Diabetes-related changes in cAMP response element-binding protein content enhance smooth muscle cell proliferation and migration. (Q43740242)

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11 November 2019

title

Diabetes-related changes in cAMP response element-binding protein content enhance smooth muscle cell proliferation and migration (English)

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11 November 2019

3

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11 November 2019

Jane Reusch

5

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11 November 2019

author name string

P A Watson

1

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11 November 2019

A Nesterova

2

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11 November 2019

D J Klemm

4

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11 November 2019

language of work or name

English

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publication date

17 September 2001

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Journal of Biological Chemistry

11 November 2019

published in

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11 November 2019

volume

276

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issue

49

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page(s)

46142-46150

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Vascular homeostasis, adhesion molecules, and macrovascular disease in non-insulin-dependent diabetes mellitus

11 November 2019

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Calmodulin-stimulated cyclic nucleotide phosphodiesterase (PDE1C) is induced in human arterial smooth muscle cells of the synthetic, proliferative phenotype

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Vascular smooth muscle cells exhibit increased growth in response to elevated glucose

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The retardation of vasculopathy induced by attenuation of insulin resistance in the corpulent JCR:LA-cp rat is reflected by decreased vascular smooth muscle cell proliferation in vivo.

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Role of oxidative stress in development of complications in diabetes

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Phosphorylated CREB binds specifically to the nuclear protein CBP

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Nuclear protein CBP is a coactivator for the transcription factor CREB

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The signal-dependent coactivator CBP is a nuclear target for pp90RSK

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Activation of cAMP and mitogen responsive genes relies on a common nuclear factor

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Differential binding of cAMP-responsive-element (CRE)-binding protein-1 and activating transcription factor-2 to a CRE-like element in the human tissue-type plasminogen activator (t-PA) gene promoter correlates with opposite regulation of t-PA by ph

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cAMP response element-binding protein is activated by Ca2+/calmodulin- as well as cAMP-dependent protein kinase

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Nerve growth factor activates a Ras-dependent protein kinase that stimulates c-fos transcription via phosphorylation of CREB.

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Insulin stimulates cAMP-response element binding protein activity in HepG2 and 3T3-L1 cell lines.

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Phosphorylation of cAMP responsive element binding protein after treatment of mesangial cells with high glucose plus TGF beta or PMA.

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Insulin-like growth factor-I induces bcl-2 promoter through the transcription factor cAMP-response element-binding protein.

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Identifiers

DOI

10.1074/JBC.M104770200

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:11560925%20AND%20SRC:MED&resulttype=core&format=json

11 November 2019

1 reference