trkb - Synonyms for trkb | Synonyms Of trkb

Examples of "trkb"
LINGO 1 negatively regulates TrkB activation through the signalling pathway of BDNF/TrKB, and anti-LINGO-1 exerts neuroprotective effects via activation of BDNF/TrkB.
TrkB binds BDNF and NT-4 more strongly than it binds NT-3. TrkC binds NT-3 more strongly than TrkB does.
TrkB binds BDNF and NT-4 more strongly than it binds NT-3. TrkC binds NT-3 more strongly than TrkB does.
Brain-derived neurotrophic factor is among the chemotactic factors that stimulate Numb-mediated chemotaxis during cell migration. BDNF can function as a chemotactic factor for neural precursors during migration by activating TrkB receptors. Numb binds to TrkB receptors to act as an endocytic regulator of TrkB and promote aPKC activation by acting as a scaffolding protein. Once phosphorylated, aPKC can also phosphorylate Numb to increase its efficacy for binding TrkB, thus promoting the precursor’s chemotactic sensitivity to BDNF.
SHC3 has been shown to interact with RICS and TrkB.
The TrkB internal ribosome entry site (IRES) is an RNA element which is present in the 5' UTR sequence of the mRNA. TrkB is a neurotrophin receptor which is essential for the development and maintenance of the nervous system. The internal ribosome entry site IRES element allows cap-independent translation of TrkB which may be needed for efficient translation in neuronal dendrites.
NAS has been shown to act as a potent TrkB receptor agonist, while serotonin and melatonin do not. Subchronic and chronic administration of NAS to adult mice induces proliferation of neural progenitor cells (NPC)s, blockage of TrkB abolished this effect suggesting that it is TrkB-dependent. NAS was also found to significantly enhance NPC proliferation in sleep-deprived mice. It is thought that the anti-depressant and neurotrophic effects of NAS are in part due to its role as a TrkB agonist.
NGF/TrkA signaling upregulates BDNF, which is transported to both peripheral and central terminals of nocireceptive sensory neurons. In the periphery, TrkB/BDNF binding and TrkB/NT-4 binding acutely sensitizing nocireceptive pathway that require the presence of mast cells.
It has been found to act as a weak TrkB receptor agonist.
Gossypetin has been found to act as an antagonist of TrkB.
NT-4 is a neurotrophic factor that signals predominantly through the TrkB receptor tyrosine kinase.
The TrkB receptor is encoded by the NTRK2 gene and is member of a receptor family of tyrosine kinases that includes TrkA and TrkC. TrkB autophosphorylation is dependent upon its ligand-specific association with BDNF, a widely expressed activity-dependent neurotic factor that regulates plasticity and is unregulated following hypoxic injury. The activation of the BDNF-TrkB pathway is important in the development of short term memory and the growth of neurons.
LM22A-4 is a synthetic, selective small-molecule partial agonist of TrkB (EC for TrkB activation = 200–500 pM; IC for inhibition of BDNF binding to TrkB = 47 nM; IA = ~85%), the main receptor of brain-derived neurotrophic factor. It has been found to possess poor blood-brain-barrier penetration when administered systemically, so LM22A-4 has been given to animals instead via intranasal administration, with central nervous system TrkB activation observed. The compound produces neurogenic and neuroprotective effects in animals, and shows beneficial effects on respiration in animal models of Rett syndrome.
Recently, studies have also indicated that TrkB receptor is associated with Alzheimer's disease.
7,8,3′-Trihydroxyflavone (7,8,3'-THF) is a flavone and small-molecule agonist of TrkB, the main receptor of brain-derived neurotrophic factor (BDNF), that was derived from 7,8-dihydroxyflavone (7,8-DHF). Relative to 7,8-DHF, 7,8,3'-THF is 2–3-fold more potent "in vitro" as a TrkB agonist. 7,3’-Dihydroxyflavone (7,3'-DHF) is also more potent than 7,8-DHF "in vitro", indicating that a 3'-hydroxy group on the B-ring enhances TrkB agonistic activity. 7,8,3'-THF has been tested "in vivo" and was found to produce TrkB-dependent neuroprotective effects in mice similarly to 7,8-DHF.
The effects of ethanol on CREB are further manifested in CREB-target genes, namely BDNF, TrkB, Arc, NPY, and CRF.
Niacin also appears to upregulate brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) expression.
A variety of close structural analogs of 7,8-DHF have also been found to act as TrkB agonists "in vitro", including diosmetin (5,7,3'-trihydroxy-4'-methoxyflavone), norwogonin (5,7,8-trihydroxyflavone), 4'-dimethylamino-7,8-dihydroxyflavone, 7,8,3'-trihydroxyflavone, 7,3'-dihydroxyflavone, 7,8,2'-trihydroxyflavone, 3,7,8,2'-tetrahydroxyflavone, and 3,7-dihydroxyflavone. The highly hydroxylated gossypetin (3,5,7,8,3',4'-hexahydroxyflavone), conversely, appears to be an antagonist of TrkB "in vitro".
The mechanism by which invading tumor cells survive the anoikis process remains largely unknown. Recent findings suggest that the protein TrkB, best known for its role in the nervous system, might be involved together with its ligand, brain-derived neurotrophic factor (BDNF). It seems that TrkB could make tumor cells resistant to anoikis by activating phosphatidylinositol 3-kinase (PI3K) signaling cascade.
TrkB has the highest affinity to the binding of brain-derived neurotrophic factor (BDNF) and NT-4. BDNF is a growth factor that has important roles in the survival and function of neurons in the central nervous system. The binding of BDNF to TrkB receptor causes many intracellular cascades to be activated, which regulate neuronal development and plasticity, long-term potentiation, and apoptosis.