Differences in expression of NGF, TrkA
, or p75NRT between samples from patients with or without PNI were assessed for significance using the Chi-square test in the case of semi-quantitative analysis or the t -test in the case of quantitative analysis.
Weichand et al., "The role of TRKA
signaling in IL-10 production by apoptotic tumor cell-activated macrophages," Oncogene, vol.
Expression levels of genes encoded with NF68, NF160, NF200, and TrkA
One of the most important events in the PTC carcinogenesis is the deregulation of the Mitogen-activated Protein Kinase (MAPK) signaling pathway with rearrangements of RET/PTC, TRKA
and mutation points in RAS and BRAF, where these nucleotide base changes contribute significantly to the PTC genotypes [30,79,83].
During the year Allergan entered into an exclusive licensing agreement with Mimetogen Pharmaceuticals, a clinical stage biotechnology company, to develop and commercialize tavilermide (MIM-D3), a topical formulation of a novel small molecule TrkA
agonist for the treatment of dry eye disease.
It is a potent, orally available, small molecule inhibitor of TrkA
is the highest affinity receptor for Nerve Growth Factor (NGF) and is widely expressed on peripheral pain sensing neurons.
Farfariello et al., "Onabotulinumtoxin-A intradetrusorial injections modulate bladder expression of NGF, TrkA
, p75 and TRPV1 in patients with detrusor overactivity," Pharmacological Research, vol.
is a member of a larger family of important signaling proteins known as tyrosine receptor kinases.
It is suggested that the neurotrophin receptor TrkB is involved because the TrkB ligand BDNF or NT4 applied to culture media specifically counteracts the up-regulatory effect of TTX on N-type channels, whereas the TrkA
ligand NGF or the TrkC ligand NT3 has no such effect (Fig.
Tropomyosin receptor kinases (TRKA
through TRKC) bind the neurotrophin family of ligands, including nerve growth factor, and have been implicated in tumorigenesis.
In addition, Pengpai (2011) showed that immediately after a single exhaustive exercise, the brain shows signs of early cortical ischemia-like changes, with significant upregulation of NGF and its cognate receptor TrkA
. After 12 h, structural damage to the cerebral cortex was more apparent, but the expression of NGF and TrkA
was significantly reduced.
(24,43) This process involves the secretion of inflammatory pain-related mediators as well as an augmented expression of pain-related molecules such as nerve growth factor and its receptor (TrkA