Results 161 to 170 of about 130,723 (312)
FDA-approved drug repurposing screen identifies inhibitors of SARS-CoV-2 pseudovirus entry. [PDF]
Singh M+3 more
europepmc +1 more source
HDAC6 and USP9X Control Glutamine Metabolism by Stabilizing GS to Promote Glioblastoma Tumorigenesis
Glioblastoma (GBM) growth relies on glutamine synthetase (GS), which is stabilized by histone deacetylase 6 (HDAC6) and deubiquitinated by ubiquitin‐specific peptidase 9, X‐linked (USP9X). HDAC6 promotes GS deacetylation, while USP9X removes its K48‐linked polyubiquitination, enhancing GS stability.
Go Woon Kim+9 more
wiley +1 more source
Development of ketobenzothiazole-based peptidomimetic TMPRSS13 inhibitors with low nanomolar potency. [PDF]
Joushomme A+11 more
europepmc +1 more source
SUMOylation of SETD8 Promotes Tumor Growth by Methylating and Stabilizing MYC in Bladder Cancer
In bladder cancer (BC), MYC serves as a novel substrate of SETD8 to be methylated at lysine 412, which enhances MYC protein stability by preventing the CHIP‐mediated degradation and ultimately promotes tumor growth. SUMOylation of SETD8 leads to SETD8 stabilization and enhances MYC methylation.
Xia Zhang+11 more
wiley +1 more source
Machine Learning-Guided Screening and Molecular Docking for Proposing Naturally Derived Drug Candidates Against MERS-CoV 3CL Protease. [PDF]
Ouassaf M+4 more
europepmc +1 more source
EccDNA‐Driven VPS41 Amplification Alleviates Genotoxic Stress via Lysosomal KAI1 Degradation
Following ionizing radiation, eccDNA‐mediated VPS41 amplification slightly increases its expression but fails to prevent apoptosis. Introducing exogenous eccDNA or VPS41 enhances VPS41‐KAI1 interaction, promoting lysosomal degradation of KAI1. This process inhibits apoptotic signaling, enhancing cell survival and resistance to radiation‐induced damage.
Bin Shi+12 more
wiley +1 more source
Recombinant chymase inhibits fibrinolysis induced by endogenous plasmin in clotted human blood. [PDF]
Vincent L+8 more
europepmc +1 more source
Aortic dissection (AD) is accompanied by a decrease in CCDC80 in vascular smooth muscle cells (VSMCs). CCDC80 can interact with JAK2, and VSMC‐specific CCDC80 deficiency accelerates the progression of AD by activating the JAK2/STAT3 pathway involved in regulating the phenotype switching and function of VSMCs.
Qingqing Xiao+18 more
wiley +1 more source