Trk Receptor

Trk receptors are a family of tyrosine kinases that regulates synaptic strength and plasticity in the mammalian nervous system. Trk receptors affect neuronal survival and differentiation through several signal cascades. However, the activation of these receptors also has significant effects on functional properties of neurons.

B0084-462361
GNF 5837
1033769-28-6
B0084-470812
Entrectinib
1108743-60-7
B0084-475140
GNE-8525
1196546-33-4
Cyclotraxin B
1203586-72-4
B0084-474404
LOXO-101 sulfate
1223405-08-0
1357920-84-3
Belizatinib
1357920-84-3
PF 06273340
1402438-74-7
TPX-0005
1802220-02-5
NTR 368
197230-90-3
219766-25-3
ANA-12
219766-25-3
263251-78-1
Tavilermide
263251-78-1
LM22B-10
342777-54-2
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GW 441756
504433-23-2
AZ 23
915720-21-7

Background


An overview of TRK receptor

The TRK receptor can regulate synaptic strength and plasticity in the mammalian nervous system, which belongs to the receptor tyrosine kinase family. The activation of TRK receptors affects the survival and differentiation of neurons through multiple signaling pathways, and also significantly affects the function of neurons. The common ligand of TRK receptors is the neurotrophic factor, a family of growth factors that play a key role in the nervous system. Their combination is highly specific. And each neurotrophic factor has a corresponding TRK receptor of different affinity. The combination of neurotrophic factors causes the activation of TRK receptors signaling pathways that eventually leads to cell survival and other functional regulation.

Inhibition of TRK receptor

7, 8-dihydroxyflavone (7, 8-DHF) is an effective and selective TRKB receptor agonist (K d≈320 nM). In vitro, 250nM of 7, 8-DHF specifically activates TRKB without activating TRKA or TRKC. In vivo, 7, 8-DHF is a biologically-active compound that activates TRKB and PI3K/Akt and MAPK downstream after intraperitoneal injection or oral administration via the blood-brain barrier 7, 8-DHF.

TRK receptor and diseases

In the central nervous system injury, the release of glutamate and the flow of Ca 2+ may be important starting factors. They can induce the expression of TRKA receptor and NGF, and the increase expression of TRKA receptor and the acute phase of injury are closely related to the overexpression of c-fos, c-jun and cytokines IL-1 and TNF-α, which belongs to the body's own balance of injury and injury resistance. Studies have shown that TRKA mediates the damage protection of the medial nucleus of the basal forebrain and the oblique band nucleus with NGF, which reduces the mortality, makes the remnant neurons atrophy and increases the TRKA receptor content. Therefore, neurons with TRKA receptor mark are first protected and supported by NGF, which resists many different types of damage.