Results 221 to 230 of about 2,866,090 (303)

ACAT1‐Mediated SP1‐K694 Lactylation Promotes M1 Macrophage Polarization via TREM1 Transcription in COPD

open access: yesAdvanced Science, EarlyView.
Upon cigarette smoke exposure(CSE), LDHA expression is increased in lung macrophages, promoting the conversion of pyruvate to lactate and elevating the lactylation level of SP1 at the K694 site. This, in turn, enhances SP1 enrichment at the TREM1 promoter, increases TREM1 expression, promoted M1 macrophage polarization, and triggers the secretion of ...
Ling Lin   +5 more
wiley   +1 more source

AARS2‐SIRT5‐Driven DLD K445 Lactylation Promotes Cuproptosis Resistance in Glioblastoma Stem Cells

open access: yesAdvanced Science, EarlyView.
Lactylation of DLD at K445 by AARS2 suppresses PDH complex activity and reduces DLAT lipoylation, thereby conferring cuproptosis resistance in glioblastoma stem cells. SIRT5‐mediated delactylation restores PDH function and enhances cuproptosis sensitivity.
Mingtian Ding   +12 more
wiley   +1 more source

WFS1 Deficiency Impairs PIAS4‐Associated SUMOylation and Increases Ubiquitin‐Mediated Spermatogenesis‐Related Protein Degradation Leading to Testicular Male Infertility

open access: yesAdvanced Science, EarlyView.
The findings establish a critical role for WFS1 in human male fertility. Mechanistically, WFS1 interacts with PIAS4 to promote the SUMOylation of key spermatogenesis‐associated proteins, which in turn competitively inhibits their K48‐linked ubiquitin‐mediated degradation during spermatogenesis.
Yunchuan Tian   +14 more
wiley   +1 more source

PLOD1 Catalytic Activity Stabilizes ENO1 by Limiting FBXW7‐dependent Degradation to Promote Glycolysis and TMZ Resistance in Glioblastoma

open access: yesAdvanced Science, EarlyView.
PLOD1 interacts with ENO1 and limits its FBXW7‐dependent ubiquitination and proteasomal degradation through a mechanism requiring PLOD1 catalytic activity. ENO1 stabilization sustains glycolysis, promoting glioblastoma cell proliferation, migration, and temozolomide resistance.
Fen Xue   +4 more
wiley   +1 more source

Mitochondrial Protection and Neural Repair via ROS‐Responsive Biomimetic Nanoparticles in Intracerebral Hemorrhage

open access: yesAdvanced Science, EarlyView.
A ROS‐responsive biomimetic nanoparticle platform co‐delivers DIDS and Mdivi‐1 to protect mitochondria and promote neural repair after intracerebral hemorrhage. By targeting LPAR1/VDAC1‐related mitochondrial dysfunction, the nanotherapy reduces oxidative injury, neuronal apoptosis, and blood‐brain barrier disruption, improving neurological recovery and
Ling Gao   +7 more
wiley   +1 more source

Home - About - Disclaimer - Privacy