Recombinant human TrkA (mutated G595R + A608D) protein (Active) is a Human Fragment protein, in the 440 to 796 aa range, expressed in Sf9, with >80% purity and suitable for SDS-PAGE, FuncS.
>80% SDS-PAGE
Sf9 cells
GST tag N-Terminus
SDS-PAGE, FuncS
Yes
Application | Reactivity | Dilution info | Notes |
---|---|---|---|
Application SDS-PAGE | Reactivity Reacts | Dilution info - | Notes - |
Application FuncS | Reactivity Reacts | Dilution info - | Notes - |
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. High affinity receptor for NGF which is its primary ligand (PubMed:1281417, PubMed:15488758, PubMed:17196528, PubMed:1849459, PubMed:1850821, PubMed:22649032, PubMed:27445338, PubMed:8325889). 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 (By similarity). Upon dimeric NGF ligand-binding, undergoes homodimerization, autophosphorylation and activation (PubMed:1281417). 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-IIIResistant to NGF, it 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.
MTC, TRK, TRKA, NTRK1, 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, gp140trk, p140-TrkA, Trk-A
Recombinant human TrkA (mutated G595R + A608D) protein (Active) is a Human Fragment protein, in the 440 to 796 aa range, expressed in Sf9, with >80% purity and suitable for SDS-PAGE, FuncS.
>80% SDS-PAGE
Sf9 cells
GST tag N-Terminus
SDS-PAGE, FuncS
Yes
The specific activity of ab269069 was 5.5 nmol/min/mg in a kinase assay using Poly (4:1 Glu, Tyr) synthetic peptide as substrate.
No
Human
pH: 7.5
Constituents: 25% Glycerol (glycerin, glycerine), 0.87% Sodium chloride, 0.79% Tris HCl, 0.31% Glutathione, 0.004% (R*,R*)-1,4-Dimercaptobutan-2,3-diol, 0.003% EDTA, 0.002% PMSF
Fragment
440 to 796
Recombinant
GST tag N-Terminus
Liquid
Affinity purified.
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. High affinity receptor for NGF which is its primary ligand (PubMed:1281417, PubMed:15488758, PubMed:17196528, PubMed:1849459, PubMed:1850821, PubMed:22649032, PubMed:27445338, PubMed:8325889). 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 (By similarity). Upon dimeric NGF ligand-binding, undergoes homodimerization, autophosphorylation and activation (PubMed:1281417). 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.
Belongs to the protein kinase superfamily. Tyr protein kinase family. Insulin receptor subfamily.
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).
Early endosome membrane, Late endosome membrane, Recycling endosome membrane
Dry Ice
-80°C
-80°C
Upon delivery aliquot
Avoid freeze / thaw cycle
This product is an active protein and may elicit a biological response in vivo, handle with caution.
This supplementary information is collated from multiple sources and compiled automatically.
TrkA also known as NTRK1 is a neurotrophin receptor and a member of the tropomyosin receptor kinase (TRK) family. It has a molecular mass of approximately 140 kDa. TrkA is expressed mostly in neuronal tissues particularly in the sensory ganglia sympathetic neurons and certain portions of the central nervous system. Mechanically TrkA activates upon binding to nerve growth factor (NGF) leading to receptor dimerization and autophosphorylation triggering downstream signaling cascades essential for neuronal growth and survival.
TrkA plays an important role in the regulation of neurotrophic signaling. TrkA existing often as part of larger signaling complexes modulates neuronal differentiation development and apoptosis. It ensures proper neural connections during development by responding to NGF which is important for neurons' health and plasticity. TrkA also aids in the response to injury by promoting neuronal repair and regeneration.
TrkA engagement activates prominent pathways like the MAPK/ERK and PI3K/AKT signaling cascades. These pathways facilitate important cellular processes like proliferation survival and metabolism. Through these pathways TrkA interacts and cooperates with proteins like SHC GRB2 and PLCγ among others to execute cellular functions. These signaling pathways enable the coordinated response needed for neural tissue maintenance and development.
TrkA abnormalities are linked to conditions like congenital insensitivity to pain with anhidrosis (CIPA) and certain cancers. Mutations in NTRK1 can disrupt NGF signaling leading to neurological deficits observed in CIPA. In cancer aberrant TrkA signaling often due to gene fusions contributes to tumorigenesis. TrkA-related signals influence oncogenic proteins such as RAS and BRAF illustrating its role in cancer progression.
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The specific activity of ab269069 was 5.5 nmol/min/mg in a kinase assay using Poly (4:1 Glu, Tyr) synthetic peptide as substrate.
SDS-PAGE analysis of ab269069.
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