Anne Grapin‐Botton

This study investigates how pancreatic progenitor cells respond to fluid shear stress, finding transcriptomic changes and reduced YAP1 activity.

This study identifies HNF1B and NPHP3 mutations as causes of a new pancreatic disease, ciliogenic pancreatopathy, characterized by acinar atrophy and adipose replacement, and links ciliary dysfunction to pancreatic dysfunction in humans and mice.

The paper investigates how lumen morphology in pancreatic organoids is controlled by the balance between cell proliferation rate and lumen pressure, showing that lower pressure and faster proliferation lead to more complex lumen shapes.

This paper uses a phase field model to predict organoid morphology by simulating cell division and lumenal pressure, identifying key parameters that determine shape and structure.

The paper compares lumen nucleation and fusion dynamics in three epithelial organoid systems under varying hydrostatic pressure conditions, revealing conserved self-organisation rules.

The paper introduces GEQO biosensors for absolute analyte quantification in single cells without requiring specialized equipment, showing they account for buffering and retain time trace information.

This paper develops a multicellular phase field model to simulate organoid morphology by integrating lumen pressure and cell proliferation, revealing how these factors determine organoid shapes and phenotypes.

The paper uses single-cell RNA-seq and live imaging to study NEUROG3 dynamics in human pancreatic endocrine progenitors, revealing differences in expression timing and proliferation patterns compared to mice.

The paper shows that apical restriction of VANGL in pancreatic ducts is essential for epithelial integrity, with loss of restriction causing cell death and extrusion.

This study identifies direct Hes1 target genes in pancreatic progenitor cells, revealing Notch signaling's role in repressing tip cell fate through repression of key regulators like Ptf1a and Gata4.