Intracellular signal transduction pathways that control pancreatic β‐cell proliferation

FEBS Letters

Sjöholm, Åke¹ 

[1] Department of Endocrinology, The Rolf Luft Center for Diabetes Research, Karolinska Institute, Karolinska Hospital, Box 60500, S-104 01 Stockholm, Sweden

关键词: Pancreatic islet;    Insulin secretion;    Protein kinase C;    Cyclic nucleotide;    Polyamine;    N-protein;    Cyclic AMP;    adenosine-3′;    5′-cyclic monophosphate;    cyclic GMP;    guanosine-3′;    5′-cyclic monophosphate;    DBI;    diazepam binding inhibitor;    DNA;    deoxyribonucleic acid;    GABA;    γ-aminobutyric acid;    GH;    growth;    hormone;    GTP;    guanosine trisphosphate;    IGF-I;    insulin-like growth factor I;    PDGF;    platelet-derived growth factor;    Sp-cAMP[S];    stimulatory diastereomer of adenosine-3′;    5′-cyclic monophosphorothioate;    TGF-β;    transforming growth factor β;    TPA;    12-O-tetradecanoylphorbol 13-acetate;   

DOI  :  10.1016/0014-5793(92)81373-T

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

This review focuses on the factors that regulate the proliferation of pancreatic islet β-cells in vitro, and in particular on the intracellular pathways that convey the mitogenic signal into a proliferative response. Substances as diverse as nutrients, polypeptides, cytokines, adrenergic agents, lithium, phorbol esters and cyclic AMP analogs are all able to stimulate or inhibit β-cell proliferation in a time- and concentration-dependent manner. The evidence for involvement of cyclic AMP, cyclic GMP, protein kinase C, inositol polyphosphates, GTP-binding proteins, polyamines and oncogenes is reviewed.

【 授权许可】

Unknown