Overview
- Peptide (C)KASRPPKMRNRPTPR, corresponding to amino acid residues 301-315 of mouse Slitrk2 (Accession Q810C0). Extracellular, N-terminus.
- Mouse and rat brain lysates, and human U-87 MG glioblastoma cell lysate (1:200-1:1000).
Western blot analysis of mouse (lanes 1 and 3) and rat (lanes 2 and 4) brain lysates:1,2. Anti-Slitrk2 (extracellular) Antibody (#ASR-082), (1:200).
3,4. Anti-Slitrk2 (extracellular) Antibody, preincubated with Slitrk2 (extracellular) Blocking Peptide (#BLP-SR082).
Western blot analysis of human U-87 MG glioblastoma cell line lysate:1. Anti-Slitrk2 (extracellular) Antibody (#ASR-082), (1:200).
2. Anti-Slitrk2 (extracellular) Antibody, preincubated with Slitrk2 (extracellular) Blocking Peptide (#BLP-SR082).
- Rat brain sections (1:200).
Slitrk2 (SLIT and NTRK-like family member 2) is a neuronal transmembrane protein widely expressed in the nervous system and found to affect neurite outgrowth1,2. Slitrk2 structure contains tandem leucine-rich repeat (LRR) domains and a single transmembrane domain2.
In mammals, the Slitrk family consists of at least six members: Slitrk1- Slitrk6. All Slitrk members apart from Slitrk3 can induce both excitatory and inhibitory synapses1.
The Slitrk family is responsible for controlling excitatory and inhibitory synapse formation by forming trans-synaptic adhesions with LAR receptor protein tyrosine phosphatases (PTPs)1,2.
Studies show that mutations in SLITRK gene family are linked to several neuropsychiatric disorders including schizophrenia, autism spectrum disorders, Tourette syndrome, and obsessive-compulsive disorder.
A single amino acid substitution in Slitrk2 (V89M) impairs synapse formation activity in cultured neurons, but does not affect surface transport, expression, or synapse inducing activity1,2.
