Disruption of Serinc1, which facilitates serine-derived lipid synthesis, fails to alter macrophage function, lymphocyte proliferation or autoimmune disease susceptibility

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• 作者：Edward P.F. Chu^a ; ^b ; Colleen M. Elso^a ; Abigail H. Pollock^c ; ^d ; May A. Alsayb^a ; ^b ; Leanne Mackin^a ; Helen E. Thomas^a ; ^b ; Thomas W.H. Kay^a ; ^b ; Pablo A. Silveira^e ; ^f ; Ashley S. Mansell^g ; ^h ; Katharina Gaus^c ; ^d ; Thomas C. Brodnicki^a ; ^b ; ^{tbrodnicki@svi.edu.au}
• 关键词：Serinc/SERINC/SERINC ; serine incorporator ; TDE2 ; tumor differentially expressed 2 ; BM-MΦs ; bone marrow derived macrophages ; gt ; gene-trap ; ANA ; anti-nuclear antibodies ; LPS ; lipopolysaccharide
• 刊名：Molecular Immunology
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：82
• 期：Complete
• 页码：19-33
• 全文大小：4556 K
• 卷排序：82

文摘

Serinc1, 2, 3 and 5 transcripts are expressed in macrophages and lymphocytes. Serinc1 deficiency does not affect lipid composition in macrophages and lymphocytes. Serinc1 deficiency does not alter macrophage function or lymphocyte proliferation. Serinc1-deficient mice do not exhibit altered susceptibility to autoimmune disease. SERINC family members may play redundant roles in immune cell function.