Vol. 6, Issue 1, Part A (2024)

The regulation of stem cell division is crucial for tissue development, maintaining homeostasis, and repair of injury. Apoptotic genes play a pivotal role in maintaining proper stem cell division through the controlled elimination of damaged or unwanted cells. Mutations in these genes can disrupt the delicate balance between self-renewal and differentiation, leading to profound effects on tissue function and development. This abstract explores key apoptotic genes such as p53, Bcl-2, and CASPASE family members, highlighting their significance in stem cell division and the consequences of mutations. The protein p53 acts as a "guardian of the genome" by monitoring DNA damage and regulating gene transcription. Its expression increases in response to DNA damage and interacts with various genes like p21/waf1, mdm2, and BAX. Another gene family under scrutiny is Bcl-2, originally identified in lymphoma patients due to chromosome translocation. Bcl-2 proteins play a role in apoptosis regulation, divided into apoptosis suppressors (e.g., Bcl-2, Bcl-XL) and promoters (e.g., BAX, Bad). BAX and Bad promote apoptosis, while Bcl-2 and Bcl-XL inhibit it. Thus, these genes' expression is involved in maintaining the balance between cell survival and cell death in many different cell types throughout the body. Two models suggest that apoptosis regulation involves interactions between these proteins, with either pro-apoptotic BAX being suppressed by hetero-dimerization or apoptosis-suppressing proteins offering dominant survival signals. Understanding the interplay between the expression of apoptotic genes and stem cell biology is essential for unraveling the molecular mechanisms that underlie developmental disorders, aging, and diseases like cancer.