The SLITRK5 Antibody, HRP conjugated is a specialized immunological reagent designed for detecting the SLITRK5 protein, a type I transmembrane protein involved in neuronal development, synaptic signaling, and bone metabolism. Horseradish Peroxidase (HRP) conjugation enables enzymatic signal amplification, making this antibody ideal for applications like ELISA and Western blotting. SLITRK5 is a member of the SLITRK family, characterized by extracellular leucine-rich repeats (LRRs) and intracellular Trk-like domains, and is implicated in neuropsychiatric disorders, epilepsy, and osteoblast differentiation .
The HRP-conjugated antibody is optimized for:
ELISA: Quantitative detection of SLITRK5 in cell lysates or tissue extracts.
Western Blotting (WB): Immunodetection of SLITRK5 protein in denatured samples.
Immunohistochemistry (IHC): Localization of SLITRK5 in tissue sections (though HRP-conjugated variants may require additional detection steps).
| Application | Key Features | Citations |
|---|---|---|
| ELISA | High sensitivity for SLITRK5 quantification | |
| WB | Detects SLITRK5 at ~107 kDa | |
| IHC | Limited direct use; requires secondary HRP detection |
SLITRK5 acts as a negative regulator of Hedgehog (Hh) signaling in osteoblasts. HRP-conjugated antibodies enable quantification of SLITRK5 levels in studies showing:
Enhanced Hh signaling in Slitrk5 knockout mice, leading to increased bone formation and fracture healing .
Direct interaction between SLITRK5 and Sonic Hedgehog (SHH), mapped to the extracellular LRR domains .
SLITRK5 modulates BDNF-dependent TrkB receptor trafficking by recruiting Rab11-FIP3, a Rab11 effector protein. Key findings include:
Basil interaction with TrkB under serum-deprived conditions.
Ligand-induced shift to cis-interactions with TrkB upon BDNF stimulation, displacing trans-interactions with PTPδ .
SLITRK5 expression is elevated in temporal lobe epilepsy (TLE) patients and pilocarpine-induced epilepsy models:
Peak expression observed 7 days post-status epilepticus in rat hippocampi .
Cytoplasmic localization in neurons, suggesting dysregulated signaling in epileptogenesis .