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TrkA/NTRK1 Protein, Antibody, ELISA Kit, cDNA Clone

Human TrkA/NTRK1 Protein

Description: Active
Expression host: Human Cells
  • Slide 1
11073-H03H-50
11073-H03H-100
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100 µg / $290
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Expression host: Human Cells
  • Slide 1
11073-H08H-50
11073-H08H-100
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100 µg / $290
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Expression host: E. coli
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11073-H07E1-50
11073-H07E1-100
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100 µg / $290
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Description: Active
Expression host: Human Cells
  • Slide 1
11073-H07H2-50
11073-H07H2-100
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100 µg / $290
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Canine TrkA/NTRK1 Protein

Expression host: Human Cells
  • Slide 1
70101-D01H-50
70101-D01H-100
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100 µg / $290
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Expression host: Human Cells
  • Slide 1
70101-D07H-50
70101-D07H-100
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100 µg / $290
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Mouse TrkA/NTRK1 Protein

Expression host: Human Cells
  • Slide 1
51103-M02H-50
51103-M02H-100
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100 µg / $290
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Expression host: Human Cells
  • Slide 1
51103-M08H-50
51103-M08H-100
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100 µg / $290
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Rat TrkA/NTRK1 Protein

Expression host: Human Cells
  • Slide 1
80404-R08H-50
80404-R08H-100
50 µg / $170
100 µg / $290
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Expression host: Human Cells
  • Slide 1
80404-R02H-50
80404-R02H-100
50 µg / $170
100 µg / $290
Add to Cart

TrkA/NTRK1 Related Areas

TrkA/NTRK1 Related Pathways

TrkA/NTRK1 Related Product

    TrkA/NTRK1 Summary & Protein Information

    TrkA/NTRK1 Related Information

    TrkA/NTRK1 Background

    Gene Summary: NTRK1 gene encodes a member of the neurotrophic tyrosine kinase receptor (NTKR) family. This kinase is a membrane-bound receptor that, upon neurotrophin binding, phosphorylates itself and members of the MAPK pathway. The presence of this kinase leads to cell differentiation and may play a role in specifying sensory neuron subtypes. Mutations in NTRK1 gene have been associated with congenital insensitivity to pain, anhidrosis, self-mutilating behavior, mental retardation and cancer. Alternate transcriptional splice variants of  NTRK1 gene have been found, but only three have been characterized to date. [provided by RefSeq, Jul 2008]
    General information above from NCBI
    Catalytic activity: ATP + a [protein]-L-tyrosine = ADP + a [protein]-L-tyrosine phosphate.
    Enzyme regulation: The pro-survival signaling effect of NTRK1 in neurons requires its endocytosis into signaling early endosomes and its retrograde axonal transport. This is regulated by different proteins including CFL1, RAC1 and SORT1. NTF3 is unable to induce this signaling probably due to the lability of the NTF3- NTRK1 complex in endosomes. SH2D1A inhibits the autophosphorylation of the receptor, and alters the recruitment and activation of downstream effectors and signaling cascades (By similarity). Regulated by NGFR (By similarity).
    Subunit structure: Exists in a dynamic equilibrium between monomeric (low affinity) and dimeric (high affinity) structures. Homodimerization is induced by binding of a NGF dimer. Interacts with SQSTM1; bridges NTRK1 to NGFR. Forms a ternary complex with NGFR and KIDINS220; this complex is affected by the expression levels of KIDINS220 and an increase in KIDINS220 expression leads to a decreased association of NGFR and NTRK1 (By similarity). Interacts with SH2D1A; regulates NTRK1 (By similarity). Interacts (phosphorylated upon activation by NGF) with SHC1; mediates SHC1 phosphorylation and activation. Interacts (phosphorylated upon activation by NGF) with PLCG1; mediates PLCG1 phosphorylation and activation. Interacts (phosphorylated) with SH2B1 and SH2B2. Interacts with GRB2. Interacts with PIK3R1. Interacts with FRS2. Interacts with SORT1; may regulate NTRK1 anterograde axonal transport. Interacts with RAB7A (By similarity).
    Domain: The transmembrane domain mediates interaction with KIDINS220 (By similarity).
    The extracellular domain mediates interaction with NGFR (By similarity).
    Subcellular location: Cell membrane; Single-pass type I membrane protein. Early endosome membrane; Single-pass type I membrane protein (By similarity). Note=Internalized to endosomes upon binding of NGF or NTF3 and further transported to the cell body via a retrograde axonal transport (By similarity).
    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.
    Post-translational: Ligand-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 (By similarity).
    Involvement in disease: Congenital insensitivity to pain with anhidrosis (CIPA) [MIM:256800]: Characterized by a congenital insensitivity to pain, anhidrosis (absence of sweating), absence of reaction to noxious stimuli, self-mutilating behavior, and mental retardation. This rare autosomal recessive disorder is also known as congenital sensory neuropathy with anhidrosis or hereditary sensory and autonomic neuropathy type IV or familial dysautonomia type II. Note=The disease is caused by mutations affecting the gene represented in this entry.
    Thyroid papillary carcinoma (TPC) [MIM:188550]: A common tumor of the thyroid that typically arises as an irregular, solid or cystic mass from otherwise normal thyroid tissue. Papillary carcinomas are malignant neoplasm characterized by the formation of numerous, irregular, finger-like projections of fibrous stroma that is covered with a surface layer of neoplastic epithelial cells. Note=The gene represented in this entry is involved in disease pathogenesis. Chromosomal aberrations involving NTRK1 are found in thyroid papillary carcinomas. Translocation t(1;3)(q21;q11) with TFG generates the TRKT3 (TRK-T3) transcript by fusing TFG to the 3'-end of NTRK1; a rearrangement with TPM3 generates the TRK transcript by fusing TPM3 to the 3'-end of NTRK1; 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.
    Sequence similarity: Belongs 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.
    General information above from UniProt

    TRKA is a member of the neurotrophic tyrosine kinase receptor (NTKR) family. It is a membrane-bound receptor that, upon neurotrophin binding, phosphorylates itself and members of the MAPK pathway. Isoform TrkA-III promotes angiogenesis and has oncogenic activity when overexpressed. 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. The presence of NTRK1 leads to cell differentiation and may play a role in specifying sensory neuron subtypes. Mutations in TRKA gene have been associated with congenital insensitivity to pain, anhidrosis, self-mutilating behavior, mental retardation and cancer. It was originally identified as an oncogene as it is commonly mutated in cancers, particularly colon and thyroid carcinomas. TRKA is required for high-affinity binding to nerve growth factor (NGF), neurotrophin-3 and neurotrophin-4/5 but not brain-derived neurotrophic factor (BDNF). Known substrates for the Trk receptors are SHC1, PI 3-kinase, and PLC-gamma-1. NTRK1 has a crucial role in the development and function of the nociceptive reception system as well as establishment of thermal regulation via sweating. It also activates ERK1 by either SHC1- or PLC-gamma-1-dependent signaling pathway. Defects in NTRK1 are a cause of congenital insensitivity to pain with anhidrosis and thyroid papillary carcinoma.

    TrkA/NTRK1 Alternative Name

    TrkA/NTRK1 Related Studies

  • Lambiase A, et al. (2005) Molecular basis for keratoconus: lack of TrkA expression and its transcriptional repression by Sp3. Natl Acad Sci. 102 (46):16795-800.
  • Benito-Gutiérrez E, et al. (2006) Origin and evolution of the Trk family of neurotrophic receptors. Mol Cell Neurosci. 31(2):179-92.
  • Martin-Zanca D, et al. (1986) A human oncogene formed by the fusion of truncated tropomyosin and protein tyrosine kinase sequences. Nature. 319(6056):743-8.
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