Basic fibroblast growth factor-induced cell death is effected through sustained activation of p38MAPK and up-regulation of the death receptor p75NTR. (Q40525596)

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scientific article published on 13 August 2004

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English	Basic fibroblast growth factor-induced cell death is effected through sustained activation of p38MAPK and up-regulation of the death receptor p75NTR.	scientific article published on 13 August 2004

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scholarly article

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Europe PubMed Central

PubMed publication ID

21 September 2017

Basic fibroblast growth factor-induced cell death is effected through sustained activation of p38MAPK and up-regulation of the death receptor p75NTR. (English)

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Europe PubMed Central

PubMed publication ID

21 September 2017

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James R Boyne

3

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Andrew J K Williamson

1

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Europe PubMed Central

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21 September 2017

Benjamin C Dibling

2

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Europe PubMed Central

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21 September 2017

Peter Selby

4

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21 September 2017

Susan A Burchill

5

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21 September 2017

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publication date

13 August 2004

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21 September 2017

Journal of Biological Chemistry

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21 September 2017

279

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Europe PubMed Central

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21 September 2017

46

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Europe PubMed Central

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21 September 2017

47912-47928

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Europe PubMed Central

PubMed publication ID

21 September 2017

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Basic fibroblast growth factor (bFGF)-induced cell death is mediated through a caspase-dependent and p53-independent cell death receptor pathway

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A lipid-anchored Grb2-binding protein that links FGF-receptor activation to the Ras/MAPK signaling pathway

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Binding of Shp2 tyrosine phosphatase to FRS2 is essential for fibroblast growth factor-induced PC12 cell differentiation

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Mitogen-activated protein kinase pathways

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Regulation of BAD phosphorylation at serine 112 by the Ras-mitogen-activated protein kinase pathway

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Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms

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Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling

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Senescence of human fibroblasts induced by oncogenic Raf.

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p38 mitogen-activated protein kinase activation is required for fibroblast growth factor-2-stimulated cell proliferation but not differentiation

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Protein kinase cascades activated by stress and inflammatory cytokines

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Pro-inflammatory cytokines and environmental stress cause p38 mitogen-activated protein kinase activation by dual phosphorylation on tyrosine and threonine

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Role of p38 and JNK mitogen-activated protein kinases in the activation of ternary complex factors

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Convergence of MAP kinase pathways on the ternary complex factor Sap-1a

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Stress-induced phosphorylation and activation of the transcription factor CHOP (GADD153) by p38 MAP Kinase

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p38 kinase mediates UV-induced phosphorylation of p53 protein at serine 389.

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The stress-activated protein kinase subfamily of c-Jun kinases

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c-Jun N-terminal phosphorylation correlates with activation of the JNK subgroup but not the ERK subgroup of mitogen-activated protein kinases

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Phosphorylation of c-jun mediated by MAP kinases.

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MKK7 is an essential component of the JNK signal transduction pathway activated by proinflammatory cytokines

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Synergistic activation of stress-activated protein kinase 1/c-Jun N-terminal kinase (SAPK1/JNK) isoforms by mitogen-activated protein kinase kinase 4 (MKK4) and MKK7

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Identification of c-Jun NH2-terminal protein kinase (JNK)-activating kinase 2 as an activator of JNK but not p38

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Cell cycle-dependent activation of Ras.

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Cellular N-Ras promotes cell survival by downregulation of Jun N-terminal protein kinase and p38

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Signal transduction by the JNK group of MAP kinases

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The activation state of p38 mitogen-activated protein kinase determines the efficiency of ATP competition for pyridinylimidazole inhibitor binding

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The primary structure of p38 gamma: a new member of p38 group of MAP kinases

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Mitogen-activated protein kinase cascades as regulators of stress responses

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10.1074/JBC.M409035200

1 reference

Europe PubMed Central

PubMed publication ID

21 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

21 September 2017

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