Yanwen Xu

This study shows MYT1 and ST18 regulate human beta-cell survival and insulin secretion under normal and stress conditions, with their genes enriched for T2D-risk loci.

This study shows that METTL14 is essential for maintaining superficial stromal cells in the mouse uterus, which are necessary for embryo implantation.

The paper uses clonal analysis to reveal species-specific differences in intestinal regeneration and stem cell dynamics in mice and humans.

This study shows CTCF is essential for early decidualization by promoting HOXA11 expression, and its loss causes infertility in mice.

This study shows NAT10 stabilizes progesterone receptor mRNA via ac4C modification, essential for uterine function and fertility in humans and mice.

The paper shows that Myt3 translation is deregulated in β-cells under obesity-induced stress, leading to β-cell dysfunction and glucose intolerance.

This study shows Atf4 protects beta-cell function under high glucose but worsens beta-cell failure when combined with free fatty acids.

The paper identifies a pathobiont-epithelial IDO1 pathway that drives region-specific susceptibility to inflammatory bowel disease in the ascending colon.

The paper introduces NSC-seq, a CRISPR-based molecular clock to track temporal and clonal events in development and precancer, revealing polyancestral initiation in colonic precancers.

The paper identifies a novel epithelial cell type, LND, in Crohn's disease that is associated with immune dysregulation and disease activity.

This paper introduces NSC-seq, a direct sgRNA capture method for single-cell CRISPR screens using standard knockout libraries, and characterizes sgRNA expression in three whole-genome libraries.

The paper develops contamination-focused metrics and software to optimize scRNA-seq experiments by reducing ambient contamination through experimental adjustments.

This paper shows that deleting Mfn1 and Mfn2 in beta cells impairs mitochondrial structure and insulin secretion, but incretins can partially compensate through EPAC2 signaling.

This study shows that Myt transcription factors prevent over-activation of stress-response genes in pancreatic β cells, maintaining their function and survival.