Eliminating elevated p53 signaling fails to rescue skeletal muscle defects or extend survival in lamin A/C-deficient mice.

Lamins A and C, encoded by the LMNA gene, are nuclear intermediate filaments that provide structural support to the nucleus and contribute to chromatin organization and transcriptional regulation. LMNA mutations cause muscular dystrophies, dilated cardiomyopathy, and other diseases. The mechanisms by which many LMNA mutations result in muscle-specific diseases have remained elusive, presenting a major hurdle in the development of effective treatments.

Nuclear damage in mutant iPSC-derived cardiomyocytes is associated with impaired lamin localization to the nuclear envelope.

The gene encodes the nuclear envelope proteins Lamins A and C, which comprise a major part of the nuclear lamina, provide mechanical support to the nucleus, and participate in diverse intracellular signaling. mutations give rise to a collection of diseases called laminopathies, including dilated cardiomyopathy (-DCM) and muscular dystrophies. Although nuclear deformities are a hallmark of -DCM, the role of nuclear abnormalities in the pathogenesis of -DCM remains incompletely understood.

Exploring the Crosstalk Between and Splicing Machinery Gene Mutations in Dilated Cardiomyopathy.

Mutations in the gene, which encodes for the nuclear lamina proteins lamins A and C, are responsible for a diverse group of diseases known as laminopathies. One type of laminopathy is Dilated Cardiomyopathy (DCM), a heart muscle disease characterized by dilation of the left ventricle and impaired systolic function, often leading to heart failure and sudden cardiac death. is the second most commonly mutated gene in DCM.

Gallotannin inhibits NFĸB signaling and growth of human colon cancer xenografts.

Gallotannin (GT), the polyphenolic hydrolyzable tannin, exhibits anti-inflammatory and anticancer activities through mechanisms that are not fully understood. Several effects modulated by GT have been shown to be linked to interference with inflammatory mediators. Considering the central role of nuclear factor kappa B (NF-ĸB) in inflammation and cancer, we investigated the effect of GT on NF-ĸB signaling in HT-29 and HCT-116 human colon cancer cells.