(Q54104814)

English

Activation of stress-activated protein kinase/c-Jun NH2-terminal kinase and p38 kinase in calphostin C-induced apoptosis requires caspase-3-like proteases but is dispensable for cell death.

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

Activation of stress-activated protein kinase/c-Jun NH2-terminal kinase and p38 kinase in calphostin C-induced apoptosis requires caspase-3-like proteases but is dispensable for cell death. (English)

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

author name string

I Ozaki

1

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

E Tani

2

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

H Ikemoto

3

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

H Kitagawa

4

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

H Fujikawa

5

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

language of work or name

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publication date

1 February 1999

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

number of pages

8

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based on heuristic

inferred from page(s)

Journal of Biological Chemistry

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

274

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

9

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

5310-5317

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

Sequential protein kinase reactions controlling cell growth and differentiation

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Ras-dependent activation of MAP kinase pathway mediated by G-protein beta gamma subunits.

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Role of transactivation of the EGF receptor in signalling by G-protein-coupled receptors

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Receptor-tyrosine-kinase- and G beta gamma-mediated MAP kinase activation by a common signalling pathway

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G(o)-protein alpha-subunits activate mitogen-activated protein kinase via a novel protein kinase C-dependent mechanism.

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Diversity in function and regulation of MAP kinase pathways

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Rapid stimulation by insulin of a serine/threonine kinase in 3T3-L1 adipocytes that phosphorylates microtubule-associated protein 2 in vitro

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Evidence that pp42, a major tyrosine kinase target protein, is a mitogen-activated serine/threonine protein kinase

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Regulatory mechanisms for ras proteins

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Phosphorylation of Bcl-2 protein and association with p21Ras in Ras-induced apoptosis

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Fas activation of the p38 mitogen-activated protein kinase signalling pathway requires ICE/CED-3 family proteases

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Ordering the cell death pathway. Differential effects of BCL2, an interleukin-1-converting enzyme family protease inhibitor, and other survival agents on JNK activation in serum/nerve growth factor-deprived PC12 cells

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Lack of correlation between activation of Jun-NH2-terminal kinase and induction of apoptosis after detachment of epithelial cells

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Signal transduction pathways regulated by mitogen-activated/extracellular response kinase kinase kinase induce cell death

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Three distinct signalling responses by murine fibroblasts to genotoxic stress

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Dissection of TNF receptor 1 effector functions: JNK activation is not linked to apoptosis while NF-kappaB activation prevents cell death

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A role for JNK/SAPK in proliferation, but not apoptosis, of IL-3-dependent cells

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Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis

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Fibroblast growth factor-2 suppression of tumor necrosis factor alpha-mediated apoptosis requires Ras and the activation of mitogen-activated protein kinase

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JNK, but not MAPK, activation is associated with Fas-mediated apoptosis in human T cells

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Positioning atypical protein kinase C isoforms in the UV-induced apoptotic signaling cascade

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Apoptosis of human glioma cells in response to calphostin C, a specific protein kinase C inhibitor

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Bcl-2 and the regulation of programmed cell death

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Introduction of soluble protein into the class I pathway of antigen processing and presentation

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SB 203580 is a specific inhibitor of a MAP kinase homologue which is stimulated by cellular stresses and interleukin-1

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Yama/CPP32 beta, a mammalian homolog of CED-3, is a CrmA-inhibitable protease that cleaves the death substrate poly(ADP-ribose) polymerase

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Cleavage of poly(ADP-ribose) polymerase by a proteinase with properties like ICE

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Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis

1 reference

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Ras-dependent induction of cellular responses by constitutively active phosphatidylinositol-3 kinase

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Reduced activation of RAF-1 and MAP kinase by a fibroblast growth factor receptor mutant deficient in stimulation of phosphatidylinositol hydrolysis

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The complexity of Raf-1 regulation

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Protein kinase C alpha activates RAF-1 by direct phosphorylation

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Protein kinase C activates the MEK-ERK pathway in a manner independent of Ras and dependent on Raf.

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Bcl-2 targets the protein kinase Raf-1 to mitochondria

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Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L)

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Abrogation of c-Raf expression induces apoptosis in tumor cells.

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The activation of p38 and apoptosis by the inhibition of Erk is antagonized by the phosphoinositide 3-kinase/Akt pathway

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Daxx, a novel Fas-binding protein that activates JNK and apoptosis

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MEK kinase 1, a substrate for DEVD-directed caspases, is involved in genotoxin-induced apoptosis

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Requirement for ceramide-initiated SAPK/JNK signalling in stress-induced apoptosis.

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Stress-signalling kinase Sek1 protects thymocytes from apoptosis mediated by CD95 and CD3

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BAX-induced cell death may not require interleukin 1 beta-converting enzyme-like proteases

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Inhibition of Ced-3/ICE-related proteases does not prevent cell death induced by oncogenes, DNA damage, or the Bcl-2 homologue Bak

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The apoptosis-necrosis paradox. Apoptogenic proteases activated after mitochondrial permeability transition determine the mode of cell death.

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Nitric oxide induces apoptosis via triggering mitochondrial permeability transition.

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The interleukin 1beta-converting enzyme inhibitor CrmA prevents Apo1/Fas- but not glucocorticoid-induced poly(ADP-ribose) polymerase cleavage and apoptosis in lymphoblastic leukemia cells

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Ceramides induce a form of apoptosis in human acute lymphoblastic leukemia cells that is inhibited by Bcl-2, but not by CrmA.

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Commitment to cell death measured by loss of clonogenicity is separable from the appearance of apoptotic markers

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Anti-apoptotic oncogenes prevent caspase-dependent and independent commitment for cell death

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DFF, a heterodimeric protein that functions downstream of caspase-3 to trigger DNA fragmentation during apoptosis

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Cleavage of CAD inhibitor in CAD activation and DNA degradation during apoptosis

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Death cycle and Swiss army knives

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Three paths to stress relief

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Ras is essential for nerve growth factor- and phorbol ester-induced tyrosine phosphorylation of MAP kinases

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CPP32/apopain is a key interleukin 1 beta converting enzyme-like protease involved in Fas-mediated apoptosis

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Target cell lysis by CTL granule exocytosis is independent of ICE/Ced-3 family proteases

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Identifiers

10.1074/JBC.274.9.5310

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

24 May 2018

http://europepmc.org/abstract/MED/10026138

ResearchGate publication ID

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