Intracellular signal transduction pathways that control pancreatic β-cell proliferation

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, lit...

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Bibliographic Details
Published in:FEBS Letters 1992-10, Vol.311 (2), p.85-90
Main Author: Sjoeholm, Aa
Format: Article
Language:English
Subjects:
12-O-tetradecanoylphorbol 13-acetate
adenosine-3′,5′-cyclic monophosphate
Amino Acids - pharmacology
Animals
beta cells
Biological and medical sciences
Cell cycle, cell proliferation
Cell Division - drug effects
Cell physiology
Cells, Cultured
control
Cyclic AMP
Cyclic AMP - physiology
cyclic GMP
Cyclic nucleotide
DBI
deoxyribonucleic acid
diazepam binding inhibitor
DNA
Fundamental and applied biological sciences. Psychology
GABA
Glucose - pharmacology
growth, hormone
GTP
GTP-Binding Proteins - physiology
guanosine trisphosphate
guanosine-3′,5′-cyclic monophosphate
IGF-I
Inositol Phosphates - metabolism
Insulin secretion
insulin-like growth factor I
Islets of Langerhans - cytology
Islets of Langerhans - metabolism
Molecular and cellular biology
N-protein
pancreas
Pancreatic islet
pathways
PDGF
Peptides - pharmacology
platelet-derived growth factor
Polyamine
Polyamines - metabolism
proliferation
Protein kinase C
Protein Kinase C - metabolism
rats
reviews
Signal Transduction
Sp-cAMP[S]
stimulatory diastereomer of adenosine-3′,5′-cyclic monophosphorothioate
TGF-β
TPA
transforming growth factor β
γ-aminobutyric acid
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Summary: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.
ISSN:0014-5793
1873-3468
DOI:10.1016/0014-5793(92)81373-T