The cell cycle inhibitory protein p21cip is not essential for maintaining beta-cell cycle arrest or beta-cell function in vivo.

The cell cycle inhibitory protein p21cip is not essential for maintaining beta-cell cycle arrest or beta-cell function in vivo. Research Abstract Details 

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The cell cycle inhibitory protein p21cip is not essential for maintaining beta-cell cycle arrest or beta-cell function in vivo. Abstract Text:

Irene Cozar-Castellano,Marcia Haught,Andrew F Stewart,

p21(cip1), a regulatory molecule upstream of the G(1/0) checkpoint, is increased in beta-cells in response to mitogenic stimulation. Whereas p21(cip1) can variably stimulate or inhibit cell cycle progression, in vitro studies suggest that p21(cip1) acts as an inhibitor in the pancreatic beta-cell. To determine the functional role of p21(cip1) in vivo, we studied p21-null mice. Surprisingly, islet mass, beta-cell replication rates, and function were normal in p21-null mice. We next attempted to drive beta-cell replication in p21-null mice by crossing them with rat insulin II promoter-murine PL-1 (islet-targeted placental lactogen transgenic) mice. Even with this added replicative stimulus of PL, p21-null islets showed no additional stimulation. A G(1/S) proteome scan demonstrated that p21(cip1) loss was not associated with compensatory increases in other cell cycle inhibitors (pRb, p107, p130, p16, p19, and p27), although mild increases in p57 were apparent. Surprisingly, p18, which had been anticipated to increase, was markedly decreased. In summary, isolated p21(cip1) loss, as for pRb, p53, p18, and p27 and other inhibitors, results in normal beta-cell development and function, either because it is not essential or because its function is subserved or complimented by another protein. These studies underscore marked inhibitory pressure and the complexity and plasticity of inhibitory pathways that restrain beta-cell replication.

The cell cycle inhibitory protein p21cip is not essential for maintaining beta-cell cycle arrest or beta-cell function in vivo. Publishing Authors By Initials

I Cozar-Castellano,M Haught,AF Stewart,

For similar animals: animal population groups: organisms, genetically modified: animals, genetically modified: mice, transgenic: mice, knockout research abstracts see: animals: animal population groups: organisms, genetically modified: animals, genetically modified: mice, transgenic: mice, knockout research

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The cell cycle inhibitory protein p21cip is not essential for maintaining beta-cell cycle arrest or beta-cell function in vivo. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Diabetes

VOLUME: 55

Page Numbers: 3271-8

Journal Abbreviation: Diabetes

ISSN: 0012-1797

DAY: 3

MONTH: Dec

YEAR: 2006

The cell cycle inhibitory protein p21cip is not essential for maintaining beta-cell cycle arrest or beta-cell function in vivo. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 372763

The cell cycle inhibitory protein p21cip is not essential for maintaining beta-cell cycle arrest or beta-cell function in vivo. Keywords Mesh Terms:

KEYWORDS: Mice, Knockout

MESH TERMS: physiology

Chemical & Substance for Abstract: The cell cycle inhibitory protein p21cip is not essential for maintaining beta-cell cycle arrest or beta-cell function in vivo. Information

Substance Name: Cyclin-Dependent Kinase Inhibitor p21

Registry Number: 0

Grant and Affiliation Information for The cell cycle inhibitory protein p21cip is not essential for maintaining beta-cell cycle arrest or beta-cell function in vivo.

AFFILIATION: Division of Endocrinology, BST E-1140, University of Pittsburgh School of Medicine, 200 Lothrop St., Pittsburgh, PA 15213, USA. cozari@dom.pitt.edu

Country: United States

AGENCY: United States NIDDK

GRANT: R01-DK-55023

ACRONYM: DK

MEDLINETA: Diabetes

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