DATASHEET
Host:
Rabbit
Target Protein:
Trk A + B + C
Clonality:
Recombinant
Isotype:
IgG
Swiss Prot:
P04629, Q16288, Q16620
Source:
KLH conjugated synthetic peptide derived from mouse Trk A
Purification:
Purified by Protein A.
Storage Buffer:
Aqueous buffered solution containing 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
Storage:
Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles.
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.
Conjugation:
AbBy Fluor-350
Excitation/ Emission:
346nm/442nm
Size:
100µL
Concentration:
Lot Dependent
Applications:
WB(1:300-5000)
IF()
Human
Mouse
Rat
For research use only. Not intended for diagnostic or therapeutic use.