人 SLITRK2 抗体对
01AB01893
SLIT and NTRK like family member 2 (SLITRK2) is an integral membrane protein predominantly expressed in neural tissues, characterized by two N-terminal leucine-rich repeat (LRR) domains similar to SLIT proteins and C-terminal regions homologous to neurotrophin receptors like NTRK1. Functionally, SLITRK2 plays a crucial role in synaptogenesis, promoting the differentiation and maintenance of excitatory synapses, and regulating neurite outgrowth at postsynaptic neurons. It is a single-pass transmembrane protein that modulates both excitatory and inhibitory presynaptic structures, with its synaptogenic activity being essential for proper neural connectivity. Pathogenic variants in SLITRK2 have been linked to neurodevelopmental disorders, including X-linked intellectual disability, as these mutations can impair membrane transport, disrupt synapse-promoting effects, and abolish the protein’s ability to regulate TrkB receptor levels, leading to deficits in memory and motor function as observed in both patients and mouse models.
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技术参数
- 靶点基因名
- SLITRK2
- 基因别名
- CXorf2; KIAA1854; SLITL1
- 蛋白别名
- SLIT and NTRK like family member 2; SLITRK2
- UniProt
- Q9H156
- 物种
- Human
产品详情
- 靶点名称
- SLITRK2
- 蛋白名称
- SLIT and NTRK like family member 2
- 蛋白别名
- SLIT and NTRK-like protein 2
- 靶点基因名
- SLITRK2
- 基因别名
- CXorf2; KIAA1854; SLITL1
- UniProt
- Q9H156
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
SLIT and NTRK like family member 2 (SLITRK2) is an integral membrane protein predominantly expressed in neural tissues, characterized by two N-terminal leucine-rich repeat (LRR) domains similar to SLIT proteins and C-terminal regions homologous to neurotrophin receptors like NTRK1. Functionally, SLITRK2 plays a crucial role in synaptogenesis, promoting the differentiation and maintenance of excitatory synapses, and regulating neurite outgrowth at postsynaptic neurons. It is a single-pass transmembrane protein that modulates both excitatory and inhibitory presynaptic structures, with its synaptogenic activity being essential for proper neural connectivity. Pathogenic variants in SLITRK2 have been linked to neurodevelopmental disorders, including X-linked intellectual disability, as these mutations can impair membrane transport, disrupt synapse-promoting effects, and abolish the protein’s ability to regulate TrkB receptor levels, leading to deficits in memory and motor function as observed in both patients and mouse models.