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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

BMX non-receptor tyrosine kinase

EphA3, Bmx, ETK
This gene encodes a non-receptor tyrosine kinase belonging to the Tec kinase family. The protein contains a PH-like domain, which mediates membrane targeting by binding to phosphatidylinositol 3,4,5-triphosphate (PIP3), and a SH2 domain that binds to tyrosine-phosphorylated proteins and functions in signal transduction. The protein is implicated in several signal transduction pathways including the Stat pathway, and regulates differentiation and tumorigenicity of several types of cancer cells. Multiple alternatively spliced variants, encoding the same protein, have been identified.[provided by RefSeq, Sep 2009] (from NCBI)
Top mentioned proteins: Eph, Tec, CAN, Btk, V1a
Papers on EphA3
Germline copy number variation analysis in Finnish families with hereditary prostate cancer.
Schleutker et al., Tampere, Finland. In Prostate, Feb 2016
RESULTS: An intronic deletion (14.7 kb) in the EPHA3 gene coding for class A ephrin receptor was observed in 11.6% of PrCa patients and in 6.1% of controls.
PTP-PEST controls EphA3 activation and ephrin-induced cytoskeletal remodelling.
Lackmann et al., Australia. In J Cell Sci, Feb 2016
Here, we demonstrate that an N-terminal fragment of PTP-PEST, generated through an ephrinA5-triggered and spatially confined cleavage mediated by caspase-3, attenuates EphA3 receptor activation and its internalisation.
Endothelial Bmx tyrosine kinase activity is essential for myocardial hypertrophy and remodeling.
Alitalo et al., Helsinki, Finland. In Proc Natl Acad Sci U S A, Nov 2015
Deletion of bone marrow kinase in chromosome X (Bmx), an arterial nonreceptor tyrosine kinase, has been shown to inhibit cardiac hypertrophy in mice.
Stochastic Interaction between Neural Activity and Molecular Cues in the Formation of Topographic Maps.
Triplett et al., San Francisco, United States. In Neuron, Oct 2015
The functional and anatomical representation of azimuth in the superior colliculus of heterozygous Islet2-EphA3 knockin (Isl2(EphA3/+)) mice is variable: maps may be single, duplicated, or a combination of the two.
EphA3 biology and cancer.
Vail et al., Australia. In Growth Factors, 2014
EphA3, originally isolated from leukemic and melanoma cells, is presently one of the most promising therapeutic targets, with multiple tumor-promoting roles in a variety of cancer types.
PH motifs in PAR1&2 endow breast cancer growth.
Bar-Shavit et al., Jerusalem, Israel. In Nat Commun, 2014
Other PH-domain signal-proteins such as Etk/Bmx and Vav3 also associate with PAR1 and PAR2 through their PH domains.
Mini-review: bmx kinase inhibitors for cancer therapy.
Willey et al., Birmingham, United States. In Recent Pat Anticancer Drug Discov, 2013
Evidence has been published that one member of this family; the Bmx kinase, may play a role in the pathogenesis of glioblastoma, prostate, breast and lung cancer.
EphA3 maintains tumorigenicity and is a therapeutic target in glioblastoma multiforme.
Boyd et al., Brisbane, Australia. In Cancer Cell, 2013
We show that the receptor tyrosine kinase EphA3 is frequently overexpressed in GBM and, in particular, in the most aggressive mesenchymal subtype.
Effects of cancer-associated EPHA3 mutations on lung cancer.
Chen et al., Nashville, United States. In J Natl Cancer Inst, 2012
Cancer-associated EPHA3 mutations attenuate the tumor-suppressive effects of normal EPHA3 in lung cancer.
Deletion of the endothelial Bmx tyrosine kinase decreases tumor angiogenesis and growth.
Alitalo et al., Helsinki, Finland. In Cancer Res, 2012
Our findings therefore indicate that Bmx activity contributes to tumor angiogenesis and growth.
EPHA3 as a novel therapeutic target in the hematological malignancies.
Giles et al., Galway, Ireland. In Expert Rev Hematol, 2012
The most promising of the Eph receptors in this regard is EPHA3, which is overexpressed in many hematologic malignancies.
BMX and its role in inflammation, cardiovascular disease, and cancer.
Gottar-Guillier et al., Basel, Switzerland. In Int Rev Immunol, 2012
This review characterizes the role of BMX in inflamamtion, cardiovascular disease and cancer.
The role of Tec family kinases in the regulation of T-helper-cell differentiation.
Ellmeier et al., Vienna, Austria. In Int Rev Immunol, 2012
ABSTRACT Members of the Tec kinase family (Tec, Btk, Itk, Rlk, and Bmx) play an important role during innate and adaptive immune responses, and mutations in Tec family kinases are linked with immunodeficiencies in humans and mice.
Cancer somatic mutations disrupt functions of the EphA3 receptor tyrosine kinase through multiple mechanisms.
Pasquale et al., Los Angeles, United States. In Biochemistry, 2012
EphA3 has ephrin- and kinase-dependent tumor suppressing activities, which are disrupted by somatic cancer mutations
Nonreceptor tyrosine kinase BMX maintains self-renewal and tumorigenic potential of glioblastoma stem cells by activating STAT3.
Bao et al., Cleveland, United States. In Cancer Cell, 2011
Constitutively active STAT3 rescued the effects of BMX downregulation, supporting that BMX signals through STAT3 in glioblastoma stem cells (GSCs).
Somatic mutations affect key pathways in lung adenocarcinoma.
Wilson et al., Saint Louis, United States. In Nature, 2008
The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes.
Monovalent, reduced-size quantum dots for imaging receptors on living cells.
Ting et al., Cambridge, United States. In Nat Methods, 2008
The small size improved access of QD-labeled glutamate receptors to neuronal synapses, and monovalency prevented EphA3 tyrosine kinase activation.
Segregation of axial motor and sensory pathways via heterotypic trans-axonal signaling.
Marquardt et al., Los Angeles, United States. In Science, 2008
in axial nerves, establishment of discrete afferent & efferent pathways depends on signaling between coextending sensory & motor projections; the axon-axon interactions require motor axonal EphA3/EphA4 activated by cognate sensory axonal ephrin-A ligands
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