Recombinant Mouse SLITRK6 Protein, CF Summary
Met1-Ser607, with a C-terminal 6-His tag
CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
|Formulation||Lyophilized from a 0.2 μm filtered solution in PBS.|
|Reconstitution||Reconstitute at 500 μg/mL in PBS.|
|Shipping||The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
2 μg/lane of Recombinant Mouse SLITRK6 was resolved with SDS-PAGE underreducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Bluestaining, showing bands at 80-90 kDa.
SLITRK6 (Slit and Trk-like family member 6) is a type I transmembrane member of the SLITRK family of proteins which contain a slit-like extracellular region and a Trk-like cytoplasmic region. Mature mouse SLITRK6 consists of a 587 amino acid (aa) extracellular domain (ECD) with 5 leucine rich repeats (LRR) flanked by N-and C-terminal LRR domains, followed by 6 more LRR flanked by another pair of N- and C-terminal LRR domains (1, 2). Within the ECD, mouse SLITRK6 shares 89% and 95% aa sequence identity with human and rat SLITRK6, respectively. SLITRK6 is strongly expressed in the auditory and vestibular sensory epithelia of the ear (3). Its expression in the inner ear promotes innervation and survival of sensory neurons (3, 4). In the brain, SLITRK6 expression is highly restricted in the thalamus, lateral geniculate nucleus, and absent in the cortex (1, 3). SLITRK6 can suppress neurite outgrowth and promote the formation of excitatory and inhibitory presynaptic structures (2, 5). Mice lacking SLITRK6 exhibit delayed retinal synaptogenesis and multiple auditory abnormalities as well as defective auditory sensory innervation, neuronal loss in the vestibular ganglia, and reduced cochlear expression of BDNF, NT-3, TrkB, and TrkC (3, 6, 7). In humans, nonsense mutations of SLITRK6 are associated with myopia and sensorial deafness (6).
- Aruga, J. et al. (2003) Gene 315:87.
- Aruga, J. and K. Mikoshiba (2003) Mol. Cell Neurosci. 24:117.
- Katayama, K.-I. et al. (2009) PLoS ONE 4:e7786.
- Morlet, T. et al. (2014) Laryngoscope. 124:95.
- Takahashi, H. et al. (2012) Nat. Neurosci. 15:389.
- Tekin, M. et al. (2013) J. Clin. Invest. 123:2094.
- Matsumoto, Y. et al. (2011) PLoS ONE 6:e16497.
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