Results 201 to 210 of about 2,804,092 (301)
LAPTM5 functions as a critical molecular scaffold bridging PGAM5 and VAMP to facilitate PGAM5‐mediated dephosphorylation of VAMP8. This cascade promotes autophagosome‐lysosome fusion, restores impaired autophagic flux, and clears damaged mitochondria, thereby mitigating cellular oxidative stress and systemic inflammation.
Lang Jiang +12 more
wiley +1 more source
Quality control in veterinary blood banks: evaluation of canine platelet concentrates stored for five days. [PDF]
Lasta CS +7 more
europepmc +1 more source
Drug Repurposing for Treating NCOR‐Related Intellectual Disability
An autism‐associated NCOR1 heterozygous mutation upregulates NRGs and activates NRG backward signaling in hypothalamic GABAergic neurons in mouse models, leading to Gabra2 downregulation and cognitive deficits, which can be therapeutically targeted by repurposing FDA‐approved drugs.
Yan Kong +15 more
wiley +1 more source
Banking feces: a new frontier for public blood banks? [PDF]
Jørgensen SMD +8 more
europepmc +1 more source
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
This diagram illustrates that MIIP suppresses tumor‐associated neutrophils infiltration and NETs formation by binding to PKR, which impairs the PKR–IKKβ interaction and attenuates NF‐κB/IL‐8 axis activation, thereby inhibiting colorectal cancer progression. This mechanism highlights a promising therapeutic target for CRC patients.
Jiaxin Li +8 more
wiley +1 more source
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
Diabetic bone defects remain a critical clinical challenge. A 3D‐printed BCPG‐MF@Y scaffold, embedding Yoda1‐functionalized manganese dioxide‐ferritin nanozymes, scavenges mtROS, suppresses the cGAS–STING pathway, and reverses cellular senescence, while Yoda1 activates Piezo1 to direct BMSCs fate to synergistically reprogram the osteoimmune ...
Qing‐Song Deng +16 more
wiley +1 more source

