p27 Regulates the transition of beta-cells from quiescence to proliferation.

p27 Regulates the transition of beta-cells from quiescence to proliferation. Research Abstract Details 

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p27 Regulates the transition of beta-cells from quiescence to proliferation. Abstract Text:

Senta Georgia,Anil Bhushan,

Diabetes results from an inadequate mass of functional beta-cells. Such inadequacy could result from loss of beta-cells due to an immune assault or the inability to compensate for insulin resistance. Thus, mechanisms that regulate the number of beta-cells will be key to understanding both the pathogenesis of diabetes and for developing therapies. In this study, we show that cell cycle regulator p27 plays a crucial role in establishing the number of beta-cells formed before birth. We show that p27 accumulates in terminally differentiated beta-cells during embryogenesis. Disabling p27 allows newly differentiated beta-cells that are normally quiescent during embryogenesis to reenter the cell cycle and proliferate. As a consequence, excess beta-cells are generated in the p27(-/-) mice, doubling their beta-cell mass at birth. The early postnatal expansion of beta-cell mass was unaffected in p27(-/-) mice, indicating that the main function of p27 is to maintain the quiescent state of newly differentiated beta-cells generated during embryogenesis. The expanded beta-cell mass was accompanied by increased insulin secretion; however, the p27(-/-) mice were glucose intolerant, as these mice were insulin insensitive. To assess the role of p27 to affect regeneration of beta-cells in models of diabetes, p27(-/-) mice were injected with streptozotocin (STZ). In contrast to control mice that displayed elevated blood glucose levels, p27(-/-) mice showed decreased susceptibility to develop STZ-induced diabetes. Furthermore, beta-cells retained the ability to reenter the cell cycle at a far greater frequency in p27(-/-) mice after developing STZ-induced diabetes compared with wild-type littermates. These data indicate that p27 is a key regulator in establishing beta-cell mass and an important target for facilitating beta-cell regeneration in therapies for diabetes.

p27 Regulates the transition of beta-cells from quiescence to proliferation. Publishing Authors By Initials

S Georgia,A Bhushan,

For similar proteins: nuclear proteins: proliferating cell nuclear antigen research abstracts see: proteins: nuclear proteins: proliferating cell nuclear antigen research

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p27 Regulates the transition of beta-cells from quiescence to proliferation. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Diabetes

VOLUME: 55

Page Numbers: 2950-6

Journal Abbreviation: Diabetes

ISSN: 0012-1797

DAY: 3

MONTH: Nov

YEAR: 2006

p27 Regulates the transition of beta-cells from quiescence to proliferation. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 372763

p27 Regulates the transition of beta-cells from quiescence to proliferation. Keywords Mesh Terms:

KEYWORDS: Proliferating Cell Nuclear Antigen

MESH TERMS: physiology

Chemical & Substance for Abstract: p27 Regulates the transition of beta-cells from quiescence to proliferation. Information

Substance Name: Insulin

Registry Number: 11061-68-0

Grant and Affiliation Information for p27 Regulates the transition of beta-cells from quiescence to proliferation.

AFFILIATION: Larry Hillblom Islet Research Center, University of California, Los Angeles, 900A Weyburn Pl., Los Angeles, CA 90095, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: R01 DK-6876

ACRONYM: DK

MEDLINETA: Diabetes

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