All TrkA reagents are produced in house and quality controlled, including 13 TrkA Antibody, 1 TrkA ELISA, 39 TrkA Gene, 10 TrkA Lysate, 11 TrkA Protein, 3 TrkA qPCR. All TrkA reagents are ready to use.
Recombinant TrkA proteins are expressed by HEK293 Cells, E. coli with fusion tags as C-His, N-human IgG1-Fc, N-His, C-human IgG1-Fc & His, C-human IgG1-Fc.
TrkAantibodies are validated with different applications, which are ELISA, IHC-P, ELISA(Cap), WB.
TrkAcDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each TrkA of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.
TrkAELISA Kit are quality controlled by 8 internation QC standard which guarantee every ELISA Kit with high quality.
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.