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Protein Names: Tumor necrosis factor ligand superfamily member 6 (Apoptosis antigen ligand) (APTL) (CD95 ligand) (CD95-L) (Fas antigen ligand) (Fas ligand) (Fas L) (CD antigen CD178) [Cleaved into: Tumor necrosis factor ligand superfamily member 6, membrane form, Tumor necrosis factor ligand superfamily member 6, soluble form (Receptor-binding Fas L ectodomain) (Soluble Fas ligand) (s Fas L), ADAM10-processed Fas L form (APL), Fas L intracellular domain (Fas L ICD) (SPPL2A-processed Fas L form) (SPA)] Gene Names: FASLG APT1LG1 CD95L FASL TNFSF6 Subunits: Homotrimer (Probable).Interacts with ARHGAP9, BAIAP2L1, BTK, CACNB3, CACNB4, CRK, DLG2, DNMBP, DOCK4, EPS8L3, FGR, FYB, FYN, HCK, ITK, ITSN2, KALRN, LYN, MACC1, MIA, MPP4, MYO15A, NCF1, NCK1, NCK2, NCKIPSD, OSTF1, PIK3R1, PSTPIP1, RIMBP3C, SAMSN1, SH3GL3, Subcellular Location: Cell membrane Interaction: FAS Summary: Fas ligand (TNF superfamily, member 6) encoded by FASLG is the ligand for FAS. Interaction of FAS with this ligand is critical in triggering apoptosis of some types of cells such as lymphocytes. Immunol., 2016 Aug, 185(2) Differential regulation of mi R-146a/FAS and mi R-21/FASLG axes in autoimmune lymphoproliferative syndrome due to FAS mutation (ALPS-FAS).[Abstract]Most cases of autoimmune lymphoproliferative syndrome (ALPS) have an inherited genetic defect involving apoptosis-related genes of the FAS pathway.
This is the first report on mi RNAs in ALPS patients.Ning Sun, Yihan Li, Yiyun Cai, Jing Chen, Yuan Shen, Jing Sun, Zheng Zhang, Jiulong Zhang, Lina Wang, Liyang Guo, Lei Yang, Li Qiang, Yanchun Yang, Gang Wang, Bo Du, Jing Xia, Han Rong, Zhaoyu Gan, Bin Hu, Jiyang Pan, Chang Li, Shufan Sun, Wei Han, Xue Xiao, Lei Dai, Guixing Jin, Yutang Zhang, Lixin Sun, Yunchun Chen, Haiying Zhao, Yamei Dang, Shenxun Shi, Kenneth S.Kendler, Jonathan Flint, Kerang Zhang Lina Wang, Dongdong Qiao, Yihan Li, Liwei Wang, Jianer Ren, Kangmei He, Jing Sun, Zhoubing Wang, Tian Tian, Ce Chen, Lei Yang, Jian Hu, Hong Deng, Qian Wang, Keqing Li, Jiyang Han, Han Rong, Zhaoyu Gan, Hong Yang, Pingliang Zhou, Jiyang Pan, Cong Zhou, Yanping Cui, Libo Song, Yuzhang Zhu, Ying Li, Xueyi Wang, Lanxian Ye, Wei Liang, Yunchun Chen, Qingjun Tang, Jing Guan, Shenxun Shi, Kenneth S.Function: Cytokine that binds to TNFRSF6/FAS, a receptor that transduces the apoptotic signal into cells.May be involved in cytotoxic T-cell mediated apoptosis and in T-cell development.TNFRSF6/FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both.
Binding to the decoy receptor TNFRSF6B/Dc R3 modulates its effects.
Disease: Defects in FASLG are the cause of autoimmune lymphoproliferative syndrome type 1B (ALPS1B) [MIM:601859]; also known as Canale-Smith syndrome (CSS).
ALPS is a childhood syndrome involving hemolytic anemia and thrombocytopenia with massive lymphadenopathy and splenomegaly.
We studied a mother and son carrying the same FAS cell surface death receptor (FAS) mutation, but with only the son manifesting the signs and symptoms of ALPS-FAS.
The aim was to analyse, by reverse transcription-quantitative polymerase chain reaction (RT-q PCR), the peripheral blood mononuclear cells (PBMC) relative expression of mi R-146a and mi R-21, including their passenger strands and respective targets (FAS and FASLG).
In comparison with healthy matched control individuals, mi R-21-3p was over-expressed significantly (P = 0·0313) in the son, with no significant change in the expression of mi R-146a, mi R-146a-3p and mi R-21.