Product nameAnti-TrkA antibody [EP1058Y]
See all TrkA primary antibodies
DescriptionRabbit monoclonal [EP1058Y] to TrkA
SpecificityThis antibody detects both phosphorylated and unphosphorylated TrkA.
Tested applicationsSuitable for: Flow Cytmore details
Predicted to work with: Mouse, Rat, Human
Synthetic peptide (the amino acid sequence is considered to be commercially sensitive) within Human TrkA aa 750 to the C-terminus. The exact sequence is proprietary. (A synthetic peptide corresponding to residues surrounding tyrosine 791 of human TrkA).
Database link: P04629
- Flow Cyt: U87MG cells.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents
Storage instructionsShipped at 4°C. Store at 4°C (stable for up to 12 months). Upon delivery aliquot. Store at +4°C. Do Not Freeze. Store In the Dark.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: PBS, 1% BSA
Concentration information loading...
PurityProtein A purified
- Rat brain normal tissue lysate - membrane extract (ab29473)
- Mouse brain tissue lysate - total protein (ab30151)
- Rat brain cerebellum tissue lysate - total protein (ab4032)
- Mouse brain tissue lysate - total protein (0 days) (ab7188)
- Mouse brain tissue lysate - total protein (14 days) (ab7189)
- Mouse brain tissue lysate - total protein (7 days) (ab7190)
Our Abpromise guarantee covers the use of ab209443 in the following tested applications.
The cellular localisation of this product has been verified in ICC/IF.
FunctionReceptor tyrosine kinase involved in the development and the maturation of the central and peripheral nervous systems through regulation of proliferation, differentiation and survival of sympathetic and nervous neurons. High affinity receptor for NGF which is its primary ligand, it can also bind and be activated by NTF3/neurotrophin-3. However, NTF3 only supports axonal extension through NTRK1 but has no effect on neuron survival. Upon dimeric NGF ligand-binding, undergoes homodimerization, autophosphorylation and activation. Recruits, phosphorylates and/or activates several downstream effectors including SHC1, FRS2, SH2B1, SH2B2 and PLCG1 that regulate distinct overlapping signaling cascades driving cell survival and differentiation. Through SHC1 and FRS2 activates a GRB2-Ras-MAPK cascade that regulates cell differentiation and survival. Through PLCG1 controls NF-Kappa-B activation and the transcription of genes involved in cell survival. Through SHC1 and SH2B1 controls a Ras-PI3 kinase-AKT1 signaling cascade that is also regulating survival. In absence of ligand and activation, may promote cell death, making the survival of neurons dependent on trophic factors.
Isoform TrkA-III is resistant to NGF, constitutively activates AKT1 and NF-kappa-B and is unable to activate the Ras-MAPK signaling cascade. Antagonizes the anti-proliferative NGF-NTRK1 signaling that promotes neuronal precursors differentiation. Isoform TrkA-III promotes angiogenesis and has oncogenic activity when overexpressed.
Tissue specificityIsoform TrkA-I is found in most non-neuronal tissues. Isoform TrkA-II is primarily expressed in neuronal cells. TrkA-III is specifically expressed by pluripotent neural stem and neural crest progenitors.
Involvement in diseaseCongenital insensitivity to pain with anhidrosis
Chromosomal aberrations involving NTRK1 are found in papillary thyroid carcinomas (PTCs) (PubMed:2869410, PubMed:7565764, PubMed:1532241). Translocation t(1;3)(q21;q11) with TFG generates the TRKT3 (TRK-T3) transcript by fusing TFG to the 3'-end of NTRK1 (PubMed:7565764). A rearrangement with TPM3 generates the TRK transcript by fusing TPM3 to the 3'-end of NTRK1 (PubMed:2869410). An intrachromosomal rearrangement that links the protein kinase domain of NTRK1 to the 5'-end of the TPR gene forms the fusion protein TRK-T1. TRK-T1 is a 55 kDa protein reacting with antibodies against the C-terminus of the NTRK1 protein (PubMed:1532241).
Sequence similaritiesBelongs to the protein kinase superfamily. Tyr protein kinase family. Insulin receptor subfamily.
Contains 2 Ig-like C2-type (immunoglobulin-like) domains.
Contains 2 LRR (leucine-rich) repeats.
Contains 1 LRRCT domain.
Contains 1 protein kinase domain.
DomainThe transmembrane domain mediates interaction with KIDINS220.
The extracellular domain mediates interaction with NGFR.
modificationsLigand-mediated autophosphorylation. Interaction with SQSTM1 is phosphotyrosine-dependent. Autophosphorylation at Tyr-496 mediates interaction and phosphorylation of SHC1.
N-glycosylated (Probable). Isoform TrkA-I is N-glycosylated.
Ubiquitinated. Undergoes polyubiquitination upon activation; regulated by NGFR. Ubiquitination regulates the internalization of the receptor.
Cellular localizationCell membrane. Early endosome membrane. Late endosome membrane. Internalized to endosomes upon binding of NGF or NTF3 and further transported to the cell body via a retrograde axonal transport. Localized at cell membrane and early endosomes before nerve growth factor (NGF) stimulation. Recruited to late endosomes after NGF stimulation. Colocalized with RAPGEF2 at late endosomes (By similarity).
- Information by UniProt
- gp140trk antibody
- High affinity nerve growth factor receptor antibody
- High affinity nerve growth factor receptor precursor antibody
Overlay histogram showing U87MG cells stained with ab209443 (red line). The cells were fixed with 4% formaldehyde (10 min)and then permeabilized with 0.1% PBS-Triton X-100 for 15 min. The cells were then incubated in 1x PBS / 10% normal goat serum to block non-specific protein-protein interactions followed by the antibody (ab209443, 1/500 dilution) for 30 min at 22°C. Isotype control antibody (black line) was rabbit IgG (monoclonal) Phycoerythrin (ab209478) used at the same concentration and conditions as the primary antibody. Unlabelled sample (blue line) was also used as a control. Acquisition of >5,000 events were collected using a 50mW Yellow/Green laser (561nm) and 586/15 bandpass filter.
ab209443 has not yet been referenced specifically in any publications.