Results 231 to 240 of about 349,794 (287)

SIRT5–RAC2 Axis Drives Monocyte‐to‐Macrophage Differentiation to Promote Inflammatory Injury in Premature Ovarian Insufficiency

open access: yesAdvanced Science, EarlyView.
SIRT5 desuccinylates and stabilizes RAC2, activating CSF1R‐dependent signaling to drive monocyte differentiation into M0 macrophages and their polarization toward pro‐inflammatory M1 phenotypes in CTX‐induced premature ovarian insufficiency. Inhibiting the SIRT5‐RAC2 axis attenuates inflammation, reduces granulosa cell apoptosis, and preserves ...
Wenjing TanTai   +15 more
wiley   +1 more source

Targeting c-Myc-p300-CARM1 complex induces ferroptosis and reduces CD8+ T cell exhaustion in esophageal squamous cell carcinoma. [PDF]

open access: yesInt J Biol Sci
Wang Y   +12 more
europepmc   +1 more source

Cytokine‐Engineered Chimeric Antigen Receptor‐T Cell Therapy: How to Balance the Efficacy and Toxicity

open access: yesAdvanced Science, EarlyView.
Cytokine‐engineered CAR‐T cells represent a promising immunotherapy against malignancies due to direct tumor killing and potent immunity response. However, significant toxicities, including CRS and ICANS, have restricted clinical applications. How to keep the risk‐benefit balance of the advanced therapy is of great importance for maximizing the benefit
Xinru Zhang   +7 more
wiley   +1 more source

Arginine Methylation Antagonizes TEAD3‐Mediated Repression to Promote Osteogenic Differentiation by Disrupting RUNX2‐Sequestrating Condensates

open access: yesAdvanced Science, EarlyView.
In the unmethylated state, TEAD forms stable, repressive condensates that sequester the osteogenic master regulator RUNX2. Arginine methylation of TEAD at R55 acts as a molecular brake, dissolving these condensates to release RUNX2 and activate the osteogenic program.
Lei Cao   +6 more
wiley   +1 more source

KDM4A promotes NEPC progression through regulation of MYC expression. [PDF]

open access: yesCancer Lett
Mak CSL   +37 more
europepmc   +1 more source

Chaperone‐Mediated Autophagic Degradation of USP9X in Macrophages Exacerbates Postmyocardial Infarction Inflammation and Cardiac Dysfunction

open access: yesAdvanced Science, EarlyView.
This study demonstrates that inflammatory stimuli induce the acetylation‐triggered, chaperone‐mediated autophagic degradation of ubiquitin‐specific peptidase 9 X‐linked (USP9X) in macrophages. USP9X acts as a macrophage “inflammation switch” after myocardial infarction (MI). USP9X loss destabilizes tumor necrosis factor receptor‐associated factor (TRAF)
Biqing Wang   +7 more
wiley   +1 more source

Targeted Mitochondrial ECSIT Overexpression Attenuates MASH by Increasing OTUD3 Expression

open access: yesAdvanced Science, EarlyView.
Mitochondrial ECSIT expression is reduced during MASH pathogenesis. Overexpression of mitochondrial ECSIT mitigates steatohepatitis and maintains hepatic metabolic homeostasis. Mechanistically, ECSIT enhances intramitochondrial OTUD3 expression to stabilize SIRT3 through deubiquitination, thus preserving mitochondrial function and impeding disease ...
Yuqing Jiang   +11 more
wiley   +1 more source

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