p16Ink4a-induced senescence of pancreatic beta cells enhances insulin secretion

被引：0
作者：
Aharon Helman
Agnes Klochendler
Narmen Azazmeh
Yael Gabai
Elad Horwitz
Shira Anzi
Avital Swisa
Reba Condiotti
Roy Z Granit
Yuval Nevo
Yaakov Fixler
Dorin Shreibman
Amit Zamir
Sharona Tornovsky-Babeay
Chunhua Dai
Benjamin Glaser
Alvin C Powers
A M James Shapiro
Mark A Magnuson
Yuval Dor
Ittai Ben-Porath
机构：
[1] Institute for Medical Research–Israel-Canada,Department of Developmental Biology and Cancer Research
[2] Hebrew University–Hadassah Medical School,Department of Internal Medicine
[3] Computation Center,Division of Diabetes, Department of Medicine
[4] Hebrew University–Hadassah Medical School,Department of Molecular Physiology and Biophysics
[5] Endocrinology and Metabolism Service,Department of Surgery
[6] Hadassah-Hebrew University Medical Center,undefined
[7] Endocrinology and Metabolism,undefined
[8] Vanderbilt University Medical Center,undefined
[9] Vanderbilt University School of Medicine,undefined
[10] Veteran Affairs Tennessee Valley Healthcare System,undefined
[11] University of Alberta,undefined
[12] Clinical Islet Transplant Program,undefined
[13] University of Alberta,undefined
[14] Center for Stem Cell Biology,undefined
[15] Vanderbilt University School of Medicine,undefined
来源：
Nature Medicine | 2016年 / 22卷
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摘要：
As beta cells age their levels of p16 rise, and the cells become senescent; rather than leading to dysfunction, this results in an increased capacity of the beta cells for glucose-stimulated insulin secretion.
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页码：412 / 420
页数：8
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