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Human TrkA / NTRK1 Protein (aa 194-413, His Tag)

MTC,p140-TrkA,TRK,Trk-A,TRK1,TRKA

Catalog Number P11073-H07H2
Organism Species Human
Host Human Cells
Synonyms MTC,p140-TrkA,TRK,Trk-A,TRK1,TRKA
Molecular Weight The recombinant human NTRK1 Ig-like C2-type 1 & 2 domains (aa 194-413) consists of 239 amino acids and has a predicted molecular mass of 26 kDa. As a result of glycosylation, it migrates as an approximately 45-50 kDa band in SDS-PAGE under reducing conditions.
predicted N His
SDS-PAGE
Purity > 95 % as determined by SDS-PAGE
Protein Construction A DNA sequence encoding the amino acid sequence (Pro 194-Glu 413) of human NTRK1 (NP_002520.2), corresponding to the Ig-like C2-type 1 & 2 domains, was expressed and purified, with a N-terminal polyhistidine tag.
Bio-activity Measured by its ability to inhibit NGF-induced proliferation of TF1 human erythroleukemic cells.
The ED50 for this effect is typically 0.5-4 μg/ml in the presence of 10 ng/mL of human NGF.
Research Area Cancer |Signal transduction |Receptor Tyrosine Kinases (RTKs)
Formulation Lyophilized from sterile PBS, pH 7.4
1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background TRKA is a member of the neurotrophic tyrosine kinase receptor (NTKR) family. It is a membrane-bound receptor that, upon neurotrophin binding, phosphorylates itself and members of the MAPK pathway. Isoform TrkA-III promotes angiogenesis and has oncogenic activity when overexpressed. Isoform TrkA-I is found in most non-neuronal tissues. Isoform TrkA-II is primarily expressed in neuronal cells. TrkA-III is specifically expressed by pluripotent neural stem and neural crest progenitors. The presence of NTRK1 leads to cell differentiation and may play a role in specifying sensory neuron subtypes. Mutations in TRKA gene have been associated with congenital insensitivity to pain, anhidrosis, self-mutilating behavior, mental retardation and cancer. It was originally identified as an oncogene as it is commonly mutated in cancers, particularly colon and thyroid carcinomas. TRKA is required for high-affinity binding to nerve growth factor (NGF), neurotrophin-3 and neurotrophin-4/5 but not brain-derived neurotrophic factor (BDNF). Known substrates for the Trk receptors are SHC1, PI 3-kinase, and PLC-gamma-1. NTRK1 has a crucial role in the development and function of the nociceptive reception system as well as establishment of thermal regulation via sweating. It also activates ERK1 by either SHC1- or PLC-gamma-1-dependent signaling pathway. Defects in NTRK1 are a cause of congenital insensitivity to pain with anhidrosis and thyroid papillary carcinoma.
Reference
  • Lambiase A, et al. (2005) Molecular basis for keratoconus: lack of TrkA expression and its transcriptional repression by Sp3. Natl Acad Sci. 102 (46):16795-800.
  • Benito-Gutiérrez E, et al. (2006) Origin and evolution of the Trk family of neurotrophic receptors. Mol Cell Neurosci. 31(2):179-92.
  • Martin-Zanca D, et al. (1986) A human oncogene formed by the fusion of truncated tropomyosin and protein tyrosine kinase sequences. Nature. 319(6056):743-8.