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The term "Apoptosis-related protein genes" refers to a comprehensive functional group of genes and their corresponding protein products that regulate and execute programmed cell death, or apoptosis [1, 2]. This broad category encompasses several distinct molecular families, most notably the B-cell lymphoma 2 (BCL-2) family—which includes both pro-apoptotic factors like BAX and BAK and anti-apoptotic factors like BCL-2 and MCL-1—as well as the Inhibitor of Apoptosis (IAP) family, such as XIAP and survivin [2, 5, 11]. These proteins collectively govern the transition from survival to death signals, typically converging on the activation of caspases, which are the executioner proteases of the apoptotic process [1, 5, 7]. In pathological states like cancer, these genes are frequently dysregulated, with anti-apoptotic proteins often overexpressed to facilitate tumor survival and resistance to therapy [1, 5]. Therapeutic strategies targeting this group involve small molecules that inhibit anti-apoptotic proteins, such as the BCL-2 inhibitor venetoclax, or IAP antagonists (SMAC mimetics) designed to restore apoptotic sensitivity in malignant cells [1, 5]. Clinical monitoring often utilizes biomarkers such as the BAX/BCL-2 expression ratio and caspase activity to assess treatment response and therapeutic efficacy [7, 9].
Inhibition of anti-apoptotic proteins (e.g., BCL-2 inhibitors), antagonism of inhibitors of apoptosis (IAPs), or direct activation of the caspase cascade to restore programmed cell death pathways.
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