Knebel et al. (2000) Characterization of a postreceptor signaling defect that impairs cfos expression in cultured fibroblasts of a patient with insulin resistance.

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Characterization of a postreceptor signaling defect that impairs cfos expression in cultured fibroblasts of a patient with insulin resistance.

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CONTRIBUTORS:

	Author:	Knebel, B
	Author:	Kotzka, J
	Author:	Avci, H
	Author:	Schiller, M
	Author:	Brüning, JC
	Author:	Hafner, Martin (Helmholtz Centre for Infection Research)
	Author:	Krone, W
	Author:	Müller-Wieland, D

JOURNAL:

Biochemical and biophysical research communications, 268(2), 577 - 582.

YEAR:

2000

PUB TYPE:

Journal Article

SUBJECT(S):

insulin action; MAPK cascades; Elk-1; gene regulation

DISCIPLINE:

Medicine

HTTP:

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WBK-45K1B5Y-13D&_user=10&_coverDate=02%2F16%2F2000&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=71367e72c2fe32f91c8d86e926954077

LANGUAGE:

English

PUB ID:

103-434-516 (Last edited on 2007/05/19 14:13:22 GMT-6)

SPONSOR(S):

ABSTRACT:
Induction of cfos expression is a definite end point of signal transduction by receptor tyrosine kinases via MAPK cascades. We have examined signal transduction to transcription factor cFos in isolated fibroblasts of a patient with an inherited syndrome of insulin resistance. MAPK phosphorylation and activity were unaltered, but inducibility of cfos transcription was strongly impaired by insulin and reduced by PDGF. Induction of the cfos promoter via MAPK is mediated by activation of the ternary complex. Abundance of SRF or Elk-1 was unaltered, but Elk-1 phosphorylation following stimulation was reduced. Transient transfections with reporter genes under control of the Elk-1 binding ets/sre cis element or expression plasmids coding for the regulatory domain of Elk-1 fused to heterologous DNA binding domains revealed a defect of Elk-1 activation in the patient cells. These data identify a novel postreceptor defect of insulin and growth factors involving activation of transcription.

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