BCL10 in cell survival after DNA damage.

The complex defense mechanism of the DNA damage response (DDR) developed by cells during long-term evolution is an important mechanism for maintaining the stability of the genome. Defects in the DDR pathway can lead to the occurrence of various diseases, including tumor development. Most cancer treatments cause DNA damage and apoptosis. However, cancer cells have the natural ability to repair this damage and inhibit apoptosis, ultimately leading to the development of drug resistance. Therefore, investigating the mechanism of DNA damage may contribute markedly to the future treatment of cancer. The CARMA-BCL10-MALT1 (CBM) complex formed by B cell lymphoma/leukemia 10 (BCL10) regulates apoptosis by activating NF-κB signaling. BCL10 is involved in the formation of complexes that antagonize apoptosis and contribute to cell survival after DNA damage, with cytoplasmic BCL10 entering the nucleus to promote DNA damage repair, including histone ubiquitination and the recruitment of homologous recombination (HR) repair factors. This article reviews the role of BCL10 in cell survival following DNA damage.

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