2019年5月13日 · A20 MYC-KO mice spontaneously develop inflammatory joint pathology resembling rheumatoid arthritis, which is characterised by immune cell infiltration, bone erosion and cartilage destruction,...

A20, also known as TNFAIP3, is a potent regulator of ubiquitin (Ub) dependent signals. A20 prevents multiple human diseases, indicating that the critical functions of this protein are clinically as well as biologically impactful.

2020年3月16日 · Here, we find that mice expressing three distinct targeted mutations of A20’s zinc finger 7 (ZF7) ubiquitin-binding motif uniformly developed digit arthritis with features common to psoriatic...

2012年10月12日 · This study showed that mice with A20-deficient myeloid cells spontaneously develop severe polyarthritis, providing potential pathophysiological mechanisms that may underlie the link between ...

2021年9月21日 · Here, we find that myeloid-specific A20-deficient mice are protected from diet-induced obesity and insulin resistance despite an inflammatory environment in their metabolic tissues. Macrophages lacking A20 show impaired mitochondrial respiratory function and metabolize more palmitate both in vitro and in vivo.

2014年7月16日 · In this study, we investigated the brain phenotype of A20 heterozygous (HT) and knockout (KO) mice. The inflammatory status of A20 wild type (WT), HT and KO brain was determined by immunostaining, quantitative PCR, and Western blot analysis. Cytokines secretion was evaluated by ELISA.

2024年4月12日 · A20 myel-KO mice are characterized by persistent Trichuris muris infection and intestinal inflammation. Myeloid A20 deficiency induces strong classical macrophage polarization which impedes anti-helminth type-2 immune activation; however, it promotes detrimental Th1/Th17 responses.

2019年12月12日 · We confirm that A20 in myeloid cells limits hypertension by restraining T cell activation during renin-angiotensin system (RAS) stimulation. Mechanistically, A20 in myeloid cells restricts the generation of pro-hypertensive cytokines, including TNF-α and IFN-γ, in CD8 + rather than CD4 + T cells that accumulate in the kidney during hypertension.

2025年3月5日 · This study investigated the involvement of A20 signaling alterations in podocytes in the development of kidney injury. The phenotypes of A20Δpodocyte (podocyte-specific knockout of A20) mice were compared with those of control mice at 6 months of age to identify spontaneous changes in kidney function.

The use of A20-deficient mice and RNA interference technologies has revealed the crucial role of A20 in a variety of pathogen- and cytokine-induced signaling pathways. Mice lacking A20 are born at normal mendelian ratios but die shortly after birth due to massive multiorgan inflammation, indicative of a key role for A20 in immune homeostasis of ...