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By immunohistochemistry, the localization of Neurotrophinss has been observed mainly in Purkinje cells; TrkA and TrkB (显示 NTRK2 ELISA试剂盒)-receptors in cells and fibers of granular and molecular layers. TrkC (显示 NTRK3 ELISA试剂盒) was faintly detected
TrkA-like immunoreactivity was the only Trk detected, and it was restricted to the somata of crypt sensory neurons, their central processes being apparently unreactive.
report describing differential expression of proteins and mRNA for NGF (显示 NGFB ELISA试剂盒) and its cognate receptors, NTRK1 and NGFR (显示 NGFR ELISA试剂盒), in the male sex organs of rabbits
Nine patients have been reported from nine unrelated families with hereditary sensory and autonomic neuropathy IV due to various mutations in NTRK1, five of which are novel.
Data suggest that kinase domains of neurotrophin (显示 BDNF ELISA试剂盒) receptor isoforms, TRKA, TRKB (显示 NTRK2 ELISA试剂盒), and TRKC (显示 NTRK3 ELISA试剂盒), exhibit a bulky phenylalanine gatekeeper, leading to a small and unattractive back pocket/binding site for antineoplastic kinase inhibitors. [REVIEW]
Pan-Trk immunohistochemistry is a time-efficient and tissue-efficient screen for NTRK fusions, particularly in driver-negative advanced malignancies and potential cases of secretory carcinoma and congenital fibrosarcoma.
analysis of NTRK1 transcripts in peripheral blood cells of the patient revealed an influence of the variant on mRNA splicing. The C>A transversion generated a novel splice-site, which led to the incorporation of 10 intronic bases into the NTRK1 mRNA and consequently to a non-functional gene product.
A novel nonsense mutation and a known splice-site mutation were detected in NTRK1 in two siblings and were shown to be associated with congenital insensitivity to pain with anhidrosis.
NT3 (显示 NTF3 ELISA试剂盒) upregulates cellular proliferation, extracellular matrix protein production, and collagen deposition in human aortic valve interstitial cells through the Trk-Akt (显示 AKT1 ELISA试剂盒)-cyclin D1 (显示 CCND1 ELISA试剂盒) cascade.
NTRK1 gene fusion in spitzoid neoplasms results in tumors with Kamino bodies and were typically arranged in smaller nests with smaller predominantly spindle-shaped cells, occasionally forming rosettes.
expression levels of tropomyosin 3 (TPM3 (显示 TPM3 ELISA试剂盒)) were higher in stage III ESCC tissue compared with stage I (P<0.05). The findings of the present study identified twelve proteins, which are closely associated with ESCC invasion and metastasis, apoptosis and cell signal transduction.
Results suggest that NTRK1 oncogenic activation through gene fusion defines a novel and distinct subset of soft tissue tumors resembling lipofibromatosis (LPF), but displaying cytologic atypia and a neural immunophenotype, provisionally named LPF-like neural tumors.
This review highlights treatment options, including clinical trials for ROS1 rearrangement, RET fusions, NTRK1 fusions, MET exon skipping, BRAF mutations, and KRAS mutations.
Foretinib protected neurons by suppressing both known degenerative pathways and a new pathway involving unliganded TrkA and transcriptional regulation of the proapoptotic BH3 family members.
nerve growth factor (NGF) signaling through neurotrophic tyrosine kinase receptor type 1 (TrkA) directs innervation of the developing mouse femur to promote vascularization and osteoprogenitor lineage progression.
retrograde signaling by target-derived nerve growth factor (NGF) is necessary for soma-to-axon transcytosis of TrkA receptors in sympathetic neurons.
These findings suggest that by interacting with PlexA4 (显示 PLXNA4 ELISA试剂盒), TrkA plays a crucial role in redirecting local Sema3A (显示 SEMA3A ELISA试剂盒) signaling to retrograde axonal transport, thereby regulating dendritic GluA2 (显示 GRIA2 ELISA试剂盒) localization and patterning.
proposal that KIF1A (显示 KIF1A ELISA试剂盒) is essential for the survival and function of sensory neurons because of the TrkA transport and its synergistic support of the NGF (显示 NGFB ELISA试剂盒)/TrkA/PI3K signaling pathway
As a result, overexpression of PTP (显示 SLC25A3 ELISA试剂盒)-MEG2 (显示 PTPN9 ELISA试剂盒) down-regulates NGF (显示 NGFB ELISA试剂盒)/TrkA signaling and blocks neurite outgrowth and differentiation
TrkA misfolding and aggregation induced by some Insensitivity to Pain with Anhidrosis mutations disrupt the autophagy homeostasis causing neurodegeneration.
USP36 (显示 USP36 ELISA试剂盒) actions extend beyond TrkA because the presence of USP36 (显示 USP36 ELISA试剂盒) interferes with Nedd4-2-dependent Kv7.2 (显示 KCNQ2 ELISA试剂盒)/3 channel regulation.
functional PAP (显示 ASAP1 ELISA试剂盒)(thorn) neurons are essential for the analgesic effect, which is mediated by NGF (显示 NGFB ELISA试剂盒)-trkA signaling.
Dimeric dipeptide mimetics of the nerve growth factor Loop 4 and Loop 1 activate TRKA with different patterns of intracellular signal transduction.
This 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 this gene have been associated with congenital insensitivity to pain, anhidrosis, self-mutilating behavior, mental retardation and cancer. Alternate transcriptional splice variants of this gene have been found, but only three have been characterized to date.
, TRK1-transforming tyrosine kinase protein
, high affinity nerve growth factor receptor
, tropomyosin-related kinase A
, tyrosine kinase receptor A
, TrkA neurotrophin receptor
, slow nerve growth factor receptor
, trkA proto-oncogene receptor
, neurotrophic tyrosine kinase receptor type 1
, tropomyosin receptor kinase
, neurotrophic tyrosine kinase, receptor, type 1
, high affinity nerve growth factor receptor-like