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人 TrkB 抗体对
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人 TrkB 抗体对

01AB02233

Neurotrophic receptor tyrosine kinase 2 (TrkB) is a transmembrane receptor that serves as the high-affinity receptor for brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4). Upon ligand binding, TrkB undergoes dimerization and autophosphorylation, activating downstream signaling cascades including the MAPK/ERK, PI3K/AKT, and PLCgamma pathways. These signals are essential for regulating neuronal survival, differentiation, synaptic plasticity, and morphology. Alternative splicing produces multiple isoforms, such as the full-length catalytic receptor and truncated versions like TrkB.T1, which modulate ligand availability and signaling. Dysregulation or oncogenic fusion of the NTRK2 gene is implicated in various malignancies, including neuroblastoma and glioma. Furthermore, altered TrkB signaling is associated with neurological and psychiatric conditions such as depression, epilepsy, and neurodegenerative diseases.

Human
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技术参数

靶点基因名
NTRK2
基因别名
TRKB
蛋白别名
neurotrophic receptor tyrosine kinase 2; TrkB
UniProt
Q16620
物种
Human

产品详情

靶点名称
TrkB
蛋白名称
neurotrophic receptor tyrosine kinase 2
蛋白别名
BDNF/NT-3 growth factors receptor; GP145-TrkB; Trk-B; Neurotrophic tyrosine kinase receptor type 2; TrkB tyrosine kinase; Tropomyosin-related kinase B
靶点基因名
NTRK2
基因别名
TRKB
UniProt
Q16620
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Neurotrophic receptor tyrosine kinase 2 (TrkB) is a transmembrane receptor that serves as the high-affinity receptor for brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4). Upon ligand binding, TrkB undergoes dimerization and autophosphorylation, activating downstream signaling cascades including the MAPK/ERK, PI3K/AKT, and PLCgamma pathways. These signals are essential for regulating neuronal survival, differentiation, synaptic plasticity, and morphology. Alternative splicing produces multiple isoforms, such as the full-length catalytic receptor and truncated versions like TrkB.T1, which modulate ligand availability and signaling. Dysregulation or oncogenic fusion of the NTRK2 gene is implicated in various malignancies, including neuroblastoma and glioma. Furthermore, altered TrkB signaling is associated with neurological and psychiatric conditions such as depression, epilepsy, and neurodegenerative diseases.