Disease relevance of SCD5

• A search was made for predictors of sudden cardiac death (SCD) among 197 men, age 40 to 79, who had multiphasic health checkups and experienced SCD 2 days to 5 1/2 years later (mean 18.1 months) [1].

High impact information on SCD5

• Unlike wild-type mice, SCD1-deficient mice failed to elevate the hepatic triglyceride monounsaturated acid (MUFA)/saturated fatty acid (SFA) ratio despite induction of the SCD2 gene [2].
• The pericentric inversion disrupts a gene (ACOD4) on chromosome 4q21 that codes for a novel acyl-CoA desaturase enzyme [3].
• The 3.0 kb human ACOD4 cDNA spans approximately 170 kb and is composed of five exons of ACOD4 [3].
• These data suggested that hSCD5 plays a role distinct from that of hSCD1 during development and in normal physiological conditions [4].
• Additionally, hSCD2 transcripts from adult and foetal tissues exhibit different sizes because of alternative splicing in the non-coding region, suggesting that hSCD2 expression is developmentally regulated [5].

Biological context of SCD5

• Interactions between Cdc42 and the scaffold protein Scd2: requirement of SH3 domains for GTPase binding [6].
• A homologous region in the stearoyl-CoA desaturase gene 2 (SCD2) promoter also mediated PUFA-specific repression in transfection experiments [7].

Anatomical context of SCD5

• Microsome fractions prepared from hSCD1 and hSCD5 transfected cells displayed similar delta 9 desaturase activity [4].

Analytical, diagnostic and therapeutic context of SCD5

• In the present study, we show using isothermal titration calorimetry that Scd2 binds two molecules of active GTP-bound Cdc42 simultaneously, but independently of one another [6].

References