Results 211 to 220 of about 902,749 (382)

Transcriptomic analysis at 48 h postmortem: a proof of concept for the identification of biomarkers to estimate time since death. [PDF]

open access: yesMol Biol Rep
Zepeta Flores N   +11 more
europepmc   +1 more source

Deacetylation of ACLY Mediates RNA M6A‐Modification of NOXA and Promotes Chemoresistance of Colorectal Cancer

open access: yesAdvanced Science, EarlyView.
This study investigates the deacetylation of ACLY at K978 acts as a novel risk in colorectal cancer chemoresistance. The deacetylation of K978 induces ACLY relocation to the nucleus and promotes its binding to RBM15, a m6A methylation modification “writer”.
Jun Wen   +8 more
wiley   +1 more source

m6A‐Modified circRAPGEF1 Interaction with IGF2BP3 Promotes Hepatocellular Carcinoma Progression via Reprogramming Aspartate Metabolism

open access: yesAdvanced Science, EarlyView.
In hepatocellular carcinoma (HCC), the m6A‐modified circRAPGEF1 destabilizes ASS1 mRNA via competitive binding to IGF2BP3, driving aspartate metabolic reprogramming in liver cancer stem cells (LCSCs). This cascade enhances stemness properties and reduces sorafenib sensitivity in LCSCs, thereby identifying circRAPGEF1 as a promising therapeutic target ...
Juanyi Shi   +13 more
wiley   +1 more source

The Gene Expression Profile of Human Umbilical Vein Endothelial Cells Stimulated by Tumor Necrosis Factor a Using DNA Microarray Analysis

open access: bronze, 2000
Takeshi Murakami   +11 more
openalex   +2 more sources

Single‐Cell Transcriptomics Reveals ITGA2‐Mediated Metabolic Reprogramming and Immune Crosstalk in Pediatric Thyroid Carcinogenesis

open access: yesAdvanced Science, EarlyView.
This study unveils ITGA2⁺ tumor cells as key drivers of pediatric thyroid cancer aggressiveness. These cells orchestrate dual oncogenic pathways: GLUT1‐mediated glycolytic reprogramming and M2 macrophage polarization. This metabolic‐immunological crosstalk promotes tumor progression and metastasis.
Zhi‐jun Zhan   +11 more
wiley   +1 more source

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