p38 MAPK activation selectively induces cell death in K-ras-mutated human colon cancer cells through regulation of vitamin D receptor (Q40575095)

21 September 2017

p38 MAPK activation selectively induces cell death in K-ras-mutated human colon cancer cells through regulation of vitamin D receptor (English)

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21 September 2017

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Xiaomei Qi

1

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21 September 2017

Jun Tang

2

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21 September 2017

Rocky Pramanik

3

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21 September 2017

Richard M Schultz

4

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21 September 2017

Senji Shirasawa

5

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21 September 2017

Takehiko Sasazuki

6

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21 September 2017

Jiahuai Han

7

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21 September 2017

Guan Chen

8

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21 September 2017

language of work or name

English

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publication date

22 March 2004

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Journal of Biological Chemistry

21 September 2017

7

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based on heuristic

inferred from page(s)

published in

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21 September 2017

279

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21 September 2017

21

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21 September 2017

22138-22144

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Essential role for oncogenic Ras in tumour maintenance

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Increasing complexity of the Ras signaling pathway.

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Activation of MAP kinase kinase is necessary and sufficient for PC12 differentiation and for transformation of NIH 3T3 cells

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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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p120 GAP modulates Ras activation of Jun kinases and transformation

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The p38 pathway provides negative feedback for Ras proliferative signaling

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Raf-independent deregulation of p38 and JNK mitogen-activated protein kinases are critical for Ras transformation

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The p38 and JNK pathways cooperate to trans-activate vitamin D receptor via c-Jun/AP-1 and sensitize human breast cancer cells to vitamin D(3)-induced growth inhibition

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Characterization of the structure and function of a novel MAP kinase kinase (MKK6)

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Cloning and characterization of the mouse vitamin D receptor promoter

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Altered growth of human colon cancer cell lines disrupted at activated Ki-ras

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Human-tumor-derived cell lines contain common and different transforming genes

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A system for stable expression of short interfering RNAs in mammalian cells

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Kaposi's Sarcoma-Associated Herpesvirus Latency-Associated Nuclear Antigen Induces Expression of the Helix-Loop-Helix Protein Id-1 in Human Endothelial Cells

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Oncogenic transformation potentiates apoptosis, S-phase arrest and stress-kinase activation by etoposide

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Selective activation of p38 mitogen-activated protein (MAP) kinase isoforms by the MAP kinase kinases MKK3 and MKK6

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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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The p38 signal transduction pathway: activation and function

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The activation of c-Jun NH2-terminal kinase (JNK) by DNA-damaging agents serves to promote drug resistance via activating transcription factor 2 (ATF2)-dependent enhanced DNA repair

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MKK3- and MKK6-regulated gene expression is mediated by the p38 mitogen-activated protein kinase signal transduction pathway

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Target cells for 1,25-dihydroxyvitamin D3 in intestinal tract, stomach, kidney, skin, pituitary, and parathyroid

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Vitamin D(3) promotes the differentiation of colon carcinoma cells by the induction of E-cadherin and the inhibition of beta-catenin signaling.

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Selective activation of Ha-ras(val12) oncogene increases susceptibilityof NIH/3T3 cells to TNF-alpha.

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Enhanced ROS production in oncogenically transformed cells potentiates c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and sensitization to genotoxic stress

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Targeted ablation of the vitamin D receptor: an animal model of vitamin D-dependent rickets type II with alopecia

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Mice lacking the vitamin D receptor exhibit impaired bone formation, uterine hypoplasia and growth retardation after weaning

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The regulation of AP-1 activity by mitogen-activated protein kinases

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Targeted disruption of the K-ras oncogene in an invasive colon cancer cell line down-regulates urokinase receptor expression and plasminogen-dependent proteolysis

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PPARgamma agonists inhibit cell growth and suppress the expression of cyclin D1 and EGF-like growth factors in ras-transformed rat intestinal epithelial cells

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

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Paclitaxel induces prolonged activation of the Ras/MEK/ERK pathway independently of activating the programmed cell death machinery

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Sustained activation of JNK/p38 MAPK pathways in response to cisplatin leads to Fas ligand induction and cell death in ovarian carcinoma cells

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Prevalence of ras gene mutations in human colorectal cancers

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21 January 2018

Identifiers

DOI

10.1074/JBC.M313964200

1 reference

21 September 2017

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