Abstract
Signaling through receptor tyrosine kinases (RTKs) is implicated in the control of various cellular functions. Immediately after activation, these RTKs are rapidly translocated from cell surface into the endosomal compartment. Then, these are sorted into lysosomes for degradation. Cbl-interacting protein of 85 kDa (CIN85) is a multiadaptor protein containing three Src homology 3 (SH3) domains, a proline-rich region and a coiled-coil domain. We have previously shown that CIN85 is involved in regulation of ligand-induced endocytosis of epidermal growth factor (EGF) receptors. To analyze the biological function of CIN85 in vivo, we generated the CIN85 knockout (KO) mouse. No significant effects of the mutation was detected on energy metabolism parameters (body weight, food consumption, feces production). CIN85 KO mice do not show any morphological phenotypes in the spleen, thymus or kidney. However, the corpus callosum (commissure of the cerebral hemispheres) was absent. Now we are analyzing the effect of this mutation [J Physiol Sci. 2008;58 Suppl:S83]
