Inhibition of arachidonate 5-lipoxygenase triggers prostate cancer cell death through rapid activation of c-Jun N-terminal kinase (Q44512411)

3 December 2017

Inhibition of arachidonate 5-lipoxygenase triggers prostate cancer cell death through rapid activation of c-Jun N-terminal kinase (English)

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3 December 2017

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Jagadananda Ghosh

1

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PubMed ID

12859962

3 December 2017

language of work or name

English

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publication date

1 July 2003

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Biochemical and Biophysical Research Communications

3 December 2017

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3 December 2017

307

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3 December 2017

2

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3 December 2017

342-349

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Decreased growth of established human prostate LNCaP tumors in nude mice fed a low-fat diet

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Do diet and androgens alter prostate cancer risk via a common etiologic pathway?

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Animal fat consumption and prostate cancer: a prospective study in Hawaii

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Chemoprevention of prostate cancer

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Adult dietary intake and prostate cancer risk in Utah: a case-control study with special emphasis on aggressive tumors.

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A prospective study of dietary fat and risk of prostate cancer

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Prospective study of plasma fatty acids and risk of prostate cancer

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Arachidonic acid stimulates prostate cancer cell growth: critical role of 5-lipoxygenase

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Inhibition of arachidonate 5-lipoxygenase triggers massive apoptosis in human prostate cancer cells

7 January 2021

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

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JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain

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Identification of MAP kinase domains by redirecting stress signals into growth factor responses

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

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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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The JUN kinase/stress-activated protein kinase pathway is required for epidermal growth factor stimulation of growth of human A549 lung carcinoma cells.

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Selective activation of c-Jun kinase mitogen-activated protein kinase by CD40 on human B cells

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Signal transduction by the c-Jun N-terminal kinase (JNK)--from inflammation to development

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JNK is involved in signal integration during costimulation of T lymphocytes.

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Jun N-terminal kinase 2 modulates thymocyte apoptosis and T cell activation through c-Jun and nuclear factor of activated T cell (NF-AT)

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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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Transcription factor AP-1 regulation by mitogen-activated protein kinase signal transduction pathways.

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Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain

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Transcription factor ATF2 regulation by the JNK signal transduction pathway

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Integration of MAP kinase signal transduction pathways at the serum response element

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Activation of the Sap-1a transcription factor by the c-Jun N-terminal kinase (JNK) mitogen-activated protein kinase

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Nuclear accumulation of NFAT4 opposed by the JNK signal transduction pathway

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Diverse functions of JNK signaling and c-Jun in stress response and apoptosis

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The small GTP-binding protein Cdc42 is required for nerve growth factor withdrawal-induced neuronal death

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Insulin-like growth factor-I and Bcl-X(L) inhibit c-jun N-terminal kinase activation and rescue Schwann cells from apoptosis

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Neuronal death in developmental models: possible implications in neuropathology

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Withdrawal of survival factors results in activation of the JNK pathway in neuronal cells leading to Fas ligand induction and cell death

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Phosphorylation of c-Jun is necessary for apoptosis induced by survival signal withdrawal in cerebellar granule neurons.

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p53 is essential for developmental neuron death as regulated by the TrkA and p75 neurotrophin receptors

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Oncogenic and transcriptional cooperation with Ha-Ras requires phosphorylation of c-Jun on serines 63 and 73

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Sequential activation of ICE-like and CPP32-like proteases during Fas-mediated apoptosis

7 January 2021

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Caspase activity is required for commitment to Fas-mediated apoptosis.

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Inhibition of the c-Jun N-terminal kinase (JNK) signaling pathway by curcumin

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c-Jun N-terminal kinase mediates apoptotic signaling induced by N-(4-hydroxyphenyl)retinamide.

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Methylglyoxal induces apoptosis in Jurkat leukemia T cells by activating c-Jun N-terminal kinase

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SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase

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Molecular mechanisms of prostate cancer cell death triggered by inhibition of arachidonate 5-lipoxygenase: involvement of Fas death receptor-mediated signals.

7 January 2021

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Bcl-2 undergoes phosphorylation by c-Jun N-terminal kinase/stress-activated protein kinases in the presence of the constitutively active GTP-binding protein Rac1.

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Translocation of SAPK/JNK to mitochondria and interaction with Bcl-x(L) in response to DNA damage

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p53 is phosphorylated in vitro and in vivo by an ultraviolet radiation-induced protein kinase characteristic of the c-Jun kinase, JNK1.

7 January 2021

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Jun NH2-terminal kinase phosphorylation of p53 on Thr-81 is important for p53 stabilization and transcriptional activities in response to stress.

7 January 2021

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Phosphorylation and inactivation of myeloid cell leukemia 1 by JNK in response to oxidative stress

7 January 2021

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C-Jun N-terminal kinase is required for phorbol ester- and thapsigargin-induced apoptosis in the androgen responsive prostate cancer cell line LNCaP.

7 January 2021

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c-Jun-dependent CD95-L expression is a rate-limiting step in the induction of apoptosis by alkylating agents

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10.1016/S0006-291X(03)01201-4

7 January 2021

Identifiers

DOI

1 reference

3 December 2017

1 reference

PubMed ID

12859962