Μεταπτυχιακές εργασίες ειδίκευσης
Τρέχουσα Εγγραφή: 4818 από 6695
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Κωδικός Πόρου |
000388725 |
Τίτλος |
The role of Usp22 de-ubiquitinase in the regulation of metabolic and carcinogenesis pathways |
Άλλος τίτλος |
Ο ρόλος της αποβουκιτινιλάτης Usp22 στη ρύθμιση του μεταβολισμού και του καρκίνου |
Συγγραφέας
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Μπάλιου Στυλιανή
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Σύμβουλος διατριβής
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Καρδάσης, Δ.
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Μέλος κριτικής επιτροπής
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Σαββάκης, Χ.
Ταλιανίδης, Ι
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Περίληψη |
USP22 is a thiol-specific protease that can remove ubiquitin from ubiquitinated histones H2A and H2B.
USP22 has been recently identified as a member of the 11-gene cancer stem cell signature proposed to
serve as a predictor of treatment resistance, tumor aggressiveness and metastatic potential of human
cancers. Studies in yeast indicate a critical role for Usp22 in transcriptional initiation and elongation.
However, its role in mammals remains elusive. We aimed to address the role of Usp22 in the mouse liver.
Our work focuses on the role of Usp22 in metabolic regulation, cell cycle progression and
hepatocarcinogenesis. Preliminary results using wild-type mice under conditions of fasting indicated
increased levels of Usp22 compared to normally fed controls. Additionally, when mice were subjected to
partial hepatectomy increased levels of Usp22 were observed. Consistent with a potential role of Usp22 in
cell proliferation, analysis of livers from mice bearing experimentally induced tumors also indicated
upregulation of Usp22, compared to normal age-matched livers. In all cases, Usp22 displayed nuclear
localization, similar to untreated livers, as assessed by immunohistochemical analysis. Our results indicate a
putative involvement of Usp22 in metabolic regulation and in cell cycle progression in murine liver. We are
currently in the process of generating three genetic models that will be useful for studies aimed at
understanding Usp22 function in liver. The first one is an Usp22 conditional liver-specific knock-out mouse,
the second is a transgenic mouse overexpressing human USP22 upon tamoxifen treatment and the third
one is a transgenic mouse overexpressing a catalytically inactive C185S mutant form of human USP22.
Phenotypic characterization, genome wide expression and occupancy analysis of these models will be
useful towards elucidating the role of Usp22 and the dynamics of histone ubiquitination in the
mammalian liver.
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Φυσική περιγραφή |
69 σ : πιν. ; 30 εκ. |
Γλώσσα |
Αγγλικά |
Θέμα |
Cell cycle progression |
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Hepatocarcinogenesis |
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Metabolic regulation |
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Usp22 |
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Εξέλιξη του κυτταρικού κύκλου |
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Ηπατοκαρκινογένεση |
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Ρύθμιση του μεταβολισμού |
Ημερομηνία έκδοσης |
2014-12-04 |
Συλλογή
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Σχολή/Τμήμα--Ιατρική Σχολή--Τμήμα Ιατρικής--Μεταπτυχιακές εργασίες ειδίκευσης
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Τύπος Εργασίας--Μεταπτυχιακές εργασίες ειδίκευσης
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Μόνιμη Σύνδεση |
https://elocus.lib.uoc.gr//dlib/e/5/d/metadata-dlib-1423205501-54181-18910.tkl
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Εμφανίσεις |
242 |