Proteomics and transcriptomics analyses of ataxia telangiectasia cells treated with Dexamethasone.

Ataxia telangiectasia (A-T) is an incurable and rare hereditary syndrome. In recent times, treatment with glucocorticoid analogues has been shown to improve the neurological symptoms that characterize this condition, but the molecular mechanism of action of these analogues remains unknown. Hence, the aim of this study was to gain insight into the molecular mechanism of action of glucocorticoid analogues in the treatment of A-T by investigating the role of Dexamethasone (Dexa) in A-T lymphoblastoid cell lines.

ATM splicing variants as biomarkers for low dose dexamethasone treatment of A-T.

Background: Ataxia Telangiectasia (AT) is a rare incurable genetic disease, caused by biallelic mutations in the Ataxia Telangiectasia-Mutated (ATM) gene. Treatment with glucocorticoid analogues has been shown to improve the neurological symptoms that characterize this syndrome. Nevertheless, the molecular mechanism underlying the glucocorticoid action in AT patients is not yet understood.

Dexamethasone improves redox state in ataxia telangiectasia cells by promoting an NRF2-mediated antioxidant response.

Ataxia telangiectasia (A-T) is a rare incurable neurodegenerative disease caused by biallelic mutations in the gene for ataxia-telangiectasia mutated (ATM). The lack of a functional ATM kinase leads to a pleiotropic phenotype, and oxidative stress is considered to have a crucial role in the complex physiopathology. Recently, steroids have been shown to reduce the neurological symptoms of the disease, although the molecular mechanism of this effect is largely unknown.

Effect of FSH and progesterone on human spermatozoa cytosolic calcium.

Ejaculated spermatozoa must undergo a number of modifications before fertilizing the oocyte: among these the capacitation and the acrosome reaction. Calcium signals play an essential role in these functional and structural modifications. Mature spermatozoa have few organelles and a very small cytoplasmic volume but maintain the homeostasis of [Ca(2+)](c) with great accuracy.