Results 301 to 310 of about 407,038 (348)

SUMOylation of SETD8 Promotes Tumor Growth by Methylating and Stabilizing MYC in Bladder Cancer

open access: yesAdvanced Science, EarlyView.
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

DHX9 helicase impacts on splicing decisions by modulating U2 snRNP recruitment in Ewing sarcoma cells. [PDF]

open access: yesNucleic Acids Res
Frezza V   +5 more
europepmc   +1 more source

Rational Design and Organoid‐Based Evaluation of a Cocktail CAR‐γδ T Cell Therapy for Heterogeneous Glioblastoma

open access: yesAdvanced Science, EarlyView.
A novel “prof” cocktail therapy is designed. It screens antigens, selects personalized antigen panels, engineers optimized CAR‐Vδ1 T cells, and tests in patient‐derived GBM organoids, offering hope for effective CAR‐T drugs against heterogeneous solid tumors. Abstract Various challenges, including tumor heterogeneity and inadequate T cell infiltration,
Guidong Zhu   +12 more
wiley   +1 more source

EccDNA‐Driven VPS41 Amplification Alleviates Genotoxic Stress via Lysosomal KAI1 Degradation

open access: yesAdvanced Science, EarlyView.
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

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

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