Results 241 to 250 of about 645,043 (338)

CCDC80 Protects against Aortic Dissection and Rupture by Maintaining the Contractile Smooth Muscle Cell Phenotype

open access: yesAdvanced Science, EarlyView.
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

TP53 minigene analysis of 161 sequence changes provides evidence for role of spatial constraint and regulatory elements on variant-induced splicing impact. [PDF]

open access: yesNPJ Genom Med
Canson DM   +7 more
europepmc   +1 more source

Inhibiting FAT1 Blocks Metabolic Bypass to Enhance Antitumor Efficacy of TCA Cycle Inhibition through Suppressing CPT1A‐Dependent Fatty Acid Oxidation

open access: yesAdvanced Science, EarlyView.
This study demonstrates that mutant FAT1 promotes ASCL2‐driven, CPT1A‐dependent fatty acid oxidation, leading to resistance to CPI‐613‐mediated TCA cycle inhibition in head and neck cancer. In vivo gene depletion of mutant FAT1 with LNP‐sgFAT1 suppresses tumor growth and restores CPI‐613 sensitivity, revealing a targetable metabolic bypass with ...
Fanghui Chen   +11 more
wiley   +1 more source

Gasdermin D‐Mediated Pyroptosis Exerts Two Opposite Effects of Resisting Enzymatic Digestion and Expanding Inflammatory Response in Acute Pancreatitis

open access: yesAdvanced Science, EarlyView.
Gasdermin D (GSDMD) does not only reduce pancreatic enzyme synthesis but also induces pancreatic acinar cells to express mucin 1 (MUC1), which forms a barrier to prevent digestive enzyme‐mediated digestion. However, GSDMD can promote the secretion of inflammatory cytokines by macrophages and aggravate pancreatic histological injury by expanding ...
Chaoxu Liu   +10 more
wiley   +1 more source

DDX3 Regulates the Cap‐Independent Translation of the Japanese Encephalitis Virus via Its Interactions with PABP1 and the Untranslated Regions of the Viral Genome

open access: yesAdvanced Science, EarlyView.
Japanese encephalitis virus (JEV) employs a cap‐independent (CI) translation strategy to evade host translational shutoff. During the shut‐off of host cellular canonical translation, DEAD‐box protein 3 (DDX3) bind to JEV UTRs to establish a closed‐loop architecture, and its interaction with poly(A)‐binding protein 1 (PABP1) to form DDX3/PABP1/eIF4G ...
Chenxi Li   +13 more
wiley   +1 more source

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