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Biochem Biophys Res Commun. 2000 Feb 16;268(2):541-6.

Signaling through the p38 and p42/44 mitogen-activated families of protein kinases in pancreatic beta-cell proliferation.

Author information

1
Endocrinology and Reproduction Research Group, Guy's, King's, & St. Thomas' School of Biomedical Sciences, Guy's Campus, London Bridge, London, SE1 9RT, United Kingdom. chris.burns@kcl.ac.uk

Erratum in

  • Biochem Biophys Res Commun 2000 May 10;271(2):558.

Abstract

The present study has focused on the role of the 42- and 44-kDa mitogen-activated protein kinases (p42/44 MAPKs) and the 38-kDa mitogen-activated protein kinase (p38 MAPK) in the proliferation of the pancreatic beta-cell line MIN6. MIN6 beta-cell proliferation was assessed by measuring 5-bromo-2'-deoxyuridine (BrdU) incorporation into cellular DNA. Inhibition of both the p42/44 MAPK pathway using the MEK inhibitor PD098059 (PD) and the p38 MAPK pathway using the p38 inhibitor SB203580 (SB) caused a marked, concentration-dependent reduction in the BrdU immunostaining observed in the presence of 15% FCS when assessed using fluorescence immunocytochemistry. These data provide direct evidence of a role for p42/44 MAPKs in the mitogenic response of MIN6 beta-cells to FCS. Furthermore, these data also suggest a novel role for the p38 MAPK pathway in MIN6 beta-cell proliferation.

PMID:
10679240
DOI:
10.1006/bbrc.2000.2179
[Indexed for MEDLINE]

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