Antibodies were produced by immunizing rabbits with synthetic phosphopeptide and KLH conjugates. Antibodies were purified by affinity-chromatography using epitope-specific phosphopeptide. Non-phospho specific antibodies were removed by chromatogramphy using non-phosphopeptide.

Concentrazione

1.0mg / ml

Formulazione

Supplied at 1.0mg / mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

Conservazione

Store at -20°C for long term preservation (recommended). Store at 4°C for short term use.

Sinonimi

AI848316, BDNF tropomyosine receptor kinase B, BDNF/NT 3 growth factors receptor, BDNF/NT-3 growth factors receptor, Brain derived neurotrophic factor receptor, C030027L06Rik, EC 2.7.10.1, GP145 TrkB, GP145-TrkB, GP145-TrkB/GP95-TrkB, GP95 TrkB, Neurotrophic receptor tyrosine kinase 2, Neurotrophic tyrosine kinase receptor type 2, Neurotrophin receptor tyrosine kinase type 2, NTRK 2, Ntrk2, NTRK2_HUMAN, Obesity, hyperphagia, and developmental delay, included, RATTRKB1, Tkrb, Trk B, Trk-B, TrkB tyrosine kinase, TRKB1, Tropomyosin related kinase B, tyrosine kinase receptor B, Tyrosine receptor kinase B

Secondari adatti

Dichiarazione di non responsabilità

Questo prodotto è solo per uso di ricerca. Non è inteso per uso diagnostico o terapeutico.

Immagini (1)

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Figure 1: Immunofluorescence - Anti-TrkB (Phospho-Tyr515) Antibody (11327)

Immunofluorescence staining of methanol-fixed Hela cells using TrkB (Phospho-Tyr515) Antibody #11327.

Pubblicazioni (1)

Visualizza pubblicazione

Sex-specific and region-specific changes in BDNF-TrkB signalling in the hippocampus of 5-HT1A receptor and BDNF single and double mutant mice.

Riferimenti: Anti-TrkB (Phospho-Tyr515) Antibody (A51482)

Astratto:

Brain-derived neurotrophic factor (BDNF) and serotonin 5-HT1A receptors are implicated in the pathophysiology of depression and the mechanism of action of antidepressant drugs. Here, we explore possible reciprocal interactions of 5-HT1A receptor knockout and the expression of BDNF, its receptor TrkB and downstream mitogen-activated protein kinase (MAPK) in the ventral (VHP) and dorsal hippocampus (DHP). We compared female and male double mutant mice (5-HT1A(-/-)/BDNF(+/-)) with single mutant mice (5-HT1A(-/-), BDNF(+/-)) and wildtype (WT) controls. Protein expression of BDNF, TrkB, phosphorylation of TrkB (pTrkB) and MAPKs (ERK1, ERK2) was examined using Western blot analysis (n=5-7). As expected, the BDNF(+/-) mice showed ~50% BDNF reduction. Loss of 5-HT1A receptors induced a significant decrease in BDNF levels in the VHP in female mice. The pTrkB/TrkB ratio was also significantly decreased in female 5-HT1A(-/-) mice and 5-HT1A(-/-)/BDNF(+/-) mice but not in males. Despite markedly reduced BDNF levels in BDNF(+/-) mice and double mutants, ERK1 activation was unchanged in the female mice. In contrast, ERK2 activation was significantly elevated in the VHP of female BDNF(+/-) mice and double mutants. Given the greater vulnerability of women to develop depression and the role of the VHP in stress responses and anxiety-related behaviours, our results may shed more light on sex differences in depression and other psychiatric disorders with BDNF and 5-HT1A receptor dysfunction.

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