Disease Progression; Mitochondrial Heat Shock Protein 70; Hsp70 Proteins; Saccharomyces cerevisiae mtHsp70 Protein; Allosteric Regulation; Mitochondrial Protein Import; Mitochondria Biogenesis; Mitochondrial HSP70 Chaperon Network; Heat Shock Proteins; mtHSp70; mtHsp70s; Parkinson's Disease; Biochemistry

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

APA (6^th Edition):

Samaddar, M. (2018). Understanding in vivo Significance of Allosteric Regulation in mtHsp70s : Revealing its Implications in Parkinson's Disease Progression. (Doctoral Dissertation). Indian Institute of Science. Retrieved from http://etd.iisc.ac.in/handle/2005/3034

Chicago Manual of Style (16^th Edition):

Samaddar, Madhuja. “Understanding in vivo Significance of Allosteric Regulation in mtHsp70s : Revealing its Implications in Parkinson's Disease Progression.” 2018. Doctoral Dissertation, Indian Institute of Science. Accessed March 09, 2021. http://etd.iisc.ac.in/handle/2005/3034.

MLA Handbook (7^th Edition):

Samaddar, Madhuja. “Understanding in vivo Significance of Allosteric Regulation in mtHsp70s : Revealing its Implications in Parkinson's Disease Progression.” 2018. Web. 09 Mar 2021.

Vancouver:

Samaddar M. Understanding in vivo Significance of Allosteric Regulation in mtHsp70s : Revealing its Implications in Parkinson's Disease Progression. [Internet] [Doctoral dissertation]. Indian Institute of Science; 2018. [cited 2021 Mar 09]. Available from: http://etd.iisc.ac.in/handle/2005/3034.

Council of Science Editors:

Samaddar M. Understanding in vivo Significance of Allosteric Regulation in mtHsp70s : Revealing its Implications in Parkinson's Disease Progression. [Doctoral Dissertation]. Indian Institute of Science; 2018. Available from: http://etd.iisc.ac.in/handle/2005/3034

21. Briassouli, Efrossini. Οι πρωτεΐνες καταπληξίας και η γλουταμίνη στην ανοσολογική απόκριση ασθενών με σήψη.

Degree: 2016, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/37296

►

Heat-Shock Proteins (HSPs) are molecular chaperones protecting cells against heat-shock (HS) or sepsis induced protein damage by activating homeostatic mechanisms, in an attempt to sustain… (more)

▼

Heat-Shock Proteins (HSPs) are molecular chaperones protecting cells against heat-shock (HS) or sepsis induced protein damage by activating homeostatic mechanisms, in an attempt to sustain a viable intracellular environment. L-Alanyl-Glutamine (L-Ala-Gln) is a pharmaco-nutrient commonly used in nutrition regimens due to its immunomodulatory effects. This study investigated whether L-Ala-Gln modulated heat shock protein-72 (HSP72) and HSP90α (HSP90α), T helper (Th)1, Th2, and Th17 cytokine expression in the peripheral blood mononuclear cells (PBMC) of patients with severe sepsis (SS). Then the lipopolysaccharide (LPS) or HS induction of HSP72 and HSP90α in PBMCs of patients with severe sepsis (SS) or trauma-related systemic inflammatory response syndrome (SIRS) were assessed, in comparison to healthy individuals (H). Finally, any pre- or post-treatment modulating glutamine (Gln) effect was investigated.High-doses of L-Gln or L-Ala-Gln do not induce any of the Th1, Th2, and Th17 cytokine in either healthy or septic human PBMCs. High Gln doses suppress HSP72 in septic and control PBMCs. HSP90α time-series expression declines, contrasting the increasing trend of HSP72 in healthy controls. HSP90α sustains increased levels in septic supernatants, showing a characteristic longitudinal behavior needed further elucidation. Regarding baseline PBMCs levels, HSP72-mRNA and lymphocyte and monocyte mHSP72 and HSP90α proteins are higher among critically ill patients, further induced by HS, not by LPS. HSP72-proteins and mRNA are positively related to serum-cytokines and negatively to supernatant-cytokines, not been influenced by HSP72-polymorphisms, cortisol or illness severity. Gln may depress l/mHSP72 after exposure to LPS and enhance them after HS-induction, but it may not affect early-induced HSP72-mRNA. Contrasting the strong HS-induction of intracellular HSP90α of healthy individuals, the HS monocyte or lymphocyte HSP90α-tolerance effect might suggest a PBMCs’ inability to respond to fever in critical illness.

Σε αυτή την μελέτη, σε μονοπύρηνα κύτταρα περιφερικού αίματος (peripheral blood mononuclear cells (PBMC)) ασθενών με σοβαρή σήψη (severe sepsis (SS)) συγκριτικά με ασθενείς με SIRS (systemic inflammatory response syndrome) που προκλήθηκε από τραύμα και υγιείς μάρτυρες, ερευνήσαμε την δράση της Gln πριν ή μετά από διέγερση με θερμικό σοκ ή με λιποπολυσακχαρίτη (lipopolysaccharide (LPS)). Συγκεκριμένα, ελέγχθηκε το ενδεχόμενο να ασκεί τροποποιητική δράση στην απάντηση της heat shock protein-72 (HSP72) και της heat shock protein-90α (HSP90α), τόσο ενδοκυττάρια και εξωκυττάρια όσο και σε επίπεδο γονιδιακής έκφρασης. Επίσης μελετήθηκε η επίδραση που έχει στις αναφερόμενες συνθήκες διέγερσης σε διάφορες φλεγμονώδεις και αντιφλεγμονώδεις κυτταροκίνες σε εξωκυττάριο επίπεδο στις προαναφερθείσες ομάδες ασθενών και υγιών μαρτύρων.Όσο αναφορά τα βασικά επίπεδα στα PBMCs ενδοκυττάριας HSP72 καθώς και έκφρασης του mRNA της HSP72 , στους ασθενείς σε κρίσιμη κατάσταση ήταν υψηλότερα και αυξήθηκαν ακόμα περισσότερο με το HS, αλλά…

Subjects/Keywords: Ανοσοπαρέμβαση στην σήψη; Γλουταμίνη; Hsp90; Heat shock proteins 70 KDa ( HSP70)

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

APA (6^th Edition):

Briassouli, E. (2016). Οι πρωτεΐνες καταπληξίας και η γλουταμίνη στην ανοσολογική απόκριση ασθενών με σήψη. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/37296

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):

Briassouli, Efrossini. “Οι πρωτεΐνες καταπληξίας και η γλουταμίνη στην ανοσολογική απόκριση ασθενών με σήψη.” 2016. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed March 09, 2021. http://hdl.handle.net/10442/hedi/37296.

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

MLA Handbook (7^th Edition):

Briassouli, Efrossini. “Οι πρωτεΐνες καταπληξίας και η γλουταμίνη στην ανοσολογική απόκριση ασθενών με σήψη.” 2016. Web. 09 Mar 2021.

Vancouver:

Briassouli E. Οι πρωτεΐνες καταπληξίας και η γλουταμίνη στην ανοσολογική απόκριση ασθενών με σήψη. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2016. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/10442/hedi/37296.

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

Council of Science Editors:

Briassouli E. Οι πρωτεΐνες καταπληξίας και η γλουταμίνη στην ανοσολογική απόκριση ασθενών με σήψη. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2016. Available from: http://hdl.handle.net/10442/hedi/37296

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

Cornell University

22. Nicklow, Erin Elizabeth. Regulation of Hsp70 chaperone cycle via reversible methionine oxidation of the nucleotide exchange factor Fes1.

Degree: PhD, Biochemistry, Molecular and Cell Biology, 2019, Cornell University

URL: http://hdl.handle.net/1813/67786

► Elevated levels of reactive oxygen species (ROS) are associated with the pathologies of many degenerative disorders (like aging, Alzheimer’s disease, atherosclerosis, and diabetes). Cells employ… (more)

▼ Elevated levels of reactive oxygen species (ROS) are associated with the pathologies of many degenerative disorders (like aging, Alzheimer’s disease, atherosclerosis, and diabetes). Cells employ a network of regulatory pathways to manage intracellular ROS levels. Identification and characterization of these fundamental pathways is necessary to determine what triggers the decline in anti-oxidant defenses associated with disease progression. Key to this understanding are the emerging roles of ROS as signaling molecules. ROS-based signaling is initiated by activation of sulfur-based redox switches, in which protein cysteine or methionine residues are post-translationally modified (oxidized) to transiently alter protein function in a manner appropriate for the physiological environment. Hsp70s are a conserved family of molecular chaperones that serve critical roles in maintaining cellular proteostasis under oxidative stress. In this dissertation, I have uncovered that a co-chaperone (Fes1) of the cytoplasmic Hsp70 system in yeast undergoes reversible methionine oxidation during excessively oxidizing cellular conditions. I have determined that three clustered methionine residues in Fes1 are oxidized to methionine sulfoxide, which inhibits Fes1 activity (and correspondingly Hsp70 chaperone activity) during stress. Importantly, I establish that Fes1 oxidation is a reversible signaling event that is regulated enzymatically by methionine sulfoxide reductase (Msr). These studies have revealed that the two yeast Msr proteins (Mxr1 and Mxr2) are both expressed in the cytosol, in contrast to prior reports of Mxr2 suggesting sole mitochondrial localization. I demonstrate that a cytoplasmic isoform of Mxr2 co-operates with Mxr1 to regulate the redox state of Fes1. Together, these studies provide a new perspective on how activities of the well-studied Hsp70 family can be attuned by ROS, and further define how methionine redox-switches, which are largely under-studied in comparison to their cysteine counterparts, are used as a means for cells to sense and respond to oxidative stress. I speculate that Fes1 oxidation may be conserved in higher eukaryotes and could serve to beneficially support cell viability during periods of oxidative stress. Elucidation of a methionine-based signaling pathway involving Fes1 furthers a general understanding of the types of events mediated by this emerging post-translational modification, for which there are few examples characterized in mechanistic detail. Advisors/Committee Members: Sevier, Carolyn S. (chair), Brown, William J. (committee member), Fromme, Joseph Chris (committee member).

Subjects/Keywords: 70 kilodalton heat shock protein (Hsp70); Fes1; methionine oxidation; methionine sulfoxide reductase; nucleotide exchange factor (NEF); reactive oxygen species (ROS); Cellular biology; Biochemistry

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

APA (6^th Edition):

Nicklow, E. E. (2019). Regulation of Hsp70 chaperone cycle via reversible methionine oxidation of the nucleotide exchange factor Fes1. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/67786

Chicago Manual of Style (16^th Edition):

Nicklow, Erin Elizabeth. “Regulation of Hsp70 chaperone cycle via reversible methionine oxidation of the nucleotide exchange factor Fes1.” 2019. Doctoral Dissertation, Cornell University. Accessed March 09, 2021. http://hdl.handle.net/1813/67786.

MLA Handbook (7^th Edition):

Nicklow, Erin Elizabeth. “Regulation of Hsp70 chaperone cycle via reversible methionine oxidation of the nucleotide exchange factor Fes1.” 2019. Web. 09 Mar 2021.

Vancouver:

Nicklow EE. Regulation of Hsp70 chaperone cycle via reversible methionine oxidation of the nucleotide exchange factor Fes1. [Internet] [Doctoral dissertation]. Cornell University; 2019. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/1813/67786.

Council of Science Editors:

Nicklow EE. Regulation of Hsp70 chaperone cycle via reversible methionine oxidation of the nucleotide exchange factor Fes1. [Doctoral Dissertation]. Cornell University; 2019. Available from: http://hdl.handle.net/1813/67786

23. Tamaki, Yoshitaka. Elimination of TDP-43 inclusions linked to amyotrophic lateral sclerosis by a misfolding-specific intrabody with dual proteolytic signals .

Degree: 2018, Kyoto University

URL: http://hdl.handle.net/2433/235059

Subjects/Keywords: Amyotrophic lateral sclerosis; TDP-43; Intrabody; Chaperone-mediated autophagy; Heat shock protein 70

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

APA (6^th Edition):

Tamaki, Y. (2018). Elimination of TDP-43 inclusions linked to amyotrophic lateral sclerosis by a misfolding-specific intrabody with dual proteolytic signals . (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/235059

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):

Tamaki, Yoshitaka. “Elimination of TDP-43 inclusions linked to amyotrophic lateral sclerosis by a misfolding-specific intrabody with dual proteolytic signals .” 2018. Thesis, Kyoto University. Accessed March 09, 2021. http://hdl.handle.net/2433/235059.

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

MLA Handbook (7^th Edition):

Tamaki, Yoshitaka. “Elimination of TDP-43 inclusions linked to amyotrophic lateral sclerosis by a misfolding-specific intrabody with dual proteolytic signals .” 2018. Web. 09 Mar 2021.

Vancouver:

Tamaki Y. Elimination of TDP-43 inclusions linked to amyotrophic lateral sclerosis by a misfolding-specific intrabody with dual proteolytic signals . [Internet] [Thesis]. Kyoto University; 2018. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/2433/235059.

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

Council of Science Editors:

Tamaki Y. Elimination of TDP-43 inclusions linked to amyotrophic lateral sclerosis by a misfolding-specific intrabody with dual proteolytic signals . [Thesis]. Kyoto University; 2018. Available from: http://hdl.handle.net/2433/235059

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

Universidade Federal de Santa Maria

24. João Gabriel Santos Rosa. EFEITOS DO ORGANOFOSFORADO PARATIONATO METÍLICO SOBRE O EIXO HIPOTÁLAMO-HIPÓFISE-INTERRENAL EM PEIXE-ZEBRA (Danio rerio).

Degree: 2013, Universidade Federal de Santa Maria

URL: http://coralx.ufsm.br/tede/tde_busca/arquivo.php?codArquivo=5425

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Compostos organofosforados como o parationato metílico são utilizados nas diversas etapas de produção para controlar pragas tanto na atividade agrícola como na aquicultura. O mecanismo… (more)

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Compostos organofosforados como o parationato metílico são utilizados nas diversas etapas de produção para controlar pragas tanto na atividade agrícola como na aquicultura. O mecanismo de ação desse tipo de composto é a inibição da enzima acetilcolinesterase. O peixe-zebra (Danio rerio) vem sendo cada vez mais usado como modelo experimental em variados campos, como desenvolvimento, genética e pesquisa farmacológica. O parationato metílico já foi caracterizado como interruptor endócrino do eixo hipotálamo-hipófise-interrenal (HHI). Foi realizado um experimento de 96 horas de exposição de peixes adultos à substância testada, na concentração de 5,2 mg/L. Foi avaliado o nível de cortisol de corpo inteiro, visando medir a resposta endócrina a um evento estressor. Também foram investigadas a expressão dos genes do receptor de glicocorticoide (GR), da proteína regulatória de esteroidogenese aguda (StAR) e a proteína do choque térmico 70 (HSP 70). Os peixes expostos que foram submetidos a um evento estressor demonstraram baixos níveis de cortisol de corpo inteiro. Além disso, os peixes estressados e expostos ao agroquímico apresentaram uma diminuição da expressão dos genes GR, StAR e HSP 70. Os dados indicam que a exposição ao parationato metílico provoca uma diminuição da capacidade de responder adequadamente a um evento estressor. Peixes que possuem uma incapacidade em produzir uma resposta satisfatória do eixo HHI, não são capazes de realizar os ajustes iônicos e metabólicos necessários à recuperação da homeostase, ficando vulneráveis ao estresse causado pelas práticas aquícolas ou por alterações ambientais.

Organophosphorus compounds such as methyl-parathion are used in the various stages of production to control pests both in agricultural activity as in aquaculture. The mechanism of action of this type of compound is the inhibition of the enzyme acetylcholinesterase. The zebrafish (Danio rerio) has been increasingly used as an experimental model in varied fields such as development, genetics and pharmacological research. The methyl-parathion has been characterized as endocrine disruptor of the hypothalamic-pituitary-interrenal axis (HHI). An experiment was carried out of 96 hours of exposure of adult fish to the substance tested, at the concentration of 5.2 mg/L. Was evaluated the whole-body cortisol level in order to measure the endocrine response to a stressful event. Were also investigated the gene expression of glucocorticoid receptor (GR), steroidogenic acute regulatory protein (StAR) and heat shock protein 70 (HSP 70). Fish exposed that have undergone a stressor event demonstrated low levels of cortisol. In addition, the fish stressed and exposed to agro-chemical showed a decreased expression of the StAR, HSP 70 and GR genes. The data indicate that exposure to methyl-parathion causes a decrease in the ability to respond appropriately to a stressor. Fish that have an inability to produce a satisfactory answer by the HHI axis are not able to make the necessary metabolic and ion adjustments for recovery the…

Advisors/Committee Members: Leonardo José Gil Barcellos, Luiz Carlos Kreutz, Angelo Luis Stapassoli Piato, Michele Fagundes.

Subjects/Keywords: Genes; Expressão; Proteína do choque térmico 70; Receptor de glicocorticoide; Proteína regulatória de esteroidogenese aguda; Danio rerio; Parationato metílico; Cortisol; FARMACIA; Danio rerio; Methyl-Parathion. Cortisol. Steroidogenic acute regulatory protein. Glucocorticoid receptor. Heat shock protein 70. Expression. Genes

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

APA (6^th Edition):

Rosa, J. G. S. (2013). EFEITOS DO ORGANOFOSFORADO PARATIONATO METÍLICO SOBRE O EIXO HIPOTÁLAMO-HIPÓFISE-INTERRENAL EM PEIXE-ZEBRA (Danio rerio). (Thesis). Universidade Federal de Santa Maria. Retrieved from http://coralx.ufsm.br/tede/tde_busca/arquivo.php?codArquivo=5425

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):

Rosa, João Gabriel Santos. “EFEITOS DO ORGANOFOSFORADO PARATIONATO METÍLICO SOBRE O EIXO HIPOTÁLAMO-HIPÓFISE-INTERRENAL EM PEIXE-ZEBRA (Danio rerio).” 2013. Thesis, Universidade Federal de Santa Maria. Accessed March 09, 2021. http://coralx.ufsm.br/tede/tde_busca/arquivo.php?codArquivo=5425.

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

MLA Handbook (7^th Edition):

Rosa, João Gabriel Santos. “EFEITOS DO ORGANOFOSFORADO PARATIONATO METÍLICO SOBRE O EIXO HIPOTÁLAMO-HIPÓFISE-INTERRENAL EM PEIXE-ZEBRA (Danio rerio).” 2013. Web. 09 Mar 2021.

Vancouver:

Rosa JGS. EFEITOS DO ORGANOFOSFORADO PARATIONATO METÍLICO SOBRE O EIXO HIPOTÁLAMO-HIPÓFISE-INTERRENAL EM PEIXE-ZEBRA (Danio rerio). [Internet] [Thesis]. Universidade Federal de Santa Maria; 2013. [cited 2021 Mar 09]. Available from: http://coralx.ufsm.br/tede/tde_busca/arquivo.php?codArquivo=5425.

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

Council of Science Editors:

Rosa JGS. EFEITOS DO ORGANOFOSFORADO PARATIONATO METÍLICO SOBRE O EIXO HIPOTÁLAMO-HIPÓFISE-INTERRENAL EM PEIXE-ZEBRA (Danio rerio). [Thesis]. Universidade Federal de Santa Maria; 2013. Available from: http://coralx.ufsm.br/tede/tde_busca/arquivo.php?codArquivo=5425

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

IUPUI

25. Hammack, Lindsay J. 20S proteasome assembly: alternative pathways and complexes.

Degree: 2017, IUPUI

URL: http://hdl.handle.net/1805/15096

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Indiana University-Purdue University Indianapolis (IUPUI)

The ubiquitin-proteasome system is responsible for the targeted degradation of proteins within the cell. The 26S proteasome, which is the… (more)

Subjects/Keywords: Proteasome; Protein Assembly; Heat shock protein

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

APA (6^th Edition):

Hammack, L. J. (2017). 20S proteasome assembly: alternative pathways and complexes. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/15096

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):

Hammack, Lindsay J. “20S proteasome assembly: alternative pathways and complexes.” 2017. Thesis, IUPUI. Accessed March 09, 2021. http://hdl.handle.net/1805/15096.

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

MLA Handbook (7^th Edition):

Hammack, Lindsay J. “20S proteasome assembly: alternative pathways and complexes.” 2017. Web. 09 Mar 2021.

Vancouver:

Hammack LJ. 20S proteasome assembly: alternative pathways and complexes. [Internet] [Thesis]. IUPUI; 2017. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/1805/15096.

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

Council of Science Editors:

Hammack LJ. 20S proteasome assembly: alternative pathways and complexes. [Thesis]. IUPUI; 2017. Available from: http://hdl.handle.net/1805/15096

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

26. Κύρου, Ιωάννα. Η επίδραση του ισχαιμικού preconditioning στους μηχανισμούς βλάβης του νωτιαίου μυελού μετά από αποκλεισμό της κατιούσας θωρακικής αορτής σε χοίρους.

Degree: 2011, University of Ioannina; Πανεπιστήμιο Ιωαννίνων

URL: http://hdl.handle.net/10442/hedi/25199

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Purpose: Herein, we investigate a possible protective role of the basal levels of Hsp70, the relationship between β-catenin and Hsp70, and the possible activation of… (more)

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Purpose: Herein, we investigate a possible protective role of the basal levels of Hsp70, the relationship between β-catenin and Hsp70, and the possible activation of β-catenin signal pathway in an early IPC experimental model, suggesting a possible role of these proteins in “first window of protection”. Methods:A total of 42 market pigs were used. Twelve animals were used in experiments for neurological evaluation and were randomly assigned to 2 groups. The remaining 30 animals were used in experiments for biological measurements and innunohistochemical studies, and were randomly assigned to 5 groups. The aortic occlusion was accomplished intravascularly with two occlusion-balloon catheters under fluoroscopic guidance. Neurologic evaluation was performed by an independent observer according to Tarlov scale. After sacrifice the lumbar spinal cords were harvested. Immunoprecipitation and western blotting studies for Hsp70, cytoskeleton elements and β-catenin, were performed in order to study their relationship and possible modifications of this in early IPC, whereas with immunohistochemical studies we investigated the cellular distribution of Hsp70 and β-catenin. Results: According to neurologic evaluation, at 24 hours, spastic paraplegia with no or slight movement of the lower limbs was observed in 84% of animals in group A, whereas an equivalent percent of animals in group B had no neurologic deficits. The differences seen in neurologic outcome between the groups A and B were statistically significant (P=0.003). The biological measurements demonstrated that Hsp70 binds to actin and to intermediate filaments of neurons (neurofilaments) and that early ischemic preconditioning influenced significantly (P =0,025) only the binding profile of Hsp70 with neurofilaments, by increasing the amount of neurofilaments that binds to Hsp70. Additionally, with immunohistochemical studies, we observed immunoreactivity of Hsp70 in cytoplasm in groups 1 and 5 and translocation of Hsp70 in nucleus in groups 2, 3 and 4. As regard β-catenin there was an increase in the samples of group 3 and a weak binding relationship with Hsp70 wich was not influenced by IPC. The immunohistochemical studies shwoed immunoreactivity for β-catenin in cytoplasm and in nucleus only in group 3. Conclusions: The results indicate that Hsp70 has an essential role in early ischemic preconditioning of spinal cord, by a) protecting the intermediate filaments of neurons (neurofilaments) that have crucial function in axonal transport, nerve conduction and in cytoskeleton stabilization and b) ensuring the functionality and the integrity of the nucleus, as contribute in the protection and repair of its structures as soon as the intensive insult begin. Moreover IPC activated the β-catenin dependent signal pathway, the active/stabilized fraction of which can offer protection through various kinases.

Στόχος: Στην παρούσα μελέτη ερευνάμε τον πιθανό προστατευτικό ρόλο των βασικών επιπέδων της Hsp70 στον νωτιαίο μυελό, την σχέση σύνδεσης της β-κατενίνης με την Hsp70 αλλά…

Subjects/Keywords: Ισχαιμία; Ισχαιμική προετοιμασία; Νωτιαίος μυελός; Παραπληγία / Παραπάρεση; Θωρακοκοιλιακός αποκλεισμός; Πειραματικό μοντέλο χοίρων; Πρωτεΐνη θερμικού στρες 70; β-κατενίνη; Ischemia; Ischemic preconditioning; Spinal cord; Paraplegia; Thoracoabdominal aorta occlusion; Experimental model; Heat shock protein 70; β-catenin

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

APA (6^th Edition):

Κύρου, . �. (2011). Η επίδραση του ισχαιμικού preconditioning στους μηχανισμούς βλάβης του νωτιαίου μυελού μετά από αποκλεισμό της κατιούσας θωρακικής αορτής σε χοίρους. (Thesis). University of Ioannina; Πανεπιστήμιο Ιωαννίνων. Retrieved from http://hdl.handle.net/10442/hedi/25199

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):

Κύρου, Ιωάννα. “Η επίδραση του ισχαιμικού preconditioning στους μηχανισμούς βλάβης του νωτιαίου μυελού μετά από αποκλεισμό της κατιούσας θωρακικής αορτής σε χοίρους.” 2011. Thesis, University of Ioannina; Πανεπιστήμιο Ιωαννίνων. Accessed March 09, 2021. http://hdl.handle.net/10442/hedi/25199.

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

MLA Handbook (7^th Edition):

Κύρου, Ιωάννα. “Η επίδραση του ισχαιμικού preconditioning στους μηχανισμούς βλάβης του νωτιαίου μυελού μετά από αποκλεισμό της κατιούσας θωρακικής αορτής σε χοίρους.” 2011. Web. 09 Mar 2021.

Vancouver:

Κύρου �. Η επίδραση του ισχαιμικού preconditioning στους μηχανισμούς βλάβης του νωτιαίου μυελού μετά από αποκλεισμό της κατιούσας θωρακικής αορτής σε χοίρους. [Internet] [Thesis]. University of Ioannina; Πανεπιστήμιο Ιωαννίνων; 2011. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/10442/hedi/25199.

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

Council of Science Editors:

Κύρου �. Η επίδραση του ισχαιμικού preconditioning στους μηχανισμούς βλάβης του νωτιαίου μυελού μετά από αποκλεισμό της κατιούσας θωρακικής αορτής σε χοίρους. [Thesis]. University of Ioannina; Πανεπιστήμιο Ιωαννίνων; 2011. Available from: http://hdl.handle.net/10442/hedi/25199

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

University of Wollongong

27. Cox, Dezerae. The interaction of small heat shock molecular chaperone proteins with a-synuclein.

Degree: PhD, 2016, University of Wollongong

URL: 0601 BIOCHEMISTRY AND CELL BIOLOGY ; https://ro.uow.edu.au/theses/4823

► Protein homeostasis, or proteostasis, is the process of maintaining the conformational and functional integrity of the proteome. Proteostasis is preserved in the face of… (more)

Subjects/Keywords: protein aggregation; neurodegeneration; heat shock proteins

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

APA (6^th Edition):

Cox, D. (2016). The interaction of small heat shock molecular chaperone proteins with a-synuclein. (Doctoral Dissertation). University of Wollongong. Retrieved from 0601 BIOCHEMISTRY AND CELL BIOLOGY ; https://ro.uow.edu.au/theses/4823

Chicago Manual of Style (16^th Edition):

Cox, Dezerae. “The interaction of small heat shock molecular chaperone proteins with a-synuclein.” 2016. Doctoral Dissertation, University of Wollongong. Accessed March 09, 2021. 0601 BIOCHEMISTRY AND CELL BIOLOGY ; https://ro.uow.edu.au/theses/4823.

MLA Handbook (7^th Edition):

Cox, Dezerae. “The interaction of small heat shock molecular chaperone proteins with a-synuclein.” 2016. Web. 09 Mar 2021.

Vancouver:

Cox D. The interaction of small heat shock molecular chaperone proteins with a-synuclein. [Internet] [Doctoral dissertation]. University of Wollongong; 2016. [cited 2021 Mar 09]. Available from: 0601 BIOCHEMISTRY AND CELL BIOLOGY ; https://ro.uow.edu.au/theses/4823.

Council of Science Editors:

Cox D. The interaction of small heat shock molecular chaperone proteins with a-synuclein. [Doctoral Dissertation]. University of Wollongong; 2016. Available from: 0601 BIOCHEMISTRY AND CELL BIOLOGY ; https://ro.uow.edu.au/theses/4823

University of Waikato

28. Kaur, Supreet. In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells .

Degree: 2015, University of Waikato

URL: http://hdl.handle.net/10289/10578

► Diabetes mellitus ( DM) is a metabolic disorder and affecting worldwide as stated by WHO that diabetes will be seventh leading cause of death in… (more)

▼ Diabetes mellitus ( DM) is a metabolic disorder and affecting worldwide as stated by WHO that diabetes will be seventh leading cause of death in 2030. Diabetes mellitus is characterized by hyperglycaemia and the production of reactive oxygen species that damages proteins, lipids and DNA. This further elicits mitochondrial specific stress, resulting in increased production of HSP60 which is a mitochondrial stress protein. The aim of this study was to investigate the mitochondrial morphology changes and heat shock protein responses of HeLa cells subjected to physiological levels of hyperglycaemia (25mM). HeLa cell growth was found to be slightly reduced with increasing glucose concentrations (10mM – 25mM ) as compared to the control (5mM). Furthermore, high glucose conditions (25mM) also affected mitochondrial activity as statistically significantly decreased mitochondrial dehydrogenase activity was observed as compared to the control. These results altogether conclude that high glucose (25mM) acted as a mitochondrial stressor. Mitochondria is a dynamic organelle that fuses and divides according to environmental stimuli and energy requirements. As a result the shape of mitochondria varies from small ovals to tubules and reticular networks. These events are mainly controlled by fission and fusion proteins and regulatory machinery. Therefore mitochondrial morphology was also analyzed by using confocal microscopy to determine the effects of high glucose (25mM) on mitochondrial morphology as compared to the control. It was found that the majority of mitochondria in the control (5mM) was tubular as compared to high glucose which showed increased mitochondrial fragmentation suggesting that growing cells in the presence of hyperglycemic conditions lead to mitochondrial stress. Mitochondrial specific stress results in selective induction of molecular chaperone, HSP60 which is mainly localized in the matrix of mitochondria. So furthermore , the expression of HSP60 was investigated. Consistent western blots results showed upregulation of HSP60 with heat shocked protein set as a positive control but not with high glucose concentration (25mM). Interestingly, HSP70 expression was found to be upregulated with high glucose (25mM) as compared to control therefore it can be concluded that there were more general cellular stress as compared to mitochondrial specific stress. This study concluded that high glucose (25mM) effects HeLa cell growth and mitochondrial activity as well as mitochondrial morphology . There are various evidence which links oxidative stress and mitochondrial dynamics and observed increased production of ROS along with short and fragmented mitochondria in high glucose conditions. Advisors/Committee Members: Martinus, Ryan Dennis (advisor).

Subjects/Keywords: Diabetes; Heat shock protein 60; mitochondrial morphology

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

APA (6^th Edition):

Kaur, S. (2015). In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells . (Masters Thesis). University of Waikato. Retrieved from http://hdl.handle.net/10289/10578

Chicago Manual of Style (16^th Edition):

Kaur, Supreet. “In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells .” 2015. Masters Thesis, University of Waikato. Accessed March 09, 2021. http://hdl.handle.net/10289/10578.

MLA Handbook (7^th Edition):

Kaur, Supreet. “In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells .” 2015. Web. 09 Mar 2021.

Vancouver:

Kaur S. In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells . [Internet] [Masters thesis]. University of Waikato; 2015. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/10289/10578.

Council of Science Editors:

Kaur S. In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells . [Masters Thesis]. University of Waikato; 2015. Available from: http://hdl.handle.net/10289/10578

Victoria University of Wellington

29. Andreassend, Sarah Kateyln. The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses.

Degree: 2017, Victoria University of Wellington

URL: http://hdl.handle.net/10063/9269

► The most lethal causative species of malaria, Plasmodium falciparum, has been reported as developing resistance against current antimalarial drugs in South-East Asia. New antimalarial drugs,… (more)

Subjects/Keywords: Malaria; Heat shock protein; Prenylated alkaloid

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

APA (6^th Edition):

Andreassend, S. K. (2017). The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses. (Masters Thesis). Victoria University of Wellington. Retrieved from http://hdl.handle.net/10063/9269

Chicago Manual of Style (16^th Edition):

Andreassend, Sarah Kateyln. “The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses.” 2017. Masters Thesis, Victoria University of Wellington. Accessed March 09, 2021. http://hdl.handle.net/10063/9269.

MLA Handbook (7^th Edition):

Andreassend, Sarah Kateyln. “The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses.” 2017. Web. 09 Mar 2021.

Vancouver:

Andreassend SK. The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses. [Internet] [Masters thesis]. Victoria University of Wellington; 2017. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/10063/9269.

Council of Science Editors:

Andreassend SK. The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses. [Masters Thesis]. Victoria University of Wellington; 2017. Available from: http://hdl.handle.net/10063/9269

University of New Mexico

30. Lanphere, Kathryn. The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise.

Degree: Health, Exercise, and Sports Sciences, 2014, University of New Mexico

URL: http://hdl.handle.net/1928/23558

► Exercise disrupts homeostasis and leads to the induction of an important catabolic system called autophagy. Autophagy is a beneficial cell survival process that is induced… (more)

▼ Exercise disrupts homeostasis and leads to the induction of an important catabolic system called autophagy. Autophagy is a beneficial cell survival process that is induced in periods of starvation. The purposes of this study are to (1) determine the time course of autophagy activation following endurance exercise at 70% of VO2max in a warm environment and (2) to determine if exercising at 50% of VO2max induces autophagy in a warm environment. Methods. Eight endurance trained subjects (2 females) participated in this study and completed a moderate intensity exercise (MIE) trial for 1h (50% of VO2max ), and a high intensity exercise (HIE) trial for 1h (70% of VO2max ). Results. Core temperature and heart rate during HIE was higher during 10-60 and 5-60 minutes, respectively, when compared to the same time during MIE and pre-HIE, p < 0.01. IL-6 levels were increased (p < 0.01) 0h post-exercise and 1h post-exercise HIE versus pre-exercise. IL-6 was increased following MIE 0h post-exercise, when compared to pre-exercise, p < 0.01. Decreases (p < 0.05) in plasma insulin were found following HIE at 2h, when compared to pre-exercise. Decreases in plasma insulin were also found at 4h post-exercise following MIE when compared to pre-exercise, p < 0.05. HIE increased (p < 0.05) autophagy marker LC3-II at 0h , 2h, and 4h post-exercise when compared to pre-exercise. MIE increased LC3-II at 1h post-exercise when compared to pre-exercise. LC3b decreased following MIE at 1h (p < 0.01) and was increased at 2h, post-exercise when compared to baseline. HSPA1A was decreased at 1h following HIE, when compared to baseline, p < 0.01. HSP70 and LC3-II were moderately and significantly related during MIE, p < 0.01. Increased Akt phosphorylation occurred 2h post-MIE when compared to pre-exercise levels, p < 0.01. Conclusions. Our data suggest that autophagy can be stimulated by exercise at both 50% VO2max and 70% VO2max. MIE induced phosphorylation of Akt post-exercise and may be activated independent of circulating insulin levels. It is unknown how or if the decreased levels we observed in plasma insulin and increases in IL-6 influence autophagy in PBMCs following exercise. Advisors/Committee Members: Mermier, Christine, Dokladny, Karol, Schneider, Suzanne, Ann, Gibson, Moseley, Pope.

Subjects/Keywords: autophagy; mTOR; endurance exercise; heat shock protein

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

APA (6^th Edition):

Lanphere, K. (2014). The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise. (Doctoral Dissertation). University of New Mexico. Retrieved from http://hdl.handle.net/1928/23558

Chicago Manual of Style (16^th Edition):

Lanphere, Kathryn. “The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise.” 2014. Doctoral Dissertation, University of New Mexico. Accessed March 09, 2021. http://hdl.handle.net/1928/23558.

MLA Handbook (7^th Edition):

Lanphere, Kathryn. “The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise.” 2014. Web. 09 Mar 2021.

Vancouver:

Lanphere K. The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise. [Internet] [Doctoral dissertation]. University of New Mexico; 2014. [cited 2021 Mar 09]. Available from: http://hdl.handle.net/1928/23558.

Council of Science Editors:

Lanphere K. The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise. [Doctoral Dissertation]. University of New Mexico; 2014. Available from: http://hdl.handle.net/1928/23558

Open Access Theses and Dissertations