ERK and AKT signaling drive MED1 overexpression in prostate cancer in association with elevated proliferation and tumorigenicity. - Wikidata - wikimedia - TriplyDB

ERK and AKT signaling drive MED1 overexpression in prostate cancer in association with elevated proliferation and tumorigenicity.

ERK and AKT signaling drive MED1 overexpression in prostate cancer in association with elevated proliferation and tumorigenicity.

http://www.wikidata.org/entity/Q39173954

about

MiR137 is an androgen regulated repressor of an extended network of transcriptional coregulators.MED1 mediates androgen receptor splice variant induced gene expression in the absence of ligand Cardiomyocyte-Specific Ablation of Med1 Subunit of the Mediator Complex Causes Lethal Dilated Cardiomyopathy in Mice.The Med1 subunit of the mediator complex induces liver cell proliferation and is phosphorylated by AMP kinase.Src promotes castration-recurrent prostate cancer through androgen receptor-dependent canonical and non-canonical transcriptional signatures.Med1 subunit of the mediator complex in nuclear receptor-regulated energy metabolism, liver regeneration, and hepatocarcinogenesis Effects of cisplatin on the LSD1-mediated invasion and metastasis of prostate cancer cells.Bone-derived soluble factors and laminin-511 cooperate to promote migration, invasion and survival of bone-metastatic breast tumor cells.MicroRNA expressions associated with progression of prostate cancer cells to antiandrogen therapy resistance.Gelsolin-like actin-capping protein is associated with patient prognosis, cellular apoptosis and proliferation in prostate cancer.The mediator complex in genomic and non-genomic signaling in cancer.Somatic MED12 mutations in prostate cancer and uterine leiomyomas promote tumorigenesis through distinct mechanisms.Looking beyond Androgen Receptor Signaling in the Treatment of Advanced Prostate Cancer

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P2860

ERK and AKT signaling drive MED1 overexpression in prostate cancer in association with elevated proliferation and tumorigenicity.

http://www.wikidata.org/entity/Q39173954

description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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2013年论文

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name

ERK and AKT signaling drive ME ...... liferation and tumorigenicity.

@en

ERK and AKT signaling drive ME ...... liferation and tumorigenicity.

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type

label

ERK and AKT signaling drive ME ...... liferation and tumorigenicity.

@en

ERK and AKT signaling drive ME ...... liferation and tumorigenicity.

@nl

prefLabel

ERK and AKT signaling drive ME ...... liferation and tumorigenicity.

@en

ERK and AKT signaling drive ME ...... liferation and tumorigenicity.

@nl

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1541-7786.MCR-12-0618

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Molecular Cancer Research

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ERK and AKT signaling drive ME ...... liferation and tumorigenicity.

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P2093

Cory Abate-Shen

http://www.w3.org/2001/XMLSchema#string

Feng Jin

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Joseph D Fondell

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Madesh Belakavadi

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Marina Chekmareva

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Michael M Ittmann

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Shazia Irshad

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Wei Yu

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P2860

Activation of TRAP/mediator subunit TRAP220/Med1 is regulated by mitogen-activated protein kinase-dependent phosphorylation

A coregulatory role for the TRAP-mediator complex in androgen receptor-mediated gene expression

MED1/TRAP220 exists predominantly in a TRAP/ Mediator subpopulation enriched in RNA polymerase II and is required for ER-mediated transcription

MED1 phosphorylation promotes its association with mediator: implications for nuclear receptor signaling

Ligand-specific allosteric regulation of coactivator functions of androgen receptor in prostate cancer cells

Amplification and overexpression of peroxisome proliferator-activated receptor binding protein (PBP/PPARBP) gene in breast cancer

Mediator-dependent nuclear receptor function

Defects of the heart, eye, and megakaryocytes in peroxisome proliferator activator receptor-binding protein (PBP) null embryos implicate GATA family of transcription factors

CDC6: from DNA replication to cell cycle checkpoints and oncogenesis

Critical role for transcription coactivator peroxisome proliferator-activated receptor (PPAR)-binding protein/TRAP220 in liver regeneration and PPARalpha ligand-induced liver tumor development

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736-747

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