Elevated JNK activation contributes to the pathogenesis of human brain tumors. - Wikidata - awgldk - TriplyDB

Elevated JNK activation contributes to the pathogenesis of human brain tumors.

Elevated JNK activation contributes to the pathogenesis of human brain tumors.

http://www.wikidata.org/entity/Q42524158

about

Ligand-Independent EGFR Signaling JNK signalling in cancer: in need of new, smarter therapeutic targets Wiring the cell signaling circuitry by the NF-kappa B and JNK1 crosstalk and its applications in human diseases The structural pathway of interleukin 1 (IL-1) initiated signaling reveals mechanisms of oncogenic mutations and SNPs in inflammation and cancer JNK-mediated phosphorylation of Cdc25C regulates cell cycle entry and G(2)/M DNA damage checkpoint.Sustained c-Jun-NH2-kinase activity promotes epithelial-mesenchymal transition, invasion, and survival of breast cancer cells by regulating extracellular signal-regulated kinase activation.Improved protein arrays for quantitative systems analysis of the dynamics of signaling pathway interactions.Epidermal growth factor receptor in glioma: signal transduction, neuropathology, imaging, and radioresistance A Cell-Cell Communication Marker for Identifying Targeted Tumor Therapies.The APC/C Ubiquitin Ligase: From Cell Biology to Tumorigenesis Targeting JNK for therapeutic depletion of stem-like glioblastoma cells Development of JNK2-selective peptide inhibitors that inhibit breast cancer cell migration Phosphorylation of Glutathione S-Transferase P1 (GSTP1) by Epidermal Growth Factor Receptor (EGFR) Promotes Formation of the GSTP1-c-Jun N-terminal kinase (JNK) Complex and Suppresses JNK Downstream Signaling and Apoptosis in Brain Tumor Cells.Effects of MAP kinase inhibitors on epidermal growth factor-induced neoplastic transformation of human keratinocytes.Epidermal growth factor receptor tyrosine phosphorylation and signaling controlled by a nuclear receptor coactivator, amplified in breast cancer 1.A mechanism for the upregulation of EGF receptor levels in glioblastomas A Novel Interaction between Pyk2 and MAP4K4 Is Integrated with Glioma Cell Migration Tissue transglutaminase is an essential participant in the epidermal growth factor-stimulated signaling pathway leading to cancer cell migration and invasion EGFRvIII expression and PTEN loss synergistically induce chromosomal instability and glial tumors.Epidermal growth factor receptor and PTEN modulate tissue factor expression in glioblastoma through JunD/activator protein-1 transcriptional activity.JNK Signaling in the Control of the Tumor-Initiating Capacity Associated with Cancer Stem Cells.p38 MAPK activation, JNK inhibition, neoplastic growth inhibition, and increased gap junction communication in human lung carcinoma and Ras-transformed cells by 4-phenyl-3-butenoic acid.Dual modulation of JNK and Akt signaling pathways by chaetoglobosin K in human lung carcinoma and ras-transformed epithelial cells.p75 neurotrophin receptor cleavage by α- and γ-secretases is required for neurotrophin-mediated proliferation of brain tumor-initiating cells.Synergistic suppression of noscapine and conventional chemotherapeutics on human glioblastoma cell growth.Interleukins in glioblastoma pathophysiology: implications for therapy.Regulation of protein translation and c-Jun expression by prostate tumor overexpressed 1.Roles of phosphorylated JNK in esophageal squamous cell carcinomas of Kazakh ethnic.Angiotensin III induces c-Jun N-terminal kinase leading to proliferation of rat astrocytes.c-Jun N-terminal kinase has a pivotal role in the maintenance of self-renewal and tumorigenicity in glioma stem-like cells.Negative regulation of constitutive NF-kappaB and JNK signaling by PKN1-mediated phosphorylation of TRAF1.Genetic alterations of the NRP/B gene are associated with human brain tumors.Phosphorylation of Bad at Thr-201 by JNK1 promotes glycolysis through activation of phosphofructokinase-1.p38 Mitogen-activated protein kinase regulation of JB6 Cl41 cell transformation promoted by epidermal growth factor.Adhesion- and stress-related adaptation of glioma radiochemoresistance is circumvented by β1 integrin/JNK co-targeting.Activation of the Ras-ERK pathway inhibits retinoic acid-induced stimulation of tissue transglutaminase expression in NIH3T3 cells.Curcumin suppresses growth and chemoresistance of human glioblastoma cells via AP-1 and NFkappaB transcription factors.Oncrasin targets the JNK-NF-κB axis to sensitize glioma cells to TNFα-induced apoptosis.RUNX1 Regulates Migration, Invasion, and Angiogenesis via p38 MAPK Pathway in Human Glioblastoma.Inhibition of JNK2 disrupts anaphase and produces aneuploidy in mammalian cells.

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Elevated JNK activation contributes to the pathogenesis of human brain tumors.

http://www.wikidata.org/entity/Q42524158

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2002年学术文章

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2002年學術文章

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2002年學術文章

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2002年學術文章

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name

Elevated JNK activation contributes to the pathogenesis of human brain tumors.

@en

Elevated JNK activation contributes to the pathogenesis of human brain tumors.

@nl

type

label

Elevated JNK activation contributes to the pathogenesis of human brain tumors.

@en

Elevated JNK activation contributes to the pathogenesis of human brain tumors.

@nl

prefLabel

Elevated JNK activation contributes to the pathogenesis of human brain tumors.

@en

Elevated JNK activation contributes to the pathogenesis of human brain tumors.

@nl

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Elevated JNK activation contributes to the pathogenesis of human brain tumors.

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Albert J Wong

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

Andrew K Godwin

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David C James

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David K Moscatello

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David R Emlet

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Isamu Okamoto

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

Lawrence C Kenyon

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Marc A Antonyak

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Marina Holgado-Madruga

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Mehdi Tnani

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P2860

JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain

Raf-1 activates MAP kinase-kinase

Constitutive activation of the 41-/43-kDa mitogen-activated protein kinase signaling pathway in human tumors

Identification of a candidate tumour suppressor gene, MMAC1, at chromosome 10q23.3 that is mutated in multiple advanced cancers

Blockade of the MAP kinase pathway suppresses growth of colon tumors in vivo

Selective activation of the JNK signaling cascade and c-Jun transcriptional activity by the small GTPases Rac and Cdc42Hs

Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis

An essential role for Rho, Rac, and Cdc42 GTPases in cell cycle progression through G1

The small GTP-binding proteins Rac1 and Cdc42 regulate the activity of the JNK/SAPK signaling pathway

The stress-activated protein kinase subfamily of c-Jun kinases

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1001123820

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