BCL2L1 Target Analysis Report Summary
About the Target
Based on the provided context information, here is a comprehensive summary of key viewpoints related to BCL2L1 (BCL-XL):
BCL-XL is a protein that plays a role in regulating apoptosis in both normal cells and during flavivirus infection [1]. It delays apoptosis in normal cells, allowing the virus to spread to neighboring cells and contribute to high pathogenicity. However, inhibiting BCL-XL accelerates apoptosis upon infection and inhibits viral dissemination [1].
BCL-XL is an isoform of Bcl-x that inhibits the activation of Bax and Bak, thus preventing the loss of mitochondrial outer membrane integrity and release of cytochrome c [2]. Therefore, BCL-XL is considered anti-apoptotic.
Another isoform of Bcl-x, Bcl-xS, can inhibit BCL-XL and, when activated, leads to the loss of mitochondrial outer membrane integrity and subsequent apoptotic cell death [2].
The expression of BCL-XL is regulated by PARK2 ubiquitin E3 ligase, which controls its levels to regulate cell death [3].
In cancer cells, pro-survival proteins like BCL-2, BCL-XL, and MCL-1 bind to and inhibit pro-apoptotic proteins, such as BAX and BAK [4]. However, when cells are treated with certain combinations of compounds, the pro-apoptotic proteins are released and activated, leading to efficient induction of apoptosis [4].
BCL-XL, along with BCL-2, is involved in B-CLL resistance to apoptosis, contributing to cell survival and resistance to cell death [5]. The interaction between NTSR2 and TrkB receptors, strengthened by BDNF activation, triggers pro-survival pathways via phosphorylation of NTSR2 and the expression of downstream anti-apoptotic proteins, including BCL-XL [5]. However, inhibiting NTSR2 can re-establish B-CLL apoptosis [5].
These findings highlight the diverse roles of BCL2L1 (BCL-XL) in regulating apoptosis, its involvement in viral pathogenicity, and its relevance in cancer and B-CLL survival.
Figure [1]
Figure [2]
Figure [3]
Figure [4]
Figure [5]
Note: If you are interested in the full version of this target analysis report, or if you'd like to learn how our AI-powered BDE-Chem can design therapeutic molecules to interact with the BCL2L1 target at a cost 90% lower than traditional approaches, please feel free to contact us at BD@silexon.ai.
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