TrkA+B+C Recombinant Rabbit monoclonal Antibody IgG
Fig1: Western blot analysis of TrkA+B+C on different lysates using anti-TrkA+B+C antibody at 1/1,000 dilution.
Lane 1: Rat brain
Lane 2: Mouse brain
Fig2: ICC staining TrkA+B+C in N2A cells (green). The nuclear counter stain is DAPI (blue). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS.
Fig3: ICC staining TrkA+B+C in SH-SY-5Y cells (green). The nuclear counter stain is DAPI (blue). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS.
Host Species; Species ReactivityRabbit; Human, Mouse, Rat
Application SummaryWB, ICC, IHC
Purification; FormulationProA affinity purified; 1*TBS (pH7.4), 1%BSA, 40%Glycerol. Preservative: 0.05% Sodium Azide.; Liquid form.
ALTnamesHigh affinity nerve growth factor receptor, Neurotrophic tyrosine kinase receptor type 1, TRK1-transforming tyrosine kinase protein, Tropomyosin-related kinase A, Tyrosine kinase receptor, Tyrosine kinase receptor A, gp140trk, p140-TrkA, BDNF/NT-3 growth factors receptor, GP145-TrkB, Neurotrophic tyrosine kinase receptor type 2, TrkB tyrosine kinase, Tropomyosin-related kinase B, NT-3 growth factor receptor, GP145-TrkC, Neurotrophic tyrosine kinase receptor type 3, TrkC tyrosine kinase
BackgroundThe 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.(ET1701-16)