Jan Lammerding

This study shows that pro-inflammatory polarization of macrophages increases nuclear stiffness despite reduced lamin A/C levels, suggesting chromatin changes drive nuclear mechanics.

This study shows that A-type and B-type lamins have opposing roles in LBR localization and dynamics, with lamin A displacing LBR from the nuclear envelope while lamin B1/B2 tether it.

The paper identifies deep nuclear envelope invaginations (DINEs) in epithelial cells, showing they organize chromatin and gene activity in response to mechanical cues like crowding and tissue maturation.

This study identifies two independent binding sites on lamin A/C that anchor emerin at the inner nuclear membrane, revealing a revised model for emerin retention.

This study shows that microtubule forces, not the LINC complex, drive nuclear damage in LMNA cardiomyopathy and that disrupting microtubules can rescue cardiac function.

Ultrack improves cell tracking across 2D, 3D, and multi-channel time-lapse recordings by integrating multiple segmentations and temporal consistency, achieving state-of-the-art performance on benchmark datasets.

This study identifies key cellular programs and pathways driving metastatic organotropism in small cell lung cancer using preclinical models and multiomic profiling.

This study identifies the A-type lamin rod domain as the key determinant of nuclear deformability, revealing its unique role in resisting large mechanical forces on the nucleus.

This study shows that N-terminal tags on Lamin A affect its nuclear structural support functions but not all its roles in mammalian cells.

This study identifies NE rupture in LMNA-DCM cardiomyocytes as a driver of transcriptomic changes and immune activation, which can be reversed by LINC complex disruption.