Genetic Coding Variant in GPR65 Alters Lysosomal pH and Links Lysosomal Dysfunction with Colitis Risk
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- 作者：Kara G. Lassen1 ; 2 ; klassen@broadinstitute.org" class="auth_mail" title="E-mail the corresponding author ; Craig I. McKenzie3 ; Muriel Mari4 ; 5 ; Tatsuro Murano1 ; 2 ; Jakob Begun2 ; 6 ; 7 ; Leigh A. Baxt2 ; Gautam Goel2 ; Eduardo J. Villablanca1 ; 2 ; 6 ; Szu-Yu Kuo1 ; Hailiang Huang1 ; 8 ; Laurence Macia3 ; Atul K. Bhan9 ; 10 ; Marcel Batten11 ; Mark J. Daly1 ; 8 ; 10 ; Fulvio Reggiori4 ; 5 ; Charles R. Mackay3 ; Ramnik J. Xavier1 ; 2 ; 6 ; 10 ; xavier@molbio.mgh.harvard.edu" class="auth_mail" title="E-mail the corresponding author
- 刊名：Immunity
- 出版年：2016
- 出版时间：21 June 2016
- 年：2016
- 卷：44
- 期：6
- 页码：1392-1405
- 全文大小：3345 K
文摘
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Genomic screen identifies role for nine genes in IBD susceptibility loci in autophagy
Gpr65-deficient mice are more susceptible to bacteria-induced colitis
Loss of GPR65 results in accumulation of aberrant phagosomes and lysosomes
GPR65 IBD risk variant confers defects in lysosomal function and pathogen defense