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Mouse TrkA / NTRK1 Protein (His Tag)

C80751,Tkr,trk,TrkA

Catalog Number P51103-M08H
Organism Species Mouse
Host Human Cells
Synonyms C80751,Tkr,trk,TrkA
Molecular Weight The recombinant mouse NTRK1 comprises 398 amino acids and has a predicted molecular mass of 43.7 kDa. The apparent molecular mass of the protein is approximately 69 kDa in SDS-PAGE under reducing conditions due to glycosylation.
predicted N Ala 34
SDS-PAGE
Purity > 95 % as determined by SDS-PAGE
Protein Construction A DNA sequence encoding the mouse NTRK1 (Met1-Gly420) was expressed with a C-terminal polyhistidine tag.
Bio-activity Measured by its ability to inhibit NGF-induced proliferation of TF‑1 human erythroleukemic cells.
The ED50 for this effect is typically 0.2-1 µg/mL in the presence of 10 ng/mL of recombinant mouse 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.