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- W4387197372 abstract "The role of FasL in initiating death signals through Fas is well characterized. However, the ‘reverse’ signaling pathway downstream of FasL in effector lymphocytes is poorly understood. Here, we identify that FasL functions as an independent activation receptor in NK cells. Activation via FasL results in the production of IFN-, GM-CSF, RANTES, MIP-1 , and MIP1- Proximal signaling of FasL requires Lck and Fyn Upon activation, FasL facilitates the phosphorylation of PI(3)K-p85/p55 subunits. A catalytically inactive PI(3)K-p110D910A mutation significantly impairs the cytokine and chemokine production by FasL. Activation of ITK and LAT downstream of FasL plays a central role in recruiting and phosphorylating PLC-2. Importantly, Fyn-mediated recruitment of ADAP links FasL to the Carma1/Bcl10/Tak1 signalosome. Lack of Carma1, CARD domain of Carma1, or Tak1 significantly reduces FasL-mediated cytokine and chemokine production. These findings, for the first time, provide a detailed molecular blueprint that defines FasL-mediated ‘reverse signaling’." @default.
- W4387197372 created "2023-09-30" @default.
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- W4387197372 date "2023-01-01" @default.
- W4387197372 modified "2023-09-30" @default.
- W4387197372 title "Novel PI(3)K-p85/p110-ITK-LAT-PLC-2 and Fyn-ADAP-Carma1-TAK1 pathways define ‘reverse signaling' via FasL" @default.
- W4387197372 doi "https://doi.org/10.1615/critrevimmunol.2023049638" @default.
- W4387197372 hasPublicationYear "2023" @default.
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