SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer. - Wikidata - awgldk - TriplyDB

SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

http://www.wikidata.org/entity/Q37542249

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P62: An emerging oncotarget for osteolytic metastasis Choosing the right cell line for renal cell cancer research p62/SQSTM1 functions as a signaling hub and an autophagy adaptor Development of synchronous VHL syndrome tumors reveals contingencies and constraints to tumor evolution p62/SQSTM1 by Binding to Vitamin D Receptor Inhibits Hepatic Stellate Cell Activity, Fibrosis, and Liver Cancer VHL deficiency augments anthracycline sensitivity of clear cell renal cell carcinomas by down-regulating ALDH2.RNA-Seq and ChIP-Seq reveal SQSTM1/p62 as a key mediator of JunB suppression of NF-κB-dependent inflammation Mitophagy and cancer.The role for autophagy in cancer.High Expression of SQSTM1/p62 Protein Is Associated with Poor Prognosis in Epithelial Ovarian Cancer.Feasibility analysis of p62 (SQSTM1)-encoding DNA vaccine as a novel cancer immunotherapy.Identification of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase as a novel autophagy regulator by high content shRNA screening.Bixin protects mice against ventilation-induced lung injury in an NRF2-dependent manner miR-490-5p suppresses tumour growth in renal cell carcinoma through targeting PIK3CA.Regulation of glucose metabolism by p62/SQSTM1 through HIF1α Mechanisms of Selective Autophagy in Normal Physiology and Cancer Absence of the Autophagy Adaptor SQSTM1/p62 Causes Childhood-Onset Neurodegeneration with Ataxia, Dystonia, and Gaze Palsy.p62/SQSTM1 enhances breast cancer stem-like properties by stabilizing MYC mRNA.VPS34 stimulation of p62 phosphorylation for cancer progression.p62/SQSTM1-Dr. Jekyll and Mr. Hyde that prevents oxidative stress but promotes liver cancer.Metabolic reprogramming of stromal fibroblasts through p62-mTORC1 signaling promotes inflammation and tumorigenesis.Autophagy-from molecular mechanisms to clinical relevance.Autophagy in the liver: functions in health and disease.Expanding perspectives on the significance of mitophagy in cancer.The KEAP1-NRF2 System in Cancer.p62 Regulates the Proliferation of Molecular Apocrine Breast Cancer Cells A novel pVHL-independent but NEMO-driven pathway in renal cancer promotes HIF stabilization.Perspectives of the Nrf-2 signaling pathway in cancer progression and therapy.Inactivation of the PBRM1 tumor suppressor gene amplifies the HIF-response in VHL-/- clear cell renal carcinoma.Expression of P62 in hepatocellular carcinoma involving hepatitis B virus infection and aflatoxin B1 exposure Sqstm1-GFP knock-in mice reveal dynamic actions of Sqstm1 during autophagy and under stress conditions in living cells.p62, Upregulated during Preneoplasia, Induces Hepatocellular Carcinogenesis by Maintaining Survival of Stressed HCC-Initiating Cells.The lncRNA HULC functions as an oncogene by targeting ATG7 and ITGB1 in epithelial ovarian carcinoma.p62/SQSTM1 Cooperates with Hyperactive mTORC1 to Regulate Glutathione Production, Maintain Mitochondrial Integrity, and Promote Tumorigenesis.The Autophagy Receptor Adaptor p62 is Up-regulated by UVA Radiation in Melanocytes and in Melanoma Cells.p62/SQSTM1 interacts with vimentin to enhance breast cancer metastasis.HIF activation causes synthetic lethality between the VHL tumor suppressor and the EZH1 histone methyltransferase.MicroRNA-17-5p contributes to osteoarthritis progression by binding p62/SQSTM1.Timing the Landmark Events in the Evolution of Clear Cell Renal Cell Cancer: TRACERx Renal.Autophagy, Metabolism, and Cancer.

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SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

http://www.wikidata.org/entity/Q37542249

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on December 2013

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

@cs

name

SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

@en

SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

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type

label

SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

@en

SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

@nl

prefLabel

SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

@en

SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

@nl

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J.CCR.2013.10.025

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SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

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A Ari Hakimi

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

Barbara Tabak

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

Chris Sander

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

Chuan Shen

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

David E Root

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

Eijiro Nakamura

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

Ella Liberzon

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

Glenn S Cowley

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

James J Hsieh

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

Kiyohiro Ando

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

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Structure and functional properties of the ubiquitin binding protein p62

The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1

Regulation of receptor for activated C kinase 1 protein by the von Hippel-Lindau tumor suppressor in IGF-I-induced renal carcinoma cell invasiveness

p62/SQSTM1 is a target gene for transcription factor NRF2 and creates a positive feedback loop by inducing antioxidant response element-driven gene transcription

Exome sequencing identifies frequent mutation of the SWI/SNF complex gene PBRM1 in renal carcinoma

Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.

Autophagy suppresses tumorigenesis through elimination of p62

pVHL acts as an adaptor to promote the inhibitory phosphorylation of the NF-kappaB agonist Card9 by CK2

Inhibition of HIF2alpha is sufficient to suppress pVHL-defective tumor growth

Autophagy suppresses RIP kinase-dependent necrosis enabling survival to mTOR inhibition

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738-750

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scholarly article

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10.1016/J.CCR.2013.10.025

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6

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24

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William G. Kaelin

Giovanni Ciriello

Aviad Tsherniak

Nikolaus Schultz

Anders Jacobsen

Patrick H Lizotte

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2013-12-01T00:00:00Z

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259317230

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24332042

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3910168

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