Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2003 Sep;24(1):117-29.
doi: 10.1016/s1044-7431(03)00129-5.

Identification and characterization of Slitrk, a novel neuronal transmembrane protein family controlling neurite outgrowth

Jun Aruga  1 , Katsuhiko Mikoshiba
Affiliations

Identification and characterization of Slitrk, a novel neuronal transmembrane protein family controlling neurite outgrowth

Jun Aruga et al. Mol Cell Neurosci. 2003 Sep.

Abstract

The Slitrk family consists of six structurally related transmembrane proteins (Slitrk1-6) in the mouse. In the extracellular region, they share two conserved leucine-rich repeat domains that have a significant homology to a secreted axonal growth-controlling protein, Slit. These proteins also have a homology to trk neurotrophin receptors in their intracellular domains, sharing a conserved tyrosine residue. Expression of Slitrk is highly restricted to neural tissues, but varies within the family. More specifically, Slitrk1 expression is in the mature neurons, whereas Slitrk2 is strongly expressed in the ventricular layer, and Slitrk6 shows compartmentalized expression in diencephalon. Over-expressed Slitrk1 induced unipolar neurites in cultured neuronal cells, whereas Slitrk2 and other Slitrk proteins inhibited neurite outgrowth. Deletion analysis showed that the functional difference between Slitrk1 and Slitrk2 lies in their intracellular domains, which are conserved in Slitrk2-6, but not in Slitrk1. These results suggest that the Slitrk proteins are the neuronal components that control the neurite outgrowth.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types

MeSH terms