p66SHC is a pro-oxidant member of the SHC family of protein adaptors that acts as a negative regulator of cell survival. In lymphocytes p66SHC exploits both its adaptor and its reactive oxygen species (ROS)-elevating function to antagonize mitogenic and survival signaling and promote apoptosis. As a result, p66SHC deficiency leads to the abnormal expansion of peripheral T and B cells and lupus-like autoimmunity. Additionally, a defect in p66SHC expression is a hallmark of B cell chronic lymphocytic leukemia, where it contributes to the accumulation of long-lived neoplastic cells. We have recently provided evidence that p66SHC exerts a further layer of control on B cell homeostasis by acting as a new mitochondrial LC3-II receptor to promote the autophagic demise of dysfunctional mitochondria. Here we discuss this finding in the context of the autophagic control of B cell homeostasis, development, and differentiation in health and disease.

Onnis, A., Cassioli, C., Finetti, F., Baldari, C.T. (2020). Regulation of Selective B Cell Autophagy by the Pro-oxidant Adaptor p66SHC. FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY, 8 [10.3389/fcell.2020.00193].

Regulation of Selective B Cell Autophagy by the Pro-oxidant Adaptor p66SHC

Onnis, A.;Cassioli, C.;Finetti, F.;Baldari, C. T.
2020-01-01

Abstract

p66SHC is a pro-oxidant member of the SHC family of protein adaptors that acts as a negative regulator of cell survival. In lymphocytes p66SHC exploits both its adaptor and its reactive oxygen species (ROS)-elevating function to antagonize mitogenic and survival signaling and promote apoptosis. As a result, p66SHC deficiency leads to the abnormal expansion of peripheral T and B cells and lupus-like autoimmunity. Additionally, a defect in p66SHC expression is a hallmark of B cell chronic lymphocytic leukemia, where it contributes to the accumulation of long-lived neoplastic cells. We have recently provided evidence that p66SHC exerts a further layer of control on B cell homeostasis by acting as a new mitochondrial LC3-II receptor to promote the autophagic demise of dysfunctional mitochondria. Here we discuss this finding in the context of the autophagic control of B cell homeostasis, development, and differentiation in health and disease.
Onnis, A., Cassioli, C., Finetti, F., Baldari, C.T. (2020). Regulation of Selective B Cell Autophagy by the Pro-oxidant Adaptor p66SHC. FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY, 8 [10.3389/fcell.2020.00193].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/1108152