Thomas R. Benzing

This study investigates actin reorganization and junctional remodeling in podocyte foot process effacement using advanced imaging techniques and shows reversible changes in actin and slit diaphragm proteins during nephrotoxic serum nephritis.

This paper shows that GLIS2 is essential for the DNA damage response in kidney cells, leading to DNA damage and cystic kidney disease in a mouse model.

This study identifies MAGI2 as a conserved biomarker for podocyte injury, showing its downregulation in glomerular diseases and differential expression in primary vs secondary FSGS.

The paper introduces a red fluorescent Lifeact marker to study actin morphology in podocytes using intravital imaging and super-resolution microscopy.

The paper develops single-cell damage scores to quantify cellular deterioration in degenerative diseases and applies them to murine and human datasets to identify molecular trajectories of damage.

The paper correlates calcium multiphoton imaging with STED imaging of the slit diaphragm in the same glomerulus to study kidney disease mechanisms.

This study shows that loss of Bbs8 in mice causes cystic kidney disease by reducing ciliary alpha-tubulin acetylation through increased HDAC2 activity.

This paper identifies a VHL-1/HIF-1/SQRD-1/COL-88 axis linking extracellular matrix formation with longevity in C. elegans, showing that loss of VHL-1 increases lifespan and alters collagen expression.

This study identifies aging-associated increases in transcriptional elongation speed across multiple species and shows that reducing this speed extends lifespan.

This paper introduces a fast and simple optical clearing and swelling protocol for 3D visualization of kidney ultrastructure using conventional confocal microscopy.

This study identifies PCK2 as a biomarker for renal function 12 months after living donor kidney transplantation using proteomic analysis of urinary extracellular vesicles.

The paper presents a comprehensive analysis of AATF's RNA interactions, revealing its role in ribosome biogenesis through binding to pre-rRNA and mRNAs of ribosome factors.

The paper develops a method to analyze individual nephron proteomes in kidney disease, identifying lysosomal protein overexpression as a key mechanism in proteinuric diseases.