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The TrkA peptide is competitive for metal binding with analogous peptides due to the N-terminal domain of NGF (show NGFB Proteins). These data provide cues for future exploration of the effect of metal ions on the activity of the NGF (show NGFB Proteins) and its specific cellular receptor.
The LMNA (show LMNA Proteins)-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 (show NGFR Proteins) controls proliferation, while the interaction of CD271 (show NGFR Proteins) with the neurotrophin (show BDNF Proteins) 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
The authors described a long-distance signaling mechanism of Porcine hemagglutinating encephalomyelitis virus-driven deficits in neurons and suggested that such Ulk1 (show ULK1 Proteins) repression may result in limited NGF (show NGFB Proteins)/TrkA retrograde signaling within activated Rab5 (show RAB5A Proteins) endosomes, explaining the progressive failure of neurite outgrowth and survival.
antibodies raised against NGF (show NGFB Proteins), TrkA, and p75 (show NGFR Proteins) (also known as CD271 (show NGFR Proteins)) 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 (show NGFB Proteins)-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 (show NTRK2 Proteins) 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 (show PLXNA4 Proteins), TrkA plays a crucial role in redirecting local Sema3A (show SEMA3A Proteins) signaling to retrograde axonal transport, thereby regulating dendritic GluA2 (show GRIA2 Proteins) localization and patterning.
proposal that KIF1A (show KIF1A Proteins) is essential for the survival and function of sensory neurons because of the TrkA transport and its synergistic support of the NGF (show NGFB Proteins)/TrkA/PI3K signaling pathway
By immunohistochemistry, the localization of Neurotrophinss has been observed mainly in Purkinje cells; TrkA and TrkB (show NTRK2 Proteins)-receptors in cells and fibers of granular and molecular layers. TrkC (show NTRK3 Proteins) 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 (show NGFB Proteins) and its cognate receptors, NTRK1 and NGFR (show NGFR Proteins), 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