Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling - Wikidata - awgldk - TriplyDB

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

http://www.wikidata.org/entity/Q34056610

about

Diversin is overexpressed in breast cancer and accelerates cell proliferation and invasion RAGE expression in human T cells: a link between environmental factors and adaptive immune responses.S100A8/A9 activate key genes and pathways in colon tumor progression.Alternative splicing of the RAGE cytoplasmic domain regulates cell signaling and function.RAGE regulates immune cell infiltration and angiogenesis in choroidal neovascularization.Apoptosis, autophagy, necroptosis, and cancer metastasis Mouse Specific Cleavage-Resistant RAGE Splice Variant.Mouse RAGE Variant 4 Is a Dominant Membrane Receptor that Does Not Shed to Generate Soluble RAGE.The role of HMGB1-RAGE axis in migration and invasion of hepatocellular carcinoma cell lines.Non-histone nuclear factor HMGB1 as a therapeutic target in colorectal cancer.Targeting of RAGE-ligand signaling impairs breast cancer cell invasion and metastasis.Regulation of Receptor for Advanced Glycation End Products (RAGE) Ectodomain Shedding and Its Role in Cell Function.Expression and subcellular localization of RAGE in melanoma cells.Role of c-Jun N-terminal kinase isoforms in the cellular activity of melanoma cell lines.All the "RAGE" in lung disease: The receptor for advanced glycation endproducts (RAGE) is a major mediator of pulmonary inflammatory responses.Interaction between Tumor Cell Surface Receptor RAGE and Proteinase 3 Mediates Prostate Cancer Metastasis to Bone.In vitro anticancer effects of a RAGE inhibitor discovered using a structure-based drug design system.Gene Expression of Sirtuin-1 and Endogenous Secretory Receptor for Advanced Glycation End Products in Healthy and Slightly Overweight Subjects after Caloric Restriction and Resveratrol Administration

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Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

http://www.wikidata.org/entity/Q34056610

description

2010 nî lūn-bûn

@nan

2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հունիսին հրատարակված գիտական հոդված

@hy

2010年の論文

@ja

2010年学术文章

@wuu

2010年学术文章

@zh-cn

2010年学术文章

@zh-hans

2010年学术文章

@zh-my

2010年学术文章

@zh-sg

2010年學術文章

@yue

name

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

@ast

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

@en

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

@nl

type

label

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

@ast

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

@en

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

@nl

prefLabel

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

@ast

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

@en

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

@nl

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P356

0008-5472.CAN-10-0595

P1433

Cancer Research

P1476

Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling

@en

P2093

Anastasia Z Kalea

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

Ann Marie Schmidt

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

Evis Harja

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

Fiona See

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

Maria Arriero

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

P2860

Receptor for advanced glycation end products (RAGE)-mediated neurite outgrowth and activation of NF-kappaB require the cytoplasmic domain of the receptor but different downstream signaling pathways

RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides

The Hallmarks of Cancer

Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins

Calcium-regulated intramembrane proteolysis of the RAGE receptor

Interaction of the RAGE cytoplasmic domain with diaphanous-1 is required for ligand-stimulated cellular migration through activation of Rac1 and Cdc42

S100A8 and S100A9 activate MAP kinase and NF-kappaB signaling pathways and trigger translocation of RAGE in human prostate cancer cells

The receptor for advanced glycation end products (RAGE) is a cellular binding site for amphoterin. Mediation of neurite outgrowth and co-expression of rage and amphoterin in the developing nervous system

N(epsilon)-(carboxymethyl)lysine adducts of proteins are ligands for receptor for advanced glycation end products that activate cell signaling pathways and modulate gene expression

Molecular basis of metastasis.

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5628-5638

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scholarly article

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10.1158/0008-5472.CAN-10-0595

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13

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70

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2010-06-22T00:00:00Z

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20570900

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P932

2919303

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