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NTRK1 might be associated with the development of nonsyndromic cleft lip with or without cleft palate.
Two novel compound heterozygous variants of NTRK1 (c.632T > A and c.1253_1254delTC) were identified in a pair of Chinese identical twins with Congenital Insensitivity to Pain and Anhidrosis.
The above results suggest that rutin preconditioning ameliorates cerebral I/R injury in OVX rats through ER-mediated BDNF-TrkB and NGF-TrkA signaling.
The TrkA peptide is competitive for metal binding with analogous peptides due to the N-terminal domain of NGF. These data provide cues for future exploration of the effect of metal ions on the activity of the NGF and its specific cellular receptor.
The LMNA-NTRK1 fusion was likely the molecular driver of tumorigenesis and metastasis in this patient, and the observed effectiveness of crizotinib treatment provides clinical validation of this molecular target.
that lipofibromatosis-like tumour represents a novel entity of NTRK1-associated neoplasms
System xC(-)-mediated TrkA activation therefore presents a promising target for therapeutic intervention in cancer pain treatment.
Results identified two known splice-site mutations, one known nonsense mutation and one novel missense mutation in three congenital insensitivity to pain with anhidrosis (CIPA) pedigrees. These findings expanded the spectrum of the NTRK1 mutations associated with CIPA patients, provided additional clues for the phenotype-genotype relationship beneath CIPA.
27 mutations in NTRK1 from Congenital insensitivity to pain with anhidrosis cohort, including 15 novel mutations, are reported.
NTRK1 was upregulated in 80% of head and neck squamous carcinoma tissue.
TRKA expression can be found in 1.6% of solid tumours and can be paralleled by NTRK1 gene rearrangements or mostly copy number gain
Cleaved intracellular domain of CD271 controls proliferation, while the interaction of CD271 with the neurotrophin receptor Trk-A modulates cell adhesiveness through dynamic regulation of a set of cholesterol synthesis genes relevant for patient survival.
These results suggest that polymorphisms in NTRK1 play an important role in pain sensitivity in young Han Chinese women
We developed a comprehensive model of acquired resistance to NTRK inhibitors in cancer with NTRK1 rearrangement and identified cabozantinib as a therapeutic strategy to overcome the resistance
TrkA plays an important role in the pathogenesis of NPM-ALK(+) T-cell lymphoma.
Results show frequent BRCA2, EGFR, and NTRK1/2/3 mutations in mismatch repair-deficient colorectal cancers , sugggesting personalized medicine strategies to treat the patients with advanced disease who may have no remaining treatment options
novel deletional mutation has enriched the spectrum of NTRK1 mutations
This study identify four novel NTRK1 mutations (IVS14+3A>T, p.Ser235*, p.Asp596Asn, and p.Leu784Serfs*79) and demonstrate that they are pathologic mutations using an mRNA splicing assay and an NTRK autophosphorylation assay.
Report a novel mechanism for the TRAIL-induced apoptosis of TrkAIII expressing NB cells that depends upon SHP/Src-mediated crosstalk between the TRAIL-receptor signaling pathway and TrkAIII.
This show evidence of variation in plasmatic monocytic TrkA expression during the progression of dementia.
intrachromosomal deletion generating a fusion between BCAN and NTRK1 drives the formation of aggressive high-grade gliomas and confers sensitivity to entrectinib
The authors described a long-distance signaling mechanism of Porcine hemagglutinating encephalomyelitis virus-driven deficits in neurons and suggested that such Ulk1 repression may result in limited NGF/TrkA retrograde signaling within activated Rab5 endosomes, explaining the progressive failure of neurite outgrowth and survival.
antibodies raised against NGF, TrkA, and p75 (also known as CD271) were used to explore the expression of these antigens in the non-decalcified young mouse femur.
these findings demonstrate that communication between osteoblasts and sensory nerves through NGF-TrkA signaling is essential for load-induced bone formation in mice.
Imipramine protected bupivacaine-induced neurotoxicity in DRG, likely via the co-activation of TrkA and TrkB signaling pathways.
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, TrkA plays a crucial role in redirecting local Sema3A signaling to retrograde axonal transport, thereby regulating dendritic GluA2 localization and patterning.
proposal that KIF1A is essential for the survival and function of sensory neurons because of the TrkA transport and its synergistic support of the NGF/TrkA/PI3K signaling pathway
As a result, overexpression of PTP-MEG2 down-regulates NGF/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 actions extend beyond TrkA because the presence of USP36 interferes with Nedd4-2-dependent Kv7.2/3 channel regulation.
functional PAP(thorn) neurons are essential for the analgesic effect, which is mediated by NGF-trkA signaling.
Dimeric dipeptide mimetics of the nerve growth factor Loop 4 and Loop 1 activate TRKA with different patterns of intracellular signal transduction.
Data show that lysophosphatidic acid (LPA) induces phosphorylation of trkA receptor (TrkA) through lysophosphatidic acid receptor 1 (LPA1) binding to TrkA
Its reduction ameliorates cognitive deficits in Alzheimer disease.
adult homozygous TrkAC knock-in mice displayed severe deficits in acute and tissue injury-induced pain, representing the first viable adult Trk mouse mutant with a pain phenotype
IL-6 may act as a new potential cumulus expansion-related transcript, which may be involved in the integration of TrkA and EGF signaling in affecting expansion of cumulus oocyte complexes.
By immunohistochemistry, the localization of Neurotrophinss has been observed mainly in Purkinje cells; TrkA and TrkB-receptors in cells and fibers of granular and molecular layers. TrkC 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.
Present results demonstrate that as for mammals neurotrophins might play a role in sensory cells of the teleostean taste buds.
report describing differential expression of proteins and mRNA for NGF and its cognate receptors, NTRK1 and NGFR, in the male sex organs of rabbits
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