Tumor necrosis factor-like weak inducer of apoptosis stimulation of glioma cell survival is dependent on Akt2 function. - Wikidata - awgldk - TriplyDB

Tumor necrosis factor-like weak inducer of apoptosis stimulation of glioma cell survival is dependent on Akt2 function.

Tumor necrosis factor-like weak inducer of apoptosis stimulation of glioma cell survival is dependent on Akt2 function.

http://www.wikidata.org/entity/Q37438218

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The TWEAK receptor Fn14 is a potential cell surface portal for targeted delivery of glioblastoma therapeutics IRS1 is highly expressed in localized breast tumors and regulates the sensitivity of breast cancer cells to chemotherapy, while IRS2 is highly expressed in invasive breast tumors A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway Proapoptotic and antiinvasive activity of Rac1 small molecule inhibitors on malignant glioma cells Predictive gene signature of response to the anti-TweakR mAb PDL192 in patient-derived breast cancer xenografts TWEAK-independent Fn14 self-association and NF-κB activation is mediated by the C-terminal region of the Fn14 cytoplasmic domain Minimizing the non-specific binding of nanoparticles to the brain enables active targeting of Fn14-positive glioblastoma cells.Reciprocal activation of transcription factors underlies the dichotomy between proliferation and invasion of glioma cells.Fn14•TRAIL effectively inhibits hepatocellular carcinoma growth.High β-catenin/Tcf-4 activity confers glioma progression via direct regulation of AKT2 gene expression.Identification of aurintricarboxylic acid as a selective inhibitor of the TWEAK-Fn14 signaling pathway in glioblastoma cells Development and characterization of a potent immunoconjugate targeting the Fn14 receptor on solid tumor cells.The Src homology 3 domain-containing guanine nucleotide exchange factor is overexpressed in high-grade gliomas and promotes tumor necrosis factor-like weak inducer of apoptosis-fibroblast growth factor-inducible 14-induced cell migration and invasio TROY (TNFRSF19) promotes glioblastoma survival signaling and therapeutic resistance.Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) promotes glioblastoma cell chemotaxis via Lyn activation.TWEAK activation of the non-canonical NF-κB signaling pathway differentially regulates melanoma and prostate cancer cell invasion.Mcl-1 mediates TWEAK/Fn14-induced non-small cell lung cancer survival and therapeutic response.The TWEAK-Fn14 system as a potential drug target.Implications of Rho GTPase Signaling in Glioma Cell Invasion and Tumor Progression.Role of Akt in human malignant glioma: from oncogenesis to tumor aggressiveness.Prognostic significance of TWEAK expression in colorectal cancer and effect of its inhibition on invasion.SGEF Is Regulated via TWEAK/Fn14/NF-κB Signaling and Promotes Survival by Modulation of the DNA Repair Response to Temozolomide Elevated expression of Fn14 in non-small cell lung cancer correlates with activated EGFR and promotes tumor cell migration and invasion.The small GTPase RhoG mediates glioblastoma cell invasion.TWEAK/Fn14 Axis-Targeted Therapeutics: Moving Basic Science Discoveries to the Clinic.The possible functions of duplicated ets (GGAA) motifs located near transcription start sites of various human genes Construction of a recombinant lentivirus containing human microRNA-7-3 and its inhibitory effects on glioma proliferation.A Novel Signaling Complex between TROY and EGFR Mediates Glioblastoma Cell Invasion.Differential expression of the TWEAK receptor Fn14 in IDH1 wild-type and mutant gliomas.FN14 expression correlates with MET in NSCLC and promotes MET-driven cell invasion.EGFRvIII-Stat5 Signaling Enhances Glioblastoma Cell Migration and Survival.PDZ-RhoGEF Is a Signaling Effector for TROY-Induced Glioblastoma Cell Invasion and Survival

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Tumor necrosis factor-like weak inducer of apoptosis stimulation of glioma cell survival is dependent on Akt2 function.

http://www.wikidata.org/entity/Q37438218

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 27 October 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Tumor necrosis factor-like wea ...... is dependent on Akt2 function.

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Tumor necrosis factor-like wea ...... is dependent on Akt2 function.

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type

label

Tumor necrosis factor-like wea ...... is dependent on Akt2 function.

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Tumor necrosis factor-like wea ...... is dependent on Akt2 function.

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prefLabel

Tumor necrosis factor-like wea ...... is dependent on Akt2 function.

@en

Tumor necrosis factor-like wea ...... is dependent on Akt2 function.

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1541-7786.MCR-09-0194

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Molecular Cancer Research

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Tumor necrosis factor-like wea ...... is dependent on Akt2 function.

@en

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Benjamin A Savitch

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

Christopher Kingsley

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

David Carpentieri

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

Galen Hostetter

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Jeffrey A Winkles

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

Joseph C Loftus

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

Matthew J Ennis

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Nhan L Tran

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

Shannon P Fortin

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

Wendy S McDonough

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

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AKT2, a putative oncogene encoding a member of a subfamily of protein-serine/threonine kinases, is amplified in human ovarian carcinomas

The human Fn14 receptor gene is up-regulated in migrating glioma cells in vitro and overexpressed in advanced glial tumors

Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery

The TNF and TNF receptor superfamilies: integrating mammalian biology

Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt

Increased fibroblast growth factor-inducible 14 expression levels promote glioma cell invasion via Rac1 and nuclear factor-kappaB and correlate with poor patient outcome

Regulation of cell death protease caspase-9 by phosphorylation

The tumor necrosis factor-like weak inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling system regulates glioma cell survival via NFkappaB pathway activation and BCL-XL/BCL-W expression

Cell death provoked by loss of interleukin-3 signaling is independent of Bad, Bim, and PI3 kinase, but depends in part on Puma

Protein kinase B alpha/Akt1 regulates placental development and fetal growth

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1871-1881

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scholarly article

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10.1158/1541-7786.MCR-09-0194

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11

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7

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2009-10-27T00:00:00Z

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38040617

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19861406

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apoptotic process

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2783270

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