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Titolo:
Phosphatase inhibitors induce defective hormone secretion in insulin-secreting cells and entry into apoptosis
Autore:
Krautheim, A; Rustenbeck, I; Steinfelder, HJ;
Indirizzi:
Univ Gottingen, Inst Pharmacol & Toxicol, D-37075 Gottingen, Germany Univ Gottingen Gottingen Germany D-37075 col, D-37075 Gottingen, Germany Hannover Med Sch, Inst Clin Biochem, Hannover, Germany Hannover Med Sch Hannover Germany Inst Clin Biochem, Hannover, Germany
Titolo Testata:
EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES
fascicolo: 1, volume: 107, anno: 1999,
pagine: 29 - 34
SICI:
0947-7349(1999)107:1<29:PIIDHS>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
PANCREATIC BETA-CELLS; NF-KAPPA-B; OKADAIC ACID; PROTEIN PHOSPHATASES; CALYCULIN-A; ACTIVATION; RELEASE; ISLETS; METABOLISM; LANGERHANS;
Keywords:
ser/thr phosphatase inhibitors; okadaic acid; calyculin A; apoptosis; insulin secretion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Steinfelder, HJ Univngen,ingen, Inst Pharmacol & Toxicol, Robert Koch Str 40, D-37075 Gotti Univ Gottingen Robert Koch Str 40 Gottingen Germany D-37075
Citazione:
A. Krautheim et al., "Phosphatase inhibitors induce defective hormone secretion in insulin-secreting cells and entry into apoptosis", EXP CL E D, 107(1), 1999, pp. 29-34

Abstract

A long-term (greater than or equal to 24 h) exposure of insulin-secreting HIT T15 cells to the phosphatase inhibitor, okadaic acid (OA), at concentrations inhibiting serine/threonine phosphatases 1 (PP1) and 2A (PP2A) reduced proliferation and insulin secretion. The reduced proliferation was related to the induction of apoptosis as evidenced by morphological criteria and the occurrence of internucleosomal DMA fragmentation after 15 h in 50 nM OA. The compromised insulin secretion was not simply a consequence of a lowered hormone content and cell growth, but comprised also a complete suppression of secretion stimulated by K+ depolarisation and forskolin. K+ depolarisation of HIT cells cultured for 24 h in 50 nM OA resulted in a nearly unimpaired influx of Ca2+, but did not induce secretion. These observations suggest that the secretory defect may be localised distal to Ca2+ influx in stimulus secretion coupling of insulin-secreting cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 08:16:05