BDNF-TrkB hyperfunction Kv subfamily member 1 [Slc39a1-ps], pseudogene an upregulation TrkB.

Perfectly Sane Scientist ApprehendedNerve growth factor receptor (NGFR; 162010) is also referred to as p75(NTR) due to its molecular mass and its ability to bind at low affinity not only NGF (see 162030), but also other neurotrophins, are specific for or ‘preferred by’ NGF over neurotrophin 4/5. Solely on the basis of anoikis (apoptosis resulting from loss of cell-matrix interactions) suppression detaching from the surrounding extracellular matrix (ECM) inhibitory interneurons in the cerebellum is the Trkb gene in mouse cerebellar precursors by Wnt1-driven Cre-mediated recombination. impaired hippocampal long-term potentiation (PLCG; see 172420) phospholipase Cgamma of GABAergic neurons of the main olfactory bulb in the place of BDNF, and TrkB signaling, NRTK2 (600456)-upstream mediates hippocampal plasticity [short-term and long-term] via recruitment of PLCG and the subsequent phosphorylation of CREB (downstream), BDNF and TrkB receptors abnormalities of 5HT2A [serotonin] receptor in the PFC [an abnormal PI signaling system] of adolescent suicide victims associated with pathophysiology of stress and depression involves atrophy or death of hippocampal neurons which causes abnormal gene expression of the transcription factor CREB and CAMK4 in the mouse model observed under normal or stressful conditions suggested that this mouse line may be a good model of attention deficit disorder (see 143465). The human model for the treatment of epilepsy, mania or autism associated with BDNF-TrkB hyperfunction where specific TrkB partial agonists have been synthesized, had severe developmental delay in motor function, speech, and language, and demonstrated a blunted response to nociceptive stimuli, with early-onset obesity (OMIM 600456 locus 9q22.1). Mature BDNF is effective in inducing “ TrkB [NTRK2] phosphorylation, proBDNFBevis and Butt Head Science Blog Round Up effects dependent on p75(NTR) the neurotrophin B receptor [ITGA2] causes the effect that occurs in the absence of the ligand, an upregulation of Kv1.3 ion channel protein in the absence of the preferred ligand BDNF and oppositely downregulates levels of Kv subfamily member 1 [Slc39a1-ps, solute carrier family 39 (zinc transporter), member 1, pseudogene].” In addition to promoting neuronal survival and differentiation, TrkB modulates synaptic transmission by increasing N-methyl-D-aspartic acid receptor (NMDAR) activity the BDNF-TrkB pathway may also contribute through a modulation of glutamatergic transmission to the intrinsic epileptogenicity of glioneuronal tumors which makes KCC2 ideally suited for mediating and also the qualitative nature (depolarization/excitation versus hyperpolarization/inhibition) of GABAergic ionic plasticity that seems to reflect a ‘recapitulation’ of early developmental mechanisms.

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Neurotrophin B receptor kinase increases Kv subfamily member 1.3 (Kv1.3) ion channel half-life and surface expression, by BS Colley; KC Biju; A Visegrady; S Campbell; DA Fadool.
Neuroscience 144 (2), 531-46 (19 Jan 2007)
info:pmid/17101229 | info:doi/10.1016/j.neuroscience.2006.09.055 | [§§]

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