(Q42487215)

English

The inhibition of ERK/MAPK not the activation of JNK/SAPK is primarily required to induce apoptosis in chronic myelogenous leukemic K562 cells

scientific article published on June 2000

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Europe PubMed Central

PubMed publication ID

1 November 2017

The inhibition of ERK/MAPK not the activation of JNK/SAPK is primarily required to induce apoptosis in chronic myelogenous leukemic K562 cells (English)

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Europe PubMed Central

PubMed publication ID

1 November 2017

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author name string

C D Kang

1

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Europe PubMed Central

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1 November 2017

S D Yoo

2

1 reference

Europe PubMed Central

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1 November 2017

B W Hwang

3

1 reference

Europe PubMed Central

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1 November 2017

K W Kim

4

1 reference

Europe PubMed Central

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1 November 2017

D W Kim

5

1 reference

Europe PubMed Central

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1 November 2017

C M Kim

6

1 reference

Europe PubMed Central

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1 November 2017

S H Kim

7

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Europe PubMed Central

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1 November 2017

B S Chung

8

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1 November 2017

publication date

1 June 2000

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1 November 2017

Leukemia Research

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Europe PubMed Central

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1 November 2017

24

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Europe PubMed Central

PubMed publication ID

1 November 2017

6

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Europe PubMed Central

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1 November 2017

527-534

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Europe PubMed Central

PubMed publication ID

1 November 2017

Regulation of the Fas apoptotic cell death pathway by Abl.

1 reference

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Taxol cytotoxicity on human leukemia cell lines is a function of their susceptibility to programmed cell death

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Selective induction of apoptosis in Philadelphia chromosome-positive chronic myelogenous leukemia cells by an inhibitor of BCR–ABL tyrosine kinase, CGP 57148

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In vivo eradication of human BCR/ABL-positive leukemia cells with an ABL kinase inhibitor

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The effect of bcr-abl antisense oligonucleotide on DNA synthesis and apoptosis in K562 chronic myeloid leukemia cells

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The MAPK signaling cascade

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Sequential protein kinase reactions controlling cell growth and differentiation

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Sounding the alarm: protein kinase cascades activated by stress and inflammation

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Interleukin-1 activates a novel protein kinase cascade that results in the phosphorylation of Hsp27.

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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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A novel kinase cascade triggered by stress and heat shock that stimulates MAPKAP kinase-2 and phosphorylation of the small heat shock proteins

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c-Jun NH2-terminal kinase regulation of the apoptotic response of small cell lung cancer cells to ultraviolet radiation

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The role of c-Jun N-terminal kinase (JNK) in apoptosis induced by ultraviolet C and gamma radiation. Duration of JNK activation may determine cell death and proliferation

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

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c-Jun NH2-terminal kinase-mediated activation of interleukin-1beta converting enzyme/CED-3-like protease during anticancer drug-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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Involvement of stress-activated protein kinase and p38 mitogen-activated protein kinase in mIgM-induced apoptosis of human B lymphocytes

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

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Mitogen-activated protein kinase-mediated Fas apoptotic signaling pathway

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Role of the Jun kinase pathway in the regulation of c-Jun expression and apoptosis in sympathetic neurons.

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Dopamine induces apoptosis through an oxidation-involved SAPK/JNK activation pathway

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Molecular mechanisms of c-Jun N-terminal kinase-mediated apoptosis induced by anticarcinogenic isothiocyanates

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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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Insulin-like Growth Factor 1 Inhibits Apoptosis Using the Phosphatidylinositol 3′-Kinase and Mitogen-activated Protein Kinase Pathways

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A requirement for NF-kappaB activation in Bcr-Abl-mediated transformation

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7 January 2021

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The Bcr-Abl tyrosine kinase activates mitogenic signaling pathways and stimulates G1-to-S phase transition in hematopoietic cells

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Bcr - Abl-mediated resistance to apoptosis is independent of PI 3-kinase activity.

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A temperature sensitive p210 BCR-ABL mutant defines the primary consequences of BCR-ABL tyrosine kinase expression in growth factor dependent cells.

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The Bcr-Abl leukemia oncogene activates Jun kinase and requires Jun for transformation

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v-Abl-mediated apoptotic suppression is associated with SHC phosphorylation without concomitant mitogen-activated protein kinase activation.

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Induction of apoptosis by a dominant negative H-RAS mutant (116Y) in K562 cells

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Identifiers

10.1016/S0145-2126(00)00010-2

1 reference

Europe PubMed Central

PubMed publication ID

1 November 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

1 November 2017

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