Regulates COPI-mediated retrograde protein traffic at the interface between the Golgi apparatus and the endoplasmic reticulum. Involved in the maintenance of the Golgi apparatus morphology. Has no detectable kinase activity in vitro. Homooligomer (By similarity). Interacts with GORAB. Interacts with COPA, COPB1 and COPB2. Interacts with AP2B1 (By similarity). Localized to the Endoplasmic reticulum-Golgi intermediate and cis-Golgi in an ARF1-independent manner. Expressed in diaphragm, quadriceps, thymus, liver, lung, spleen, kidney, heart and brain. Prominently expressed in neurons, and enriched at central nervous system synapses and neuromuscular junctions. The protein kinase domain is predicted to be catalytically inactive. Defects in Scyl1 are the cause of the muscle deficient phenotype (mdf). Mice exhibit progressive neuromuscular atrophy, hindlimb paralysis, gait ataxia, abnormal hindlimb posture and tremor. Pathology of mdf comprises cerebellar atrophy, Purkinje cell loss and optic nerve atrophy. Belongs to the protein kinase superfamily.