Mark H. Ginsberg

This study identifies MACS as a non-canonical IL-2 signaling pathway that promotes Treg differentiation and function through AP-1-dependent mechanisms.

This study uses EGFP-talin1 knock-in mice to show talin-1 dynamics during neutrophil migration in vivo, revealing its polarization during directional movement.

This study shows RAP1 regulates platelet PtdSer exposure and procoagulant activity through RHOA/integrin-dependent and -independent mechanisms.

This study shows that sustained RIAM-talin engagement reprograms adhesion dynamics and force transmission, with Rap1 playing a separable role in adhesion turnover and traction force generation.

This study shows that silencing KRIT1 in endothelial cells under disturbed flow restores KLF2 and KLF4 expression, mimicking the transcriptomic profile of cells under laminar flow.

The paper shows that genetic inactivation of the beta1 adrenergic receptor reduces cerebral cavernous malformations in zebrafish, supporting propranolol's therapeutic effect through beta1 receptor antagonism.

This study identifies an IL-2 mutant that disrupts alternative signaling by blocking CD25-CCR7 complex formation while preserving canonical signaling.

The paper shows that mTORC1 signaling hypersensitivity to leucine drives an onco-circuit in T cell malignancy, and a low leucine diet is therapeutic without impairing T cell immunity.

This study shows that mosaic inactivation of ccm2 in zebrafish leads to abortive intussusceptive angiogenesis, causing multi-cavernous vascular malformations similar to human cerebral cavernous malformations.

This paper describes a new mechanism for forming large diameter blood vessels through endothelial struts that act as scaffolds during vasculogenesis.

The paper shows that astrocytes contribute to cerebral cavernous malformations (CCMs) through VEGF production driven by endothelial NO, highlighting non-cell-autonomous mechanisms.