TrkA, B, C antibody

Catalog No. ABIN6945222

Product Details

Target: TrkA, B, C

Reactivity: Rat, Mouse, Human

Host: Rabbit

Clonality: Monoclonal

Conjugate: Un-conjugated

Application: Western Blotting (WB), Immunofluorescence (Cultured Cells) (IF (cc)), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)), Immunohistochemistry (IHC)

Cross-Reactivity: Human, Mouse, Rat

Purification: Purified by Protein A.

Immunogen: Human TrkA + TrkB + TrkC aa 800 to the C-terminus

Clone: 5T6

Isotype: IgG

Application Details

Application Notes: WB 1:300-5000
IHC-P 1:200-400
IF(ICC) 1:50-200
IHC()

Restrictions: For Research Use only

Handling

Format: Liquid

Concentration: 1 μg/μL

Buffer: Aqueous buffered solution containing 1xTBS ( pH 7.4), 1 % BSA, 40 %Glycerol and 0.05 % Sodium Azide.

Preservative: ProClin

Precaution of Use: This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE, which should be handled by trained staff only.

Storage: 4 °C,-20 °C

Storage Comment: Shipped at 4°C. Store at -20°C for one year. Avoid repeated freeze/thaw cycles.

Expiry Date: 12 months

Target Details

Target: TrkA, B, C

Alternative Name: TrkA+B+C

Background:

Synonyms: BDNF/NT-3 growth factors receptor antibody, gp140trk antibody, GP145-TrkB antibody, GP145-TrkC antibody, High affinity nerve growth factor receptor antibody, MTC antibody, Neurotrophic tyrosine kinase receptor type 1 antibody, Neurotrophic tyrosine kinase receptor type 2 antibody, Neurotrophic tyrosine kinase receptor type 3 antibody, NT-3 growth factor receptor antibody, NTRK1 antibody, NTRK2 antibody, NTRK3 antibody, p140-TrkA antibody, TRK antibody, Trk-A antibody, Trk-B antibody, Trk-C antibody

Background: The 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.

UniProt: P04629, Q16288, Q16620