M. Gaestel

MK2 deficiency decreases mortality during the inflammatory phase after myocardial infarction in mice

This study shows MK2 deficiency reduces mortality and alters cytokine levels during the inflammatory phase after myocardial infarction in mice.

5-iodotubercidin sensitizes cells to RIPK1-dependent necroptosis by interfering with NFkappaB signaling

This study identifies 5-iodotubercidin as a compound that sensitizes cells to RIPK1-dependent necroptosis by inhibiting NFκB signaling in MK2-deficient cells.

Enforced dimerization of CD45 by the adenovirus E3/49K protein inhibits T cell receptor signaling

This study shows that the adenovirus E3/49K protein binds to CD45, enforcing its dimerization and inhibiting T cell receptor signaling.

On the therapeutic potential of MAPK4 in triple-negative breast cancer

The paper critiques Wang et al.'s study on ERK4's role in TNBC, arguing that methodological flaws undermine their conclusion that ERK4 is a therapeutic target.

PRMT5-mediated regulatory arginine methylation of RIPK3

This study identifies PRMT5-mediated arginine methylation of RIPK3 as a feedback mechanism regulating RIPK1 activity and function in cell death pathways.

Targeting aggressive B-cell lymphomas through pharmacological activation of the mitochondrial protease OMA1

This study identifies OMA1 activators that induce apoptosis in DLBCL cells via the ATF4-ISR pathway, showing efficacy in preclinical models.

ERK3-MK5 signaling regulates myogenic differentiation and muscle regeneration by promoting FoxO3 degradation

Expression, subcellular localization, and phosphorylation of MK5 in adult cardiac ventricular fibroblasts

This study investigates MK5 expression, localization, and phosphorylation in cardiac myofibroblasts and myocytes, finding that p38/{beta} mediates T182-MK5 phosphorylation and activation.

MK2-deficient mice are bradycardic and display delayed hypertrophic remodelling in response to a chronic increase in afterload

This study examines the cardiac phenotype of MK2-deficient mice, finding altered autonomic regulation, increased metabolic gene expression, reduced mitochondrial Ca2+-sensitivity, and delayed hypertrophic remodeling in response to pressure overload.

Germline deletion reveals a non-essential role of the atypical MAPK6/ERK3

The paper shows that ERK3 is not essential for viability, fertility, or T-cell function, contradicting previous reports of perinatal lethality due to a different genetic construct.