Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
about
Phosphorylation by casein kinase I promotes the turnover of the Mdm2 oncoprotein via the SCF(beta-TRCP) ubiquitin ligaseHypoxia-inducible factors and the response to hypoxic stressEarly events in the pathogenesis of chronic obstructive pulmonary disease. Smoking-induced reprogramming of airway epithelial basal progenitor cellsAcquisition order of Ras and p53 gene alterations defines distinct adrenocortical tumor phenotypesPHD2: from hypoxia regulation to disease progressionProlyl hydroxylase-2 (PHD2) exerts tumor-suppressive activity in pancreatic cancerProlyl hydroxylation by EglN2 destabilizes FOXO3a by blocking its interaction with the USP9x deubiquitinase.Tumor suppressor SPOP ubiquitinates and degrades EglN2 to compromise growth of prostate cancer cellsA nontranscriptional role for HIF-1α as a direct inhibitor of DNA replicationProlyl hydroxylase PHD3 enhances the hypoxic survival and G1 to S transition of carcinoma cells.Suppression of glioma progression by Egln3Deficiency of a transmembrane prolyl 4-hydroxylase in the zebrafish leads to basement membrane defects and compromised kidney functionLoss of PHD3 allows tumours to overcome hypoxic growth inhibition and sustain proliferation through EGFR.EGLN2 and RNF150 genetic variants are associated with chronic obstructive pulmonary disease risk in the Chinese population.The prolyl hydroxylase enzymes are positively associated with hypoxia-inducible factor-1α and vascular endothelial growth factor in human breast cancer and alter in response to primary systemic treatment with epirubicin and tamoxifen.Expression and DNA methylation levels of prolyl hydroxylases PHD1, PHD2, PHD3 and asparaginyl hydroxylase FIH in colorectal cancer.Genetic and functional studies implicate HIF1α as a 14q kidney cancer suppressor geneAnti-estrogen resistance in breast cancer is induced by the tumor microenvironment and can be overcome by inhibiting mitochondrial function in epithelial cancer cells.Expression of prolyl hydroxylases (PHDs) is selectively controlled by HIF-1 and HIF-2 proteins in nucleus pulposus cells of the intervertebral disc: distinct roles of PHD2 and PHD3 proteins in controlling HIF-1α activity in hypoxiaIdentification of Small-Molecule PHD2 Zinc Finger Inhibitors that Activate Hypoxia Inducible Factor.Chromosome 19q13 disruption alters expressions of CYP2A7, MIA and MIA-RAB4B lncRNA and contributes to FAP-like phenotype in APC mutation-negative familial colorectal cancer patients.Regulation of cell proliferation by hypoxia-inducible factorsEglN2 associates with the NRF1-PGC1α complex and controls mitochondrial function in breast cancerNew cancer targets emerging from studies of the Von Hippel-Lindau tumor suppressor protein.Estrogen receptor β sustains epithelial differentiation by regulating prolyl hydroxylase 2 transcriptionDeletion or Inhibition of the Oxygen Sensor PHD1 Protects against Ischemic Stroke via Reprogramming of Neuronal Metabolism.A screen for inducers of p21(waf1/cip1) identifies HIF prolyl hydroxylase inhibitors as neuroprotective agents with antitumor properties.EglN2 positively regulates mitochondrial function in breast cancer.Function and expression of prolyl hydroxylase 3 in cancers.Variants in two adjacent genes, EGLN2 and CYP2A6, influence smoking behavior related to disease risk via different mechanisms.SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.Smoking dysregulates the human airway basal cell transcriptome at COPD risk locus 19q13.2.pVHL suppresses kinase activity of Akt in a proline-hydroxylation-dependent manner.EglN2 contributes to triple negative breast tumorigenesis by functioning as a substrate for the FBW7 tumor suppressor.Cancer and altered metabolism: potential importance of hypoxia-inducible factor and 2-oxoglutarate-dependent dioxygenasesHypoxia-inducible factor prolyl hydroxylases as targets for neuroprotection by "antioxidant" metal chelators: From ferroptosis to stroke.Prolyl 4-hydroxylases, master regulators of the hypoxia response.Cell cycle progression in response to oxygen levels.Recent Advances in Developing Inhibitors for Hypoxia-Inducible Factor Prolyl Hydroxylases and Their Therapeutic Implications.PHD1 regulates p53-mediated colorectal cancer chemoresistance.
P2860
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P2860
Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
2009年學術文章
@zh
2009年學術文章
@zh-hant
name
Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
@en
Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
@nl
type
label
Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
@en
Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
@nl
prefLabel
Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
@en
Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
@nl
P2093
P2860
P50
P1433
P1476
Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
@en
P2093
Andrea L Richardson
Archana Bommi-Reddy
Christoph Geisen
David E Root
Hiu-Wing Cheung
Jiayun Liu
Jinming Gu
Kornelia Polyak
Lianjie Li
P2860
P304
P356
10.1016/J.CCR.2009.09.029
P577
2009-11-01T00:00:00Z