Anti-TrkA+B+C Antibody [JJ084-04]
ET1701-16
ApplicationsImmunoFluorescence, Western Blot, ImmunoHistoChemistry, ImmunoHistoChemistry Paraffin
Product group Antibodies
ReactivityHuman, Mouse, Rat
TargetNTRK1
Overview
- SupplierHUABIO
- Product NameAnti-TrkA+B+C Antibody [JJ084-04]
- Delivery Days Customer7
- ApplicationsImmunoFluorescence, Western Blot, ImmunoHistoChemistry, ImmunoHistoChemistry Paraffin
- Applications SupplierWB,IF-Cell,IHC-P
- CertificationResearch Use Only
- ClonalityMonoclonal
- Clone IDJJ084-04
- Concentration1 mg/ml
- ConjugateUnconjugated
- Gene ID4914
- Target nameNTRK1
- Target descriptionneurotrophic receptor tyrosine kinase 1
- Target synonymsMTC, TRK, TRK1, TRKA, Trk-A, p140-TrkA, high affinity nerve growth factor receptor, Oncogene TRK, TRK1-transforming tyrosine kinase protein, gp140trk, neurotrophic tyrosine kinase, receptor, type 1, tropomyosin receptor kinase A, tropomyosin-related kinase A, tyrosine kinase receptor A
- HostRabbit
- IsotypeIgG
- Protein IDP04629
- Protein NameHigh affinity nerve growth factor receptor
- Scientific DescriptionThe family of Trk receptor tyrosine kinases consists of TrkA, TrkB, and TrkC. While the sequence of these family members is highly conserved, they are activated by different neurotrophins: TrkA by NGF, TrkB by BDNF or NT4, and TrkC by NT3. In the adult nervous system, the Trk receptors regulate synaptic strength and plasticity. TrkA regulates proliferation and is important for development and maturation of the nervous system. Point mutations, deletions, and chromosomal rearrangements (chimeras) cause ligand-independent receptor dimerization and activation of TrkA. TrkA is activated in many malignancies including breast, ovarian, prostate, and thyroid carcinomas. TrkB is overexpressed in tumors such as neuroblastoma, prostate adenocarcinoma and pancreatic ductal adenocarcinoma. In neuroblastomas overexpression of TrkB correlates with unfavorable disease outcome when autocrine loops signaling tumor survival are potentiated by additional overexpression of brain-derived neurotrophic factor (BDNF). An alternatively spliced truncated TrkB isoform lacking the kinase domain is overexpressed in Wilms tumors and this isoform may act as a dominant-negative to TrkB signaling. Altered TrkC expression and corresponding gene mutations are seen in various forms of cancer, with increased expression a positive prognostic indicator in patients with medulloblastoma.
- ReactivityHuman, Mouse, Rat
- Reactivity SupplierHuman,Mouse,Rat
- Storage Instruction-20°C,2°C to 8°C
- UNSPSC41116161