Article
The Alzheimer's disease-protective CD33 splice variant mediates adaptive loss of function via diversion to an intracellular pool.
The Journal of biological chemistry - 15 Sept 2017
Siddiqui Shoib S, Springer Stevan A, Verhagen Andrea, Sundaramurthy Venkatasubramaniam, Alisson-Silva Frederico, Jiang Weiping, Ghosh Pradipta, Varki Ajit
Abstract excerpt
The immunomodulatory receptor Siglec-3/CD33 influences risk for late-onset Alzheimer's disease (LOAD), an apparently human-specific post-reproductive disease. CD33 generates two splice variants: a full-length CD33M transcript produced primarily by the "LOAD-risk" allele and a shorter CD33m isoform lacking the sialic acid-binding domain produced primarily from the "LOAD-protective" allele. An SNP that modulates...
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