Document Detail

Regulation of beta cell replication.
MedLine Citation:
PMID:  18824066     Owner:  NLM     Status:  MEDLINE    
Beta cell mass, at any given time, is governed by cell differentiation, neogenesis, increased or decreased cell size (cell hypertrophy or atrophy), cell death (apoptosis), and beta cell proliferation. Nutrients, hormones and growth factors coupled with their signalling intermediates have been suggested to play a role in beta cell mass regulation. In addition, genetic mouse model studies have indicated that cyclins and cyclin-dependent kinases that determine cell cycle progression are involved in beta cell replication, and more recently, menin in association with cyclin-dependent kinase inhibitors has been demonstrated to be important in beta cell growth. In this review, we consider and highlight some aspects of cell cycle regulation in relation to beta cell replication. The role of cell cycle regulation in beta cell replication is mostly from studies in rodent models, but whether these findings can be extended to human beta cells remains to be shown.
Ying C Lee; Jens Høiriis Nielsen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2008-09-07
Journal Detail:
Title:  Molecular and cellular endocrinology     Volume:  297     ISSN:  0303-7207     ISO Abbreviation:  Mol. Cell. Endocrinol.     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2008-12-22     Completed Date:  2009-02-25     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7500844     Medline TA:  Mol Cell Endocrinol     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  18-27     Citation Subset:  IM    
Department of Biomedical Sciences, University of Copenhagen, Blegdamsvej 3, Building 6.5, DK-2200 Copenhagen N., Denmark.
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MeSH Terms
Cell Aging
Cell Division*
Cyclin D
Cyclin-Dependent Kinases / metabolism
Cyclins / metabolism
Insulin-Secreting Cells / cytology*,  enzymology
Proto-Oncogene Proteins / metabolism
Reg. No./Substance:
0/Cyclin D; 0/Cyclins; 0/Proto-Oncogene Proteins; EC Kinases

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