Effect of CA3 overexpression on signalling pathways in different cell lines

Carbonic Anhydrase 3 (CA3) was an understudied member of the carbonic anhydrase family. It is highly expressed in muscle tissue and contains two surface-exposed cysteine residues, which can undergo glutathionylation. The redox modification protects cells under oxidative stress. Recent studies have shown that CA3 interacts with Bcl-2–Associated Athanogene 3 (BAG3) and squalene epoxidase (SQLE), implicating CA3 in the pathogenesis of myasthenia gravis and non-alcoholic fatty liver disease. CA3 overexpression has also been reported to reduce hypoxia-induced apoptosis in cardiomyocytes. In this study, we performed RNA-seq profiling on HEK293T, MDA-MB-231, and SVCT cell lines following CA3 overexpression. HEK293T cells were analyzed only under normoxic conditions, whereas MDA-MB-231 and SVCT cells were cultured under both normoxia and hypoxia. Overall design: RNA-seq profiling on HEK293T, MDA-MB-231, and SVCT cell lines following CA3 overexpression. HEK293T cells were analyzed only under normoxic conditions, whereas MDA-MB-231 and SVCT cells were cultured under both normoxia and hypoxia.