|Application ||WB, IHC, IF|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||87497 Da|
|Other Names||High 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, Trk-A, gp140trk, p140-TrkA, NTRK1, MTC, TRK, TRKA|
|Target/Specificity||A synthetic peptide corresponding to residues surrounding tyrosine 791 of human Trk A was used as an immunogen. This antibody detects both phosphorylated and unphosphorylated Trk A.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Trk-A Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||MTC, TRK, TRKA|
|Function||Receptor 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 (PubMed:27676246). 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.|
|Cellular Location||Cell membrane; Single-pass type I membrane protein. Early endosome membrane; Single-pass type I membrane protein Late endosome membrane; Single-pass type I membrane protein. Note=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).|
|Tissue Location||Isoform 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.|
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Provided below are standard protocols that you may find useful for product applications.
The Trk proto-oncogene encodes a 140 kDa, membrane-spanning protein tyrosine kinase that is expressed only in neural tissues. Nerve growth factor (NGF) stimulates phosphorylation of Trk A in neural cell lines and in embryonic dorsal root ganglia. Affinity cross-linking and equilibrium binding experiments with 125I-labeled NGF indicate that Trk A binds NGF specifically in cultured cells with a dissociation constant of 10(-9) molar. The identification of Trk A as an NGF receptor indicates that this protein participates in the primary signal transduction mechanism of NGF (1). Trk A was found to be expressed in the nervous system and phosphorylated in response to NGF (Nerve Growth Factor). Somatic rearrangement(s) of the TRKA gene (also designated NTRK1) are responsible for formation of some oncogenes (2). Trk A is expressed in neural and nonneuronal tissues. Like RET, Trk A is often activated by rearrangements that involve one of at least five other genes in papillary thyroid carcinoma (PTC) (3).
1. Kaplan DR, et al. Science 252(5005):554-8, 1991
2. Indo Y, et al, Jpn J Hum Genet 42(2):343-51, 1997
3. Gimm O, et al. J Clin Endocrin Metab 84(8):2784-7, 1999
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