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By immunohistochemistry, the localization of Neurotrophinss has been observed mainly in Purkinje cells; TrkA (show NTRK1 ELISA Kits) and TrkB-receptors in cells and fibers of granular and molecular layers. TrkC (show NTRK3 ELISA Kits) was faintly detected
BDNF (show BDNF ELISA Kits)-TrkB influences the expression level of components of chemokine (show CCL1 ELISA Kits) signaling including Cxcr4b, and the generation of progenitors of mechanoreceptors, at the level of expression of Atoh1a-Atp2b1a.
Light regulates the expression of the BDNF (show BDNF ELISA Kits)/TrkB2 system in the adult zebrafish retina.
Study showed that complex relationships exist between BDNF (show BDNF ELISA Kits)/TrkB gene expression and interneuron marker gene expression that appear to be dependent on the presence of testosterone at adolescence
Data suggest that high expression of TRKB (not TRKA (show NTRK1 ELISA Kits) or TRKC (show NTRK3 ELISA Kits)) in lung squamous cell carcinoma is correlated with vascular invasion, lymph node metastasis, advanced stage of tumor, and poor prognosis; overall survival of patients with TRKB-high expression is significantly shorter than those with TRKB-low expression; RNA interference against TRKB or BDNF (show BDNF ELISA Kits) (TRKB agonist) inhibits cell proliferation of tumor cell line.
Among the adaptations observed following consumption of drugs of abuse or alcohol abuse, BDNF (show BDNF ELISA Kits) levels are widely altered in both brain and periphery. Data suggest that BDNF (show BDNF ELISA Kits)/TRKB signaling in neurons in specific areas of brain (hippocampus, nucleus accumbens) is altered in protracted withdrawal from drug/alcohol abuse. [REVIEW]
Data suggest that kinase domains of neurotrophin (show BDNF ELISA Kits) receptor isoforms, TRKA (show NTRK1 ELISA Kits), TRKB, and TRKC (show NTRK3 ELISA Kits), exhibit a bulky phenylalanine gatekeeper, leading to a small and unattractive back pocket/binding site for antineoplastic kinase inhibitors. [REVIEW]
Pan-Trk (show NTRK1 ELISA Kits) immunohistochemistry is a time-efficient and tissue-efficient screen for NTRK fusions, particularly in driver-negative advanced malignancies and potential cases of secretory carcinoma and congenital fibrosarcoma.
High TRKB expression is associated with Small Cell Lung Cancer.
Co-immunoprecipitation and biochemical fractionation data suggested that p75 (show CUX1 ELISA Kits) TM stimulates TrkB phosphorylation at the cell membrane.
High NTRK2 expression is associated with astrocytomas.
overexpression of TrkB, but not of BDNF (show BDNF ELISA Kits), is significantly associated with a poor survival outcome for TNBC patients.
In the current work, we provide a global analysis of the physiological consequences of TrkB receptor activation in vitro and discuss the dynamic consequences of TrkB activation in vivo. Finally, we propose a clinically-feasible option for increasing BDNF (show BDNF ELISA Kits) expression in the hypothalamus to more readily utilize the oncolytic effects of BDNF (show BDNF ELISA Kits).
ShcD binds to active Ret (show RET ELISA Kits), TrkA (show NTRK1 ELISA Kits), and TrkB neurotrophic factor (show NTF3 ELISA Kits) receptors predominantly via its phosphotyrosine-binding (PTB (show PTBP1 ELISA Kits)) domain.
The three receptor sets considered (mAChR (show CHRM3 ELISA Kits), AR and TrkB receptors) intervene in modulating the conditions of the competition between nerve endings.
Signaling through postsynaptic trkB receptors is considered to be an essential part of a cellular mechanism for maintaining the contacts of some, but not all, synaptic contacts onto motoneurons
findings show that BDNF (show BDNF ELISA Kits)-TrkB signaling, rather than Dopamine signaling, in the Ventral Tegmental Area -Nuc (show SREBF2 ELISA Kits). Accumbens circuit is crucial for facilitating depressive-like depressive-like outcomes after Chronic Social Defeat Stress and they establish BDNF (show BDNF ELISA Kits)-TrkB signaling as a pathologic mechanism during periods of chronic stress.
inhibition of Sig (show PICALM ELISA Kits)-1 R prevented cocaine-induced TrkB activation in hippocampal neurons.
After spinal cord injury, astrocyte-specific TrkB knock-out mice showed reduced hyperpathic responses and improved motor coordination.
Results imply that oleanolic acid ameliorates scopolamine-induced memory impairment by modulating the brain-derived neurotrophic factor (show BDNF ELISA Kits) -ERK1/2 (show MAPK1/3 ELISA Kits)-cAMP response element-binding protein (show CREB ELISA Kits) pathway through tropomyosin receptor kinase (show NTRK1 ELISA Kits) B activation in mice, suggesting that oleanolic acid would be a potential therapeutic agent for the treatment of cognitive deficits.
Data show that c-Jun NH2-terminal kinase (JNK (show MAPK8 ELISA Kits))-interacting protein-3 (JIP3 (show MAPK8IP3 ELISA Kits)) participates in the migration of cortical neurons during cortical development by mediating TrkB receptor axonal anterograde transport.
findings reveal a spine-autonomous, autocrine signalling mechanism involving NMDAR (show GRIN1 ELISA Kits)-CaMKII (show CAMK2G ELISA Kits)-dependent BDNF (show BDNF ELISA Kits) release from stimulated dendritic spines and subsequent TrkB activation on these same spines that is crucial for structural and functional plasticity
Following ethanol administration, phosphorylation of TrkB in the striatum was significantly reduced in wild-type mice.
Results suggest that the therapeutic actions of atypical antidepressant drugs involve various neurocircuits, some of which, but not all, appears to involve BDNF (show BDNF ELISA Kits)/TrkB and downstream neuroplastic signaling
These observations provided evidence that brain-derived naeurotrophic factor(BDNF (show BDNF ELISA Kits)) and its receptor (BDNF (show BDNF ELISA Kits) receptor) secreted by bovine sperm was important in regulation of insulin (show INS ELISA Kits) and leptin (show LEP ELISA Kits).
Expressed in ganglionic neuron-like tumor cells, which may activate an embryonic autocrine pathwy involving bdnf (show BDNF ELISA Kits)-Trk-B
This gene encodes a member of the neurotrophic tyrosine receptor kinase (NTRK) family. This kinase is a membrane-bound receptor that, upon neurotrophin binding, phosphorylates itself and members of the MAPK pathway. Signalling through this kinase leads to cell differentiation. Mutations in this gene have been associated with obesity and mood disorders. Alternate transcriptional splice variants encoding different isoforms have been found for this gene.
neurotrophin receptor B xTrkB-alpha
, BDNF/NT-3 growth factors receptor
, neurotrophic tyrosine kinase, receptor, type 2
, BDNF/NT-3 growth factors receptor-like
, neurotrophic tyrosine kinase receptor type 2
, trkB tyrosine kinase
, tyrosine kinase receptor
, BDNF-tropomyosine receptor kinase B
, tropomyosin-related kinase B
, tyrosine kinase receptor B
, neural receptor protein-tyrosine kinase (trkB)
, trkB protein