Results 201 to 210 of about 1,337,477 (299)

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

Reversing the great degradation of nature by reducing factors related to cropland expansion. [PDF]

open access: yesProc Natl Acad Sci U S A
Polasky S   +8 more
europepmc   +1 more source

[Parallel import of drugs].

open access: yesTidsskrift for den Norske laegeforening : tidsskrift for praktisk medicin, ny raekke, 1999
T, Rygnestad, G, Fredriksen, O, Spigset
openaire   +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

Chemotherapy‐Activated GSK3β‐DNMT1 Signaling Upregulates CD47 to Evade Macrophage Phagocytosis and Drive Temozolomide Resistance in Glioblastoma

open access: yesAdvanced Science, EarlyView.
Temozolomide treatment activates GSK3β, driving DNMT1 phosphorylation, destabilization, and CD47 promoter hypomethylation in glioblastoma. This epigenetic shift upregulates CD47, enabling TMZ‐treated GBM cells to evade macrophage phagocytosis, survive chemotherapy, and acquire resistance.
Jie Li   +11 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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