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Validated All-in-One™ qPCR Primer for NTRK1(NM_002529.4) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes a member of the neurotrophic tyrosine kinase receptor (NTKR) family. This kinase is a membrane-bound receptor that, upon neurotrophin binding, phosphorylates itself and members of the MAPK pathway. The presence of this kinase leads to cell differentiation and may play a role in specifying sensory neuron subtypes. Mutations in this gene have been associated with congenital insensitivity to pain, anhidrosis, self-mutilating behavior, mental retardation and cancer. Alternate transcriptional splice variants of this gene have been found, but only three have been characterized to date. [provided by RefSeq].
Gene References into function
- congenital insensitivity to pain with anhidrosis (CIPA): novel mutations of the TRKA (NTRK1) gene, a putative uniparental disomy, and a linkage of the mutant TRKA and PKLR genes in a family with CIPA and pyruvate kinase deficiency
- TrkA is expressed in pleural and peritoneal effusions and in advanced-stage ovarian carcinoma.
- biologic effects of trkA neurotrophin receptor activation by nerve growth factor in a newly established Askin tumor cell line
- Cys436 of the trkA is responsible for the rapid transfer of the transmembrane occupancy signal to the SHC adaptor protein for activation of the Ras-Erk pathway and DNA synthesis.
- genetics of hereditary sensory and autonomic neuropathy type IV: clinical, biological and molecular aspects of mutations (REVIEW)
- role in tyrosine phosphorylation and processing of beta-APP
- TrkA as a life and death receptor: receptor dose as a mediator of function.
- No mutation in the TRKA (NTRK1) gene encoding a receptor tyrosine kinase for nerve growth factor in a patient with hereditary sensory and autonomic neuropathy type V.
- These results suggest that Grit, a novel TrkA-interacting protein, regulates neurite outgrowth by modulating the Rho family of small GTPases.
- Most of the GFAP-positive cells express TrkA, whereas a rare, novel subpopulation of astrocytes was found to be devoid of TrkA. Those results support the idea that astrocytes play an important neurotrophic role in the retina.
- Nerve growth factor decreases N-myc levels in TRKA-infected neuroblastoma cells and decreases cell proliferation via a MAPK path.
- Constitutively activated Scr facilitates NGF-induced phosphorylation of TRKA.
- CIPA patients had a branch site mutation in intron 7 (IVS7-33 T-->A) of the NTRK1 gene and a marked reduction of small myelinated and unmyelinated fibers and a relatively increased axon size. This is the first CIPA family encountered in Taiwan
- genes are rearranged in papillary thyroid cancer.
- a role for TrkA activation in a subset of melanomas as a predictor of an aggressive phenotype and poor outcome
- a novel alternative TrkA splice variant, TrkAIII, that exhibits expression restricted to undifferentiated early neural progenitors, human neuroblastomas, and a subset of other neural crest-derived tumors
- expression of NGF and its receptors, TrkA and p75NTR, in hepatocellular carcinomas (HCC); NGF and its receptors are thought to have a role in cellular interactions involving HCC cells, hepatic stellate cells, arterial cells and nerve cells in HCC tissues
- upregulation of proapoptotic genes and angiogenesis inhibitors
- mechanism that regulates aberrant or increased TrkA expression in various cancer cell lines and in the course of pancreatic cancer progression.
- These results strongly indicate that the expression level of PS1 protein has a cross talk with the Trk-dependent neuroprotective intracellular signaling pathway.
- TrkA induces apoptosis of neuroblastoma cells through a p53-dependent mechanism
- Data show that nerve growth factor activation of the TrkA receptor involves two distinct signalling pathways, and that both are necessary to induce airway smooth muscle cell proliferation.
- Congenital insensitivity to pain with anhidrosis (CIPA) is an autosomal recessive disorder caused by mutations in the neurotrophic tyrosine receptor kinase 1 (NTRK1) gene which encodes the receptor for nerve growth factor (NGF).
- Phosphorylated TrkA is localized at the mitotic apparatus in a human glioma cell line.
- Trk receptor signaling involves an inducible switch mechanism through an unconventional substrate that distinguishes neurotrophin action from other growth factor receptors
- Novel frameshift and splice site mutations in the neurotrophic tyrosine kinase receptor type 1 gene (NTRK1) associated with hereditary sensory neuropathy type IV.
- frequency of NTRK1 rearrangements in papillary thyroid carcinoma for the Polish population
- Overexpression in salivary adenoid cystic carcinoma may constitute a reason for perineural invasion
- Some trkA immunoreactivity was observed in the outer membrane of cells in the basal and spinal layers of the epidermis in atopic dermatitis (AD). In the papillary dermis, a larger number of cells demonstrated strong trkA immunoreactivity.
- Expression of TrkA in pancreatic cancer is a marker of tumor aggressiveness.
- Light and electron microscopy immunohistochemistry showed that human tonsillar samples were positive for TrkA.
- These results indicate that Fyn is activated by G-protein-coupled receptor stimulation and is responsible for transactivation of TrkA receptors on intracellular membranes.
- Human lung adenocarcinomas express TrkA and TrkB, but not TrkC; A549 cells, express mRNA transcripts encoding nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), TrkA, TrkB, and p75, and high protein levels of TrkA and TrkB.
- Findings report, for the first time, the expression pattern of NGF and TrkA proteins in human scalp skin and hair follicle.
- These data strongly indicate that these anti-neutral glycosphingolipids antibodies have a functional impact on nerve growth factor (NGF)-Trk-mediated intracellular signal transduction pathway.
- Data provide further evidence regarding the clinical role of p-TrkA in ovarian carcinoma.
- CEP-701 could be used to reduce the metastasis formation in advanced prostatic cncer by inhibiting NTRK1.
- We propose that TrkA and p75 likely communicate through convergence of downstream signaling pathways and/or shared adaptor molecules, rather than through direct extracellular interactions.
- TrkA is located in carrier vesicles, including ring-like vesicles near the plasma membrane, and dense core vesicles around the nucleius in a glioma cell line.
- trkA(NGFR) and p75(NTR) have roles with nerve growth factor in the healing process as a result of injury [review]
- TrkA signaling appears to be proapoptotic in the absence of Ku70.
- Data show that functional cooperation between TrkA and p75(NTR) accelerates neuronal differentiation by increased transcription of GAP-43 and p21(CIP/WAF) genes via ERK1/2 and AP-1 activities.
- Our findings suggest that TrkA activation in human glioblastomas might be beneficial therapeutically, especially as several of the currently used chemotherapeutics also induce autophagic cell death.
- NGF mRNA and its high-affinity tyrosine kinase receptor (trkA) expression were selectively increased in obstructive sleep apnea.
- TrkA is a determinant of pancreatic adenocarcinoma chemoresistance and small interfering RNA induces better response to gemcitabine.
- We show here high expression of TRKA in Hodgkin-Reed/Sternberg cell lines as compared to normal B cells and other B cell lymphomas, without major increases in TRKA gene dosage.
- Differential expression throughout the epithelium suggests a role in epithelial differentiation
- in astrocytomas, Trk receptors (TrkA, TrkB, TrkC) expression, but not p75NTR may promote tumor growth independently of grade
- Diffusible TrkA and TrkA-blocking agents neutralize infection in cellular and animal models of acute Chagas' disease.
- nuclear localization of the intracellular domain of Trk-A is observed constitutively in liver cells such as hepatocytes and activated stellate cells, while in other cell types it could be induced in response to soluble factors
- missense, insertion and deletion mutation in NTRK1 associated with congenital insensitivity to pain with anhidrosis
- upregulation and activation in oral lichen planus is one of the pathways that can activate protein kinase B and thereby rescue epithelial cells from untimely cell death
- Melanoma cells express the low-affinity (p75NTR) and the high-affinity tyrosine kinase NT receptors (Trk).
- A potential role of all neurotrophins, through their different receptors, in pituitary functions.
- TrkA receptor endolysosomal degradation is both ubiquitin and proteasome dependent
- NGF/TrkA signaling contributes to aberrant signaling in chronic myelogenous leukemia.
- The impact of Trk receptor expression on nonhomologous end joining-mediated DNA double-strand breaks repair, was analyzed.
- Expression of Trk-A and Trk-B by cells of the nondegenerate and degenerate intervertebral disc suggests an autocrine role for neurotrophins in regulation of disc cell biology.
- NTRK1 gene is associated with Alzheimer's disease in Italian population.
- Overexpression of TrkA caused massive cell death via both apoptosis and autophagy.
- In glomerulonephritis, TrkA is overexpressed, whereas p75 did not show any difference versus controls. By contrast in hemodialysis, TrkA expression is associated with increased p75 levels.
