Results 111 to 120 of about 147,336 (310)
SETDB1 is progressively downregulated in ALD, correlating with disease severity. SETDB1 deficiency impairs LAP by disrupting Rubicon membrane localization, leading to defective lipid droplet clearance. Concurrently, loss of SETDB1 reduces nuclear LC3B, causing R‐loop accumulation and cGAS‐STING‐driven inflammation. Lipidated LC3B mediates LAP‐dependent
Yi Zhang +17 more
wiley +1 more source
TRMT6‐mediated m1A modification in CDK9 mRNA enhances its mRNA stability and translation efficiency, thereby increasing the protein levels of CDK9. Upregulated CDK9 promotes the progression of HCC by elevating the levels of oncogenic factors including p‐STAT3, MCL1, and BCL‐2. On the other hand, CDK9 phosphorylates TARDBP at Ser254 to activate HBV core
Rui Zhang +12 more
wiley +1 more source
A genome‐wide microRNA CRISPR screen identifies miR‐18a as a master regulator of cross‐resistance in melanoma. Loss of miR‐18a activates the AJUBA–YAP/Hippo axis to confer BRAFi resistance and enhances THBS1–CD47 interaction to impair CD8+ T cell immunity. hnRNP A1 is identified as an upstream regulator of miR‐18a processing.
Zhao Wang +19 more
wiley +1 more source
A Rare Allele of ST5 From Wild Rice Enhances Salt Tolerance in Rice
A novel salt‐tolerance gene ST5W, characterized by a unique 36‐bp promoter insertion, is found exclusively in a small subset of Oryza rufipogon and is absent in cultivated rice. Field trials confirm ST5W significantly enhances rice yield across diverse genetic backgrounds under saline conditions.
Meng Xing +26 more
wiley +1 more source
Targeting the PDK1/c‐Myc/SOX10 Signaling in Oligodendrocytes Alleviates Neuropathic Pain
This work reveals that oligodendrocyte homeostasis, mediated by PDK1, is a critical determinant of neuropathic pain (NPP) pathogenesis. Disruption of PDK1 in oligodendrocytes impairs SOX10‐dependent myelination programs through c‐Myc accumulation, leading to disrupted myelination and the pathophysiology of NPP.
Pingping Qiao +7 more
wiley +1 more source

