Results 241 to 250 of about 4,334,118 (337)

Single-cell multi-omics identifies metabolism-linked epigenetic reprogramming as a driver of therapy-resistant medulloblastoma. [PDF]

open access: yesNat Commun
Veo B   +11 more
europepmc   +1 more source

Metformin promotes mitochondrial integrity through AMPK‐signaling in Leber's hereditary optic neuropathy

open access: yesFEBS Open Bio, EarlyView.
Metformin mediates mitochondrial quality control in Leber's hereditary optic neuropathy (LHON) fibroblasts carrying mtDNA mutations. At therapeutic levels, metformin activates AMPK signaling to restore mitochondrial dynamics by promoting fusion and restraining fission, while preserving mitochondrial mass, enhancing autophagy/mitophagy and biogenesis ...
Chatnapa Panusatid   +3 more
wiley   +1 more source

Engineering tandem VHHs to target different epitopes to enhance antibody‐dependent cell‐mediated cytotoxicity

open access: yesFEBS Open Bio, EarlyView.
Tandem VHH targeting distinct EGFR epitopes were engineered into a monovalent bispecific antibody (7D12‐EGA1‐Fc) with more potent ADCC without increasing affinity to EGFR. Structural modeling of 7D12‐EGA1‐Fc showed cross‐linking of separate EGFR domains to enhance CD16a engagement on NK cells.
Yuqiang Xu   +5 more
wiley   +1 more source

FGFR Like1 drives esophageal cancer progression via EMT, PI3K/Akt, and notch signalling: insights from clinical data and next‐generation sequencing analysis

open access: yesFEBS Open Bio, EarlyView.
Clinical analysis reveals significant dysregulation of FGFRL1 in esophageal cancer (EC) patients. RNAi‐coupled next‐generation sequencing (NGS) and in vitro study reveal FGFRL1‐mediated EC progression via EMT, PI3K/Akt, and Notch pathways. Functional assays confirm its role in tumor growth, migration, and invasion.
Aprajita Srivastava   +3 more
wiley   +1 more source

Chromatin architecture reprogramming reveals novel epigenetic dependencies in breast cancer. [PDF]

open access: yesGenes Dev
Garcia-Martinez L   +10 more
europepmc   +1 more source

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