IndraLab

Statements


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sparser
"In future studies, determining the precise role and mechanisms by which A20 inhibits cell death promises to be an exciting avenue of research."

eidos
"CYLD unravels M1 chains , increasing the sensitivity of cells to TNF-induced cell death , whereas A20 prevents the removal effect , thus inhibiting cell death ( Elliott et al ., 2021 ) ."

reach
"The phenotype of this patient characterized by autoinflammation might be explained by increased cell proliferation and cell death caused by reduced TNFAIP3 (A20) expression."

sparser
"We considered two major hypotheses, how the increased NF-κB activation of A20-deficient pathogen-specific CD8 + T cells might cause reduced numbers of T EM and T CM : (i) A20 regulates the development of SLEC and MPEC CD8 + T cells, and (ii) A20 inhibits cell death and enables persistence of CD8 + T cells."

sparser
"Therefore, A20 inhibits RIP3-dependent necroptotic cell death. xref This finding sheds new light on the importance of RIP3 ubiquitination in the process of necroptosis ( xref )."

sparser
"Although most studies have focused on the role of A20 in the inhibition of NF-κB and inflammatory signaling, little is known about how A20 inhibits cell death."

sparser
"Given that A20 inhibits T effector cell death in CD4 + T cells, unleashing T effector cell–mediated inflammatory activity, our data complement the picture of A20 as a potent regulator of T cell–mediated inflammation, inducing T effector cell survival while reducing T reg cell generation."

eidos
"While the cell biological mechanisms by which A20 restricts cell death remain incompletely understood , some clues are provided by the observations that several death signaling proteins undergo physiological ubiquitination , and ubiquitinated death signaling complexes are dependent upon A20 ."

reach
"Upon searching the microarray for candidate genes involved in apoptosis downstream of PGC-1alpha4, we identified Birc2 (Ciap1) and Tnfaip3 (also known as A20), two anti-apoptotic proteins that prevent cell death downstream of inflammatory signaling."