Activated c-Abl tyrosine kinase in malignant solid tumors. - Wikidata - thesis-toulmin - TriplyDB

Activated c-Abl tyrosine kinase in malignant solid tumors.

Activated c-Abl tyrosine kinase in malignant solid tumors.

http://www.wikidata.org/entity/Q37129818

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ABL tyrosine kinases: evolution of function, regulation, and specificity Heme controls the regulation of protein tyrosine kinases Jak2 and Src Evidence for a direct involvement of hMSH5 in promoting ionizing radiation induced apoptosis Mitochondria, calcium, and tumor suppressor Fus1: At the crossroad of cancer, inflammation, and autoimmunity Inhibition of c-Abl kinase activity renders cancer cells highly sensitive to mitoxantrone Role of ABL family kinases in cancer: from leukaemia to solid tumours The oleocanthal-based homovanillyl sinapate as a novel c-Met inhibitor c-Abl Kinase Is a Regulator of αvβ3 Integrin Mediated Melanoma A375 Cell Migration.Misfolding, Aggregation, and Disordered Segments in c-Abl and p53 in Human Cancer.Activated Abl kinase inhibits oncogenic transforming growth factor-beta signaling and tumorigenesis in mammary tumors.c-Abl tyrosine kinase regulates cardiac growth and development.Global Regulation of Differential Gene Expression by c-Abl/Arg Oncogenic Kinases.The Ron receptor tyrosine kinase activates c-Abl to promote cell proliferation through tyrosine phosphorylation of PCNA in breast cancer Saracatinib Impairs Head and Neck Squamous Cell Carcinoma Invasion by Disrupting Invadopodia Function Drosophila Abelson kinase mediates cell invasion and proliferation through two distinct MAPK pathways.Interaction of proliferation cell nuclear antigen (PCNA) with c-Abl in cell proliferation and response to DNA damages in breast cancer.Abl kinases are required for invadopodia formation and chemokine-induced invasion.c-Abl phosphorylation of ΔNp63α is critical for cell viability Src activates Abl to augment Robo1 expression in order to promote tumor cell migration.Geminin overexpression promotes imatinib sensitive breast cancer: a novel treatment approach for aggressive breast cancers, including a subset of triple negative Growth factor dependent regulation of centrosome function and genomic instability by HuR.The Cain and Abl of epithelial-mesenchymal transition and transforming growth factor-β in mammary epithelial cells Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR.The Emerging Role of ABL Kinases in Solid Tumors.Crk and ABI1: binary molecular switches that regulate abl tyrosine kinase and signaling to the cytoskeleton.SRC points the way to biomarkers and chemotherapeutic targets.Activation of abl family kinases in solid tumors.Abl kinases regulate autophagy by promoting the trafficking and function of lysosomal components N-myristoylated c-Abl tyrosine kinase localizes to the endoplasmic reticulum upon binding to an allosteric inhibitor.Dynamin 2 and c-Abl are novel regulators of hyperoxia-mediated NADPH oxidase activation and reactive oxygen species production in caveolin-enriched microdomains of the endothelium.Tyrosine kinase c-Abl regulates the survival of plasma cells Invading one step at a time: the role of invadopodia in tumor metastasis.c-Abl inhibits breast cancer tumorigenesis through reactivation of p53-mediated p21 expression Novel Src/Abl tyrosine kinase inhibitor bosutinib suppresses neuroblastoma growth via inhibiting Src/Abl signaling.Abl interconnects oncogenic Met and p53 core pathways in cancer cells.c-Abl and Arg are activated in human primary melanomas, promote melanoma cell invasion via distinct pathways, and drive metastatic progression.Benefits of Multifaceted Chemopreventives in the Suppression of the Oral Squamous Cell Carcinoma (OSCC) Tumorigenic Phenotype.Multi-talented DEAD-box proteins and potential tumor promoters: p68 RNA helicase (DDX5) and its paralog, p72 RNA helicase (DDX17)Atomic view of the energy landscape in the allosteric regulation of Abl kinase.Interaction of Abl Tyrosine Kinases with SOCS3 Impairs Its Suppressor Function in Tumorigenesis

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Activated c-Abl tyrosine kinase in malignant solid tumors.

http://www.wikidata.org/entity/Q37129818

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on 07 April 2008

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Activated c-Abl tyrosine kinase in malignant solid tumors.

@en

Activated c-Abl tyrosine kinase in malignant solid tumors.

@nl

type

label

Activated c-Abl tyrosine kinase in malignant solid tumors.

@en

Activated c-Abl tyrosine kinase in malignant solid tumors.

@nl

prefLabel

Activated c-Abl tyrosine kinase in malignant solid tumors.

@en

Activated c-Abl tyrosine kinase in malignant solid tumors.

@nl

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Activated c-Abl tyrosine kinase in malignant solid tumors.

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J Lin

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R Arlinghaus

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P2860

The PAG gene product, a stress-induced protein with antioxidant properties, is an Abl SH3-binding protein and a physiological inhibitor of c-Abl tyrosine kinase activity

Oncogenic activation of c-Abl in non-small cell lung cancer cells lacking FUS1 expression: inhibition of c-Abl by the tumor suppressor gene product Fus1

Molecular responses to hypoxia in tumor cells

Molecular and cellular aspects of the insulin-like growth factor I receptor

Nuclear-cytoplasmic shuttling of C-ABL tyrosine kinase

The Abl family kinases: Mechanisms of regulation and signaling

c-Abl is activated by growth factors and Src family kinases and has a role in the cellular response to PDGF

Myristoylation of the fus1 protein is required for tumor suppression in human lung cancer cells.

Treatment with Imatinib in NSCLC is associated with decrease of phosphorylated PDGFR-beta and VEGF expression, decrease in interstitial fluid pressure and improvement of oxygenation

Overexpression of candidate tumor suppressor gene FUS1 isolated from the 3p21.3 homozygous deletion region leads to G1 arrest and growth inhibition of lung cancer cells.

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4385-4391

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scholarly article

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10.1038/ONC.2008.86

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2008-04-07T00:00:00Z

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5460563

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18391983

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