The emerging role of alternative splicing in senescence and aging

Role of Aberrant Alternative Splicing in Cancer

Alternative splicing can alter genome sequence and as a consequence, many genes change to oncogenes. This event can also affect protein function and diversity. The growing number of study elucidate the pathological influence of impaired alternative splicing events on numerous disease including cancer. Here, we would like to highlight the significant role of alternative splicing in cancer biolog...

The Splicing Factor SRSF1 as a Marker for Endothelial Senescence

Aging is the major risk factor per se for the development of cardiovascular diseases. The senescence of the endothelial cells (ECs) that line the lumen of blood vessels is the cellular basis for these age-dependent vascular pathologies, including atherosclerosis and hypertension. During their lifespan, ECs may reach a stage of senescence by two different pathways; a replicative one derived from...

Pre-mRNA splicing modulations in senescence.

Aging and associated diseases involve multilevel changes in the complex phenomenon of alternative splicing. Here, we review the potential genomic and environmental origins of such changes and discuss the research implications of these findings.

Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts.

Hutchinson-Gilford progeria syndrome (HGPS), a devastating premature aging disease, is caused by a point mutation in the lamin A gene (LMNA). This mutation constitutively activates a cryptic splice donor site, resulting in a mutant lamin A protein known as progerin. Recent studies have demonstrated that progerin is also produced at low levels in normal human cells and tissues. However, the caus...

A novel DNA damage-induced alternative splicing pathway that regulates p53 and cellular senescence markers