Trk-A Antibody (YA1489)
(Synonyms: NTRK1; MTC; TRK; TRKA; 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 Antibody (YA1489) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Trk-A.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF, IP, FC
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
IP
IP: Immunoprecipitation
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FC
FC: Flow Cytometry
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|---|---|---|---|---|---|
| Dilution Ratio | 1:500-1:1000 | 1:50-1:100 | 1:50-1:200 | 1:50 | 1:50-1:100 |
Product Details
Trk-A Antibody (YA1489) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Trk-A.
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Host Rabbit
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Clonality Recombinant,Monoclonal
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 145 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 87 kDa
Entrez Gene: 4914 Human ;
SwissProt: P04629 Human ; Q16288 Human ; Q16620 Human ;
OMIM: 256800 Human
A synthesized peptide derived from human TrkA aa700-796.
Endogenous
Affinity Chromatography
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
TrkA (tropomyosin receptor kinase A; encoded by NTRK1) is a high-affinity receptor tyrosine kinase for nerve growth factor (NGF) that regulates neuronal survival, differentiation, and sensory neuron function through ligand-induced receptor dimerization and autophosphorylation[1][2]. Mechanistically, NGF-TrkA signaling activates major downstream pathways including RAS/MAPK, PI3K/AKT, and PLCγ, thereby controlling transcriptional programs that support neuronal growth, maintenance, and synaptic function[1][2][3]. Through these signaling cascades, TrkA plays a central role in the development and maintenance of nociceptive neurons and contributes to neurotrophin-dependent cellular responses in the peripheral and central nervous systems[1][2]. In disease contexts, dysregulation of NGF/TrkA signaling has been implicated in chronic pain disorders and neurodegenerative conditions, including experimental models of Alzheimer's disease in which impaired TrkA signaling is associated with cholinergic neuronal dysfunction and synaptic deficits[3][4][5]. Compared with related neurotrophin receptors, TrkA is distinguished by its preferential activation by NGF, whereas TrkB primarily responds to BDNF and NT-4/5 and TrkC is activated predominantly by NT-3, enabling receptor-specific biological outcomes[6]. For experimental applications, both agonists and antagonists targeting the NGF-TrkA axis have been widely utilized to investigate neurotrophic signaling, neuronal survival mechanisms, and pain-related pathways, making TrkA an important molecular target in translational neuroscience research[4][5].
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Subcellular Localization
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; Recycling endosome membrane; Single-pass type I membrane protein
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Expression
Tissue_specificity: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
Induction:Isoform TrkA-III is up-regulated upon hypoxia in cells normally expressing it -
Isoforms & Post-Translational Modification
P04629 has 4 isomers: P04629-1: 87497 Da (predicted); P04629-2: 86880 Da (predicted); P04629-3: 83993 Da (predicted); P04629-4: 77145 Da (predicted).
Ligand-mediated autophosphorylation (PubMed:1281417, PubMed:15488758, PubMed:27676246, PubMed:28177573, PubMed:2927393, PubMed:7510697, PubMed:8155326, PubMed:8325889). Interaction with SQSTM1 is phosphotyrosine-dependent. Autophosphorylation at Tyr-496 mediates interaction and phosphorylation of SHC1 (PubMed:15488758, PubMed:7510697, PubMed:8155326, PubMed:8325889);N-glycosylated (PubMed:2927393). Isoform TrkA-I and isoform TrkA-II are N-glycosylated;Ubiquitinated (PubMed:27445338). Undergoes polyubiquitination upon activation; regulated by NGFR (PubMed:27445338). Ubiquitination by NEDD4L leads to degradation (PubMed:27445338). Ubiquitination regulates the internalization of the receptor (By similarity) -
Subunit
Exists in a dynamic equilibrium between monomeric (low affinity) and dimeric (high affinity) structures. Homodimerization is induced by binding of a NGF dimer (PubMed:10490030, PubMed:1281417, PubMed:17196528).
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SwissProt ID
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Synonyms
NTRK1; MTC; TRK; TRKA; 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
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Research Field
Neuroscience
Documentation
[1]. Norman BH, et al. Targeting the Nerve Growth Factor (NGF) Pathway in Drug Discovery. Potential Applications to New Therapies for Chronic Pain. J Med Chem. 2017 Jan 12;60(1):66-88. [Content Brief]
[2]. Indo Y. NTRK1 Congenital Insensitivity to Pain with Anhidrosis. 2008 Aug 5 [updated 2020 Apr 30]. In: Adam MP, et al. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993–2026. PMID: 20301726. [Content Brief]
[3]. Latina V, et al. Impaired NGF/TrkA Signaling Causes Early AD-Linked Presynaptic Dysfunction in Cholinergic Primary Neurons. Front Cell Neurosci. 2017 Mar 15;11:68. doi: 10.3389/fncel.2017.00068. PMID: 28360840; PMCID: PMC5350152. [Content Brief]
[4]. Baño V, et al. Characterization and Structural Performance in Bending of CLT Panels Made from Small-Diameter Logs of Loblolly/Slash Pine. Materials (Basel). 2018 Nov 30;11(12):2436. [Content Brief]
[5]. Mantyh PW, et al. Antagonism of nerve growth factor-TrkA signaling and the relief of pain. Anesthesiology. 2011 Jul;115(1):189-204. [Content Brief]
[6]. Clinical Guidelines on the Identification, et al. National Institutes of Health. Obes Res. 1998 Sep;6 Suppl 2:51S-209S. Erratum in: Obes Res 1998 Nov;6(6):464. PMID: 9813653. [Content Brief]
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