Bcl XL Mouse

B-Cell Leukemia/Lymphoma XL (BCL-xL) is a member of the B-cell lymphoma 2 (BCL-2) family of proteins, which play a crucial role in regulating apoptosis, or programmed cell death. BCL-xL is an anti-apoptotic protein that helps cells survive under stress conditions by preventing the release of cytochrome c from the mitochondria, thereby inhibiting the intrinsic pathway of apoptosis .

BCL-xL is characterized by the presence of four BCL-2 homology (BH) domains, which are essential for its anti-apoptotic function. These domains allow BCL-xL to interact with pro-apoptotic proteins, such as BAX and BAK, and inhibit their activity. By doing so, BCL-xL prevents mitochondrial outer membrane permeabilization (MOMP) and the subsequent release of cytochrome c, which is a critical step in the activation of caspases and the execution of apoptosis .

In many cancers, including B-cell malignancies such as chronic lymphocytic leukemia (CLL) and diffuse large B-cell lymphoma (DLBCL), BCL-xL is often overexpressed. This overexpression helps cancer cells evade apoptosis, contributing to tumor growth and resistance to chemotherapy . Targeting BCL-xL to induce apoptosis in cancer cells has been a significant focus of cancer research. For instance, the development of small-molecule inhibitors like navitoclax (ABT-263) has shown promise in restoring apoptotic cell death in cancer cells by inhibiting BCL-xL .

Recombinant BCL-xL proteins, such as those derived from mouse models, are widely used in research to study the mechanisms of apoptosis and to develop new therapeutic strategies. These recombinant proteins are produced using genetic engineering techniques, where the BCL-xL gene is inserted into a suitable expression system, such as bacteria or mammalian cells, to produce large quantities of the protein for experimental purposes .

The study of BCL-xL and its role in apoptosis has led to the development of targeted therapies for cancer treatment. By inhibiting BCL-xL, researchers aim to sensitize cancer cells to chemotherapy and promote their elimination through apoptosis. This approach has shown potential in preclinical models and is being explored in clinical trials for various hematologic malignancies .