Calb1, also known as calbindin 1, is a calcium-binding protein. It plays a crucial role in regulating calcium-ion homeostasis, which is essential for numerous cellular processes such as autophagy, cell proliferation, and senescence. It is associated with pathways like the Ca2+-dependent calcineurin/NFAT pathway [3].

In ovarian cancer, knockdown of CALB1 inhibited cell proliferation and colony formation, while overexpression promoted these processes and inhibited senescence by modulating p21 and p27 expression levels. Mechanistically, CALB1 interacts with MDM2 and promotes the interaction between p53 and MDM2, suggesting it may act as an oncogene in ovarian cancer by inhibiting the p53 pathway [1].

In oocytes, knockdown of CALB1 led to reduced calcium-ion levels in the endoplasmic reticulum and mitochondria, resulting in mitochondrial dysfunction and meiotic defects. Overexpression of CALB1 in aging oocytes partially rescued age-related defective phenotypes, indicating its importance in maintaining oocyte quality during aging [2].

In conclusion, Calb1 is vital for maintaining calcium-ion homeostasis, which impacts various biological processes. Its role in ovarian cancer and oocyte aging, as revealed through functional studies including knockdown experiments, highlights its significance in understanding cancer development and age-related reproductive health issues.