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Neurotrophic tyrosine kinase, receptor, type 3

trkC, NTRK3
This gene encodes a member of the neurotrophic tyrosine receptor kinase (NTRK) family. This kinase is a membrane-bound receptor that, upon neurotrophin binding, phosphorylates itself and members of the MAPK pathway. Signalling through this kinase leads to cell differentiation and may play a role in the development of proprioceptive neurons that sense body position. Mutations in this gene have been associated with medulloblastomas, secretory breast carcinomas and other cancers. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2011] (from NCBI)
Top mentioned proteins: trkA, TrkB, neurotrophin-3, Brain-derived neurotrophic factor, NGF
Papers on trkC
Molecular characterization of sporadic pediatric thyroid carcinoma with the DNA/RNA ThyroSeq v2 next-generation sequencing assay.
Nikiforov et al., Pittsburgh, United States. In Pediatr Dev Pathol, 14 Oct 2015
These gene fusions included ETV6/NTRK3 (n=3) and TPR/NTRK1 (n=1).
Neurotrophin-3 Enhances the Synaptic Organizing Function of TrkC-Protein Tyrosine Phosphatase σ in Rat Hippocampal Neurons.
Takahashi et al., Vancouver, Canada. In J Neurosci, 09 Oct 2015
UNLABELLED: Neurotrophin-3 (NT-3) and its high-affinity receptor TrkC play crucial trophic roles in neuronal differentiation, axon outgrowth, and synapse development and plasticity in the nervous system.
Secretory Breast Carcinoma: A Histopathologic and Genomic Spectrum Characterized by a Joint Specific ETV6-NTRK3 Gene Fusion.
MacGrogan et al., Sherbrooke, Canada. In Am J Surg Pathol, 18 Sep 2015
Histologic and immunohistochemical analyses, fluorescence in situ hybridization using break-apart probes specific to ETV6 on 12p13, reverse transcription polymerase chain reaction with in-house probes specific to the ETV6-NTRK3 gene fusion, and DNA copy number variation by array comparative genomic hybridization analyses were performed on all cases.
Diagnostic utility of phosphorylated signal transducer and activator of transcription 5 immunostaining in the diagnosis of mammary analogue secretory carcinoma of the salivary gland: A comparative study of salivary gland cancers.
Kage et al., Kurume, Japan. In Cancer Cytopathol, 07 Sep 2015
BACKGROUND: Mammary analogue secretory carcinoma (MASC) with an ETS variant gene 6 (ETV6)-neurotrophic tyrosine kinase receptor type 3 (NTRK3) translocation is a newly described type of salivary gland cancer.
[The Role of Neurotrophins and Neurexins Genes in the Risk of Paranoid Schizophrenia in Russians and Tatars].
Khusnutdinova et al., In Genetika, Jul 2015
In this paper we investigated 48 polymorphic variants of genes of the neurotrophins and neurexins family (BDNF, NTRK2, NTRK3, NGF, NXPH1, and NRXN1) in Russian and Tatar cases and in a control group living in the Republic of Bashkortostan.
The p75 neurotrophin receptor: at the crossroad of neural repair and death.
Williams et al., Chapel Hill, United States. In Neural Regen Res, May 2015
The strong repair and pro-survival functions of neurotrophins at their primary receptors, TrkA, TrkB and TrkC, have made them attractive candidates for treatment of nervous system injury and disease.
Fetal presentation of congenital fibrosarcoma of the meninges: case report and literature review.
Laquerrière et al., In Clin Neuropathol, Mar 2015
A reverse transcription polymerase chain reaction assay was performed to detect the gene fusion ETV6-NTRK3 transcript.
Dynamic nature of the p75 neurotrophin receptor in response to injury and disease.
Williams et al., Chapel Hill, United States. In J Neuroimmune Pharmacol, Dec 2014
Neurotrophins and their respective tropomyosin related kinase (Trk) receptors (TrkA, TrkB, and TrkC) and the p75 neurotrophin receptor (p75(NTR)) play a fundamental role in the development and maintenance of the nervous system making them important targets for treatment of neurodegenerative diseases.
Neurodevelopment. Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling.
Luo et al., Stanford, United States. In Science, Dec 2014
We show that the neurotrophin receptor tropomyosin-related kinase C (TrkC) is required for dendritic growth and branching of mouse cerebellar Purkinje cells.
Molecular genetics of ependymomas and pediatric diffuse gliomas: a short review.
Yokoo et al., Maebashi, Japan. In Brain Tumor Pathol, Oct 2014
As for non-brainstem high-grade tumors, in addition to H3F3A, TP53, and ATRX mutations, which were frequently observed in older children, recurrent fusions involving NTRK1, NTRK2, and NTRK3 were reported in infants younger than 3 years of age.
Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia.
Mullighan et al., Memphis, United States. In N Engl J Med, Oct 2014
Cell lines and human leukemic cells expressing ABL1, ABL2, CSF1R, and PDGFRB fusions were sensitive in vitro to dasatinib, EPOR and JAK2 rearrangements were sensitive to ruxolitinib, and the ETV6-NTRK3 fusion was sensitive to crizotinib.
The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma.
St. Jude Children's Research Hospital–Washington University Pediatric Cancer Genome Project et al., Memphis, United States. In Nat Genet, May 2014
Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants.
The role of rab proteins in neuronal cells and in the trafficking of neurotrophin receptors.
Cogli et al., Lecce, Italy. In Membranes (basel), 2013
Neurotrophins exert their role by binding to their receptors, the Trk family of receptor tyrosine kinases (TrkA, TrkB, and TrkC) and p75NTR, a member of the tumor necrosis factor (TNF) receptor superfamily.
Chaperones as thermodynamic sensors of drug-target interactions reveal kinase inhibitor specificities in living cells.
Lindquist et al., Cambridge, United States. In Nat Biotechnol, 2013
Demonstrating the value of the assay, we identify ETV6-NTRK3 as a target of the FDA-approved drug crizotinib (Xalkori).
Small-molecule modulation of neurotrophin receptors: a strategy for the treatment of neurological disease.
Massa et al., Stanford, United States. In Nat Rev Drug Discov, 2013
One strategy to overcome these limitations is to target individual neurotrophin receptors — such as tropomyosin receptor kinase A (TRKA), TRKB, TRKC, the p75 neurotrophin receptor or sortilin — with small-molecule ligands.
Expression of neurotrophin receptors by retinoinvasive uveal melanoma.
Finger et al., New York City, United States. In Melanoma Res, 2012
expression of neurotrophin receptors Pan-Trk, p75 neurotrophin receptor (p75(NTR) and ciliary neurotrophic factor receptor-alpha in ulveal melanoma does not show a role in growth.
A tripartite complex composed of ETV6-NTRK3, IRS1 and IGF1R is required for ETV6-NTRK3-mediated membrane localization and transformation.
Sorensen et al., Vancouver, Canada. In Oncogene, 2012
find that both IRS1 and kinase active IGF1R are required for ETV6-NTRK3 transformation, that tyrosine phosphorylated IRS1 is present in high molecular weight complexes with EN and IGF1R, and that EN colocalizes with IGF1R at the plasma membrane
Transcriptional regulation of TRKC by SOX2 in human embryonic stem cells.
Donovan et al., Irvine, United States. In Stem Cell Res, 2012
SOX2 utilizes a specific binding motif to directly interact with the TRKC regulatory region.
Cograft of neural stem cells and schwann cells overexpressing TrkC and neurotrophin-3 respectively after rat spinal cord transection.
Teng et al., Guangzhou, China. In Biomaterials, 2011
Transplantation of overexpressing neurotrophin-3-Schwann cells + trkC-neural stem cells in Gelfoam into the lesion gap immediately following injury results in significantly improved relay of the cortical motor evoked potential.
Neurotrophin receptor TrkC is an entry receptor for Trypanosoma cruzi in neural, glial, and epithelial cells.
Pereiraperrin et al., Boston, United States. In Infect Immun, 2011
TrkC is implicated as a functional PDNF receptor in cell entry, independently of sialic acid recognition, mediating broad T. cruzi infection both in vitro and in vivo.
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