Results 191 to 200 of about 19,933,051 (310)

An RNA‐Binding Protein RBMS1 Promotes Endothelial Cell Autophagy to Maintain Vascular Homeostasis and Suppress Deep Vein Thrombosis

open access: yesAdvanced Science, EarlyView.
RBMS1, an RNA‐binding protein, restores vascular endothelial homeostasis by enhancing ATG3‐mediated autophagy, thereby attenuating thrombus formation and suggesting a potential avenue for further therapeutic exploration in DVT. ABSTRACT Deep vein thrombosis (DVT) is a prevalent vascular disorder characterized by aberrant coagulation within the deep ...
Chu Chu   +13 more
wiley   +1 more source

Macrophage PARP7 Alleviates Septic Cardiomyopathy by Interacting With TBK1 and Suppressing TBK1‐Driven Inflammatory Response

open access: yesAdvanced Science, EarlyView.
In septic cardiomyopathy, PARP7 directly binds TBK1 and mediates its ADP‐ribosylation, thereby repressing TBK1‐driven proinflammatory signaling in macrophages. ABSTRACT Septic cardiomyopathy is a life‐threatening complication of sepsis, and an uncontrolled inflammatory response represents a key pathogenic mechanism. PARP7 negatively regulates the IFN‐I
Jibo Han   +10 more
wiley   +1 more source

Restoration of m6A‐Modified circPSMB1 Suppresses Chordoma Progression and Enables Local Nanotherapeutic Intervention

open access: yesAdvanced Science, EarlyView.
An m6A‐modified circRNA, circPSMB1, is identified as a tumor suppressor in chordoma. METTL3‐dependent m6A promotes circPSMB1 interaction with HNRNPA2B1, limiting c‐MYC expression and malignant progression. An injectable HMnO2‐based nanohydrogel enables local circPSMB1 delivery and tumor microenvironment‐responsive therapy, offering a promising strategy
Yingchuang Tang   +7 more
wiley   +1 more source

OAF Blocks SIAH1‐Mediated Degradation of SCPX, a Therapeutic Strategy for MASLD

open access: yesAdvanced Science, EarlyView.
This study shows OAF directly binds to SCPX and inhibits its interaction with the E3 ligase SIAH1, thereby protecting SCPX from ubiquitin‐dependent degradation and stabilizing its levels. This OAF‐SCPX axis represents a novel pathway in lipid homeostasis, highlighting OAF as a promising therapeutic candidate for MASLD.
Zongxi Li   +11 more
wiley   +1 more source

Oncogene c‑Myc: From molecular mechanism to targeted therapy (Review). [PDF]

open access: yesMol Med Rep
Lu J   +7 more
europepmc   +1 more source

Natural Product Toosendanin Suppresses the Malignant Development of Skin Melanoma by Targeting BNC2 for Degradation

open access: yesAdvanced Science, EarlyView.
BNC2 exhibits context‐dependent opposing functions across multiple cancer types. This study reveals BNC2 as an oncogenic driver of melanoma proliferation and metastasis through transcriptional activation of PIK3CA. The natural compound TSN simultaneously degrades BNC2 and its oncogenic partner SMAD3 via CRBN‐dependent ubiquitination.
Hui Dai   +7 more
wiley   +1 more source

RFC5 and STAT3 form a transcriptional complex to drive NSCLC progression via c-Myc. [PDF]

open access: yesiScience
Yan J   +10 more
europepmc   +1 more source

Multi‐Technique Integration Identifies O‐GlcNAc Transferase in Fibroblast‐Like Synoviocytes as a Therapeutic Target for Rheumatoid Arthritis

open access: yesAdvanced Science, EarlyView.
AI‑guided single‑cell transcriptomics identifies OGT as a key regulator enriched in rheumatoid arthritis fibroblast‑like synoviocytes (RA‐FLSs). Inflammatory stimuli activate the OGT–SAP130 axis, which modulates the H3K27ac/H3K27me3 balance and epigenetically silences BTG2, promoting aggressive transformation of RA‑FLSs.
Duoli Xie   +14 more
wiley   +1 more source

YTHDC1 Orchestrates Glucose and Glutamate Rewiring to Overcome Lethal Metabolic Stress in Triple‐Negative Breast Cancer

open access: yesAdvanced Science, EarlyView.
Lai et al. find that m6A reader YTHDC1 is specifically overexpressed in triple‐negative breast cancer (TNBC) and orchestrates glucose and glutamine metabolism in an m6A‐dependent manner to confer robust adaptability to lethal metabolic stress. Leveraging YTHDC1 knockdown‐induced metabolic vulnerability, an ATF4 mRNA‐targeted nanotherapy is developed to
Zheng‐Hao Lai   +12 more
wiley   +1 more source

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