TrkA, B, C anticorps

N° du produit ABIN6945222

Détail du produit

Antigène: TrkA, B, C

Reactivité: Rat, Souris, Humain

Hôte: Lapin

Clonalité: Monoclonal

Conjugué: Inconjugué

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

Réactivité croisée: Humain, Souris, Rat

Purification: Purified by Protein A.

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

Clone: 5T6

Isotype: IgG

Information d'application

Indications d'application: WB 1:300-5000
IHC-P 1:200-400
IF(ICC) 1:50-200
IHC()

Restrictions: For Research Use only

Stockage

Format: Liquid

Concentration: 1 μg/μL

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

Agent conservateur: ProClin

Précaution d'utilisation: This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE, which should be handled by trained staff only.

Stock: 4 °C,-20 °C

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

Date de péremption: 12 months

Détail du antigène

Antigène: TrkA, B, C

Autre désignation: TrkA+B+C

Sujet:

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