SLITRK3 / Unconjugated /
Product Details
Description | SLIT and NTRK-like family 3 (Slitrk3) is a member a protein family consisting of six homologous transmembrane proteins (Slitrk1-6) that share two conserved leucine-rich repeat domains in the extracellular domain and have significant homology to Slit, a secreted axonal growth-controlling protein. These proteins are also homologous to trk neurotrophin receptors in their intracellular domains. Expression of Slitrk proteins is highly restricted to neural and brain tumor tissues, but varies within the protein family. Like every other Slitrk protein except Slitrk1, overexpression of Slitrk3 inhibited neurite outgrowth in cultured neurons, suggesting that these proteins are involved in the control of neurite outgrowth. This antibody is predicted to have no cross-reactivity to other Slitrk proteins. | |
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Conjugate | Unconjugated | |
Clone | ||
Target Species | Human, Mouse | |
Applications | ELISA, WB, IHC | |
Supplier | Aviva Systems Biology | |
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About SLITRK3
This gene encodes a member of the Slitrk family of structurally related transmembrane proteins that are involved in controlling neurite outgrowth. The encoded protein contains two leucine-rich repeat (LRR) domains and a C-terminal domain that is partially similar to Trk neurotrophin receptor protein. Enhanced expression of this gene was found in tissue from several different types of tumors. Alternative splicing results in multiple transcript variants, all encoding the same protein. [provided by RefSeq, Jan 2016]
This gene encodes a member of the Slitrk family of structurally related transmembrane proteins that are involved in controlling neurite outgrowth. The encoded protein contains two leucine-rich repeat (LRR) domains and a C-terminal domain that is partially similar to Trk neurotrophin receptor protein. Enhanced expression of this gene was found in tissue from several different types of tumors. Alternative splicing results in multiple transcript variants, all encoding the same protein. [provided by RefSeq, Jan 2016]
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