p38 MAP kinase modulates Smad-dependent changes in human prostate cell adhesion (Q73741501)

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:12894225%20AND%20SRC:MED&resulttype=core&format=json

6 November 2019

title

p38 MAP kinase modulates Smad-dependent changes in human prostate cell adhesion (English)

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6 November 2019

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Steven A Hayes

1

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6 November 2019

Xiaoke Huang

2

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6 November 2019

Suman Kambhampati

3

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6 November 2019

Leonidas C Platanias

4

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6 November 2019

Raymond C Bergan

5

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6 November 2019

language of work or name

English

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publication date

1 July 2003

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6 November 2019

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6 November 2019

volume

22

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6 November 2019

page(s)

4841-4850

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6 November 2019

issue

31

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1206730

6 November 2019

exact match

0 references

cites work

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Cross-talk between the p42/p44 MAP kinase and Smad pathways in transforming growth factor beta 1-induced furin gene transactivation

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Docking sites on substrate proteins direct extracellular signal-regulated kinase to phosphorylate specific residues

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Selective targeting of MAPKs to the ETS domain transcription factor SAP-1

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Involvement of the p38 mitogen-activated protein kinase pathway in transforming growth factor-beta-induced gene expression

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Cell adhesion protein receptors as targets for transforming growth factor-beta action

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Transforming growth factor-beta-induced osteoblast elongation regulates osteoclastic bone resorption through a p38 mitogen-activated protein kinase- and matrix metalloproteinase-dependent pathway.

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Transforming growth factor beta upregulates the integrin-mediated adhesion of human prostatic carcinoma cells to type I collagen

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Stress-induced phosphorylation of STAT1 at Ser727 requires p38 mitogen-activated protein kinase whereas IFN-gamma uses a different signaling pathway

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Novel homologues of CSBP/p38 MAP kinase: activation, substrate specificity and sensitivity to inhibition by pyridinyl imidazoles

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Transforming growth factor beta-induced phosphorylation of Smad3 is required for growth inhibition and transcriptional induction in epithelial cells

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Focal adhesion kinase (FAK) phosphorylation is not required for genistein-induced FAK-beta-1-integrin complex formation.

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Prostate cancer chemoprevention agents exhibit selective activity against early stage prostate cancer cells.

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Over expression of endoglin in human prostate cancer suppresses cell detachment, migration and invasion

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The role of transforming growth factor-beta1, -beta2, and -beta3 in androgen-responsive growth of NRP-152 rat prostatic epithelial cells

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Transforming growth factor-beta-mediated mast cell migration depends on mitogen-activated protein kinase activity.

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Arachidonic acid activates mitogen-activated protein (MAP) kinase-activated protein kinase 2 and mediates adhesion of a human breast carcinoma cell line to collagen type IV through a p38 MAP kinase-dependent pathway

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Transforming growth factor-beta induces collagenase-3 expression by human gingival fibroblasts via p38 mitogen-activated protein kinase

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Prostate cancer cell growth inhibition by tamoxifen is associated with inhibition of protein kinase C and induction of p21(waf1/cip1)

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A highly specific inhibitor of human p38 MAP kinase binds in the ATP pocket

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Regulation of biglycan gene expression by transforming growth factor-beta requires MKK6-p38 mitogen-activated protein Kinase signaling downstream of Smad signaling

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Transforming growth factor-beta 1 (TGF-beta1)-mediated inhibition of glial cell proliferation and down-regulation of intercellular adhesion molecule-1 (ICAM-1) are interrupted by interferon-gamma (IFN-gamma)

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Involvement of p38 MAP kinase in TGF-beta-stimulated VEGF synthesis in aortic smooth muscle cells

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