Results 291 to 300 of about 635,202 (354)

Synergistic Effects of Insulin-like Growth Factor-1 and Platelet-Derived Growth Factor-BB in Tendon Healing. [PDF]

open access: yesInt J Mol Sci
Rieber J   +7 more
europepmc   +1 more source

Unraveling the Morphological and Functional Maturation Mechanisms Underlying Human Neural Development Using iPSCs‐Derived Neuronal Model

open access: yesAdvanced Science, EarlyView.
Using human induced pluripotent stem cells (hiPSCs)‐derived neuronal model, Tian and colleagues reveal that voltage‐gated calcium channels Cav1.2 and Cav1.3, and their mediated calcium ion influx, are essential for early morphogenesis of human neuronal development, while ECEL1 underlies human neuronal functional developmental maturation through CALM3 ...
Yue Tian   +5 more
wiley   +1 more source

Serum Insulin-Like Growth Factor 1 and the Prognosis of Patients With Advanced Liver Diseases: A Meta-Analysis. [PDF]

open access: yesClin Transl Gastroenterol
Liu Y   +7 more
europepmc   +1 more source

WDR5‐H3K4me3 Epigenetic Axis Promotes TRMT6‐Dependent tRNA M1A Modification to Facilitate Triple‐Negative Breast Cancer Progression by Suppressing Ferroptosis

open access: yesAdvanced Science, EarlyView.
Upregulated TRMT6 forms aberrant hypermethylation of a specific tRNA pool and serves as a predictor of poor prognosis in TNBC. This m1A modification in tRNAs enhances translation of FTH1 and FTL, reducing the pool of bioavailable Fe2⁺. Reduced Fe2+ availability impairs RSL3‐induced lipid peroxidation and tumor progression.
Yuqing Lei   +12 more
wiley   +1 more source

Dual Targeting of Mutant p53 and SNRPD2 via Engineered Exosomes Modulates Alternative Splicing to Suppress Ovarian Cancer

open access: yesAdvanced Science, EarlyView.
Mutant p53 drives oncogenic splicing to promote the progression of ovarian cancer by partnering with the spliceosome factor SNRPD2. Therefore, it is engineered iRGD‐exosomes to co‐deliver siRNAs against both targets. This approach restored tumor‐suppressive mRNA isoforms, effectively enhanced sensitivity to cisplatin, and ultimately blocked tumor ...
Wei Zhao   +14 more
wiley   +1 more source

Metabolic Reprogramming Driven by Trophoblasts and Decidual XCR1+PMN‐MDSC Crosstalk Controls Adverse Outcomes Associated With Advanced Maternal Age

open access: yesAdvanced Science, EarlyView.
The interaction between trophoblasts and decidual polymorphonuclear myeloid‐derived suppressor cells (dPMN‐MDSCs) via the XCL1–XCR1 axis is crucial for fetal development during the third trimester. Disruption of this axis impairs FOXO1 activity and causes metabolic imbalance in dPMN‐MDSCs, contributing to adverse outcomes associated with advanced ...
Meiqi Chen   +12 more
wiley   +1 more source

Flipping the Switch: MeCP2‐Mediated Lactylation Rewires Microglial Metabolism and Inflammation via the HK2/mTOR Axis in Poststroke Neuroinflammation

open access: yesAdvanced Science, EarlyView.
Stroke‐induced lactate accumulation promotes p300‐mediated lactylation of methyl‐CpG binding protein 2 (MeCP2) at lysine 210, which reprograms microglial metabolism toward glycolysis and activates the hexokinase 2 (HK2)/mTOR axis. This cascade promotes proinflammatory responses and impairs neurofunctional outcomes.
Zengyu Zhang   +12 more
wiley   +1 more source

Discovery of a Novel DNMT1 Inhibitor with Improved Efficacy in Treating β‐Thalassemia

open access: yesAdvanced Science, EarlyView.
Context of Research: β‐thalassemia affects millions worldwide. DNMT inhibitors are effective HbF‐inducers that benefit patients with β‐thalassemia. Existing DNMT inhibitors are not approved for β‐thalassemia treatment due to dose‐limiting toxicity.What We Find: DMT207 traps DNMT1 into helix‐kinked inactive conformation and enhances its interaction with
Yijie Shen   +19 more
wiley   +1 more source

Cancer Stem Cells Shift Metabolite Acetyl‐Coenzyme A to Abrogate the Differentiation of CD103+ T Cells

open access: yesAdvanced Science, EarlyView.
Lei et al. demonstrate that cancer stem cells (CSCs) play a pivotal role in impairing the differentiation of CD103+ T cells in patients with non‐small‐cell lung cancer. The key mechanism involves CSC‐derived acetyl‐CoA, which disrupts CD103+ T cell differentiation by sequentially inducing acetylation and ubiquitination of the Blimp‐1 protein. Targeting
Jiaxin Lei   +10 more
wiley   +1 more source

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