Bcl-2-like protein 1 (BCL2L1), encoded by the BCL2L1 gene, belongs to the BCL-2 protein family. BCL-2 family members form heterozygous or homologous dimers and participate in various cell activities as anti-apoptotic or pro-apoptotic regulators. BCL2L1 is expressed at the outer mitochondrial membrane, involved the regulation of mitochondrial membrane potential, controlling the production of reactive oxygen species and release of cytochrome C by mitochondria.
Basic Information of BCL2L1 | |
Protein Name | Bcl-2-like protein 1 |
Gene Name | BCL2L1 |
Aliases | Bcl2-L-1, Apoptosis regulator Bcl-X, BCL2L, BCLX |
Organism | Homo sapiens (Human) |
UniProt ID | Q07817 |
Transmembrane Times | 0 |
Length (aa) | 233 |
Sequence | MSQSNRELVVDFLSYKLSQKGYSWSQFSDVEENRTEAPEGTESEMETPSAINGNPSWHLADSPAVNGATGHSSSLDAREVIPMAAVKQALREAGDEFELRYRRAFSDLTSQLHITPGTAYQSFEQVVNELFRDGVNWGRIVAFFSFGGALCVESVDKEMQVLVSRIAAWMATYLNDHLEPWIQENGGWDTFVELYGNNAAAESRKGQERFNRWFLTGMTVAGVVLLGSLFSRK |
BCL2-family proteins have been revealed to regulate programmed cell death or apoptosis. Some members of the family (e.g. Bcl-2, Bcl-XL, and Mcl-1) display antiapoptotic functions, while others (e.g. Bax, Bak, and Bok ) exhibit proapoptotic effects. Located at the outer mitochondrial membrane, BCL2L1 controls the generation of reactive oxygen species and release of cytochrome C, which is associated with cell apoptosis. It has been reported BCL2L1 inhibits cell death and seems to regulate cell death through blocking the voltage-dependent anion channel (VDAC) and preventing the release of the caspase activator, CYC1, from the mitochondrial membrane. Besides, BCL2L1 also functions as a regulator of G2 checkpoint and progression to cytokinesis during mitosis.
Fig.1 Bcl-2-like protein 1 structure.
Rno-miR-665 can affect isophenols by counteracting the negative localization of apoptotic BCL2L1, so it can be a potential target for children's anesthesia.
This study suggested the poor response to drug therapy by targeting BCL2L1 may be associated with up-regulated miR-184 in osteosarcoma patients.
Authors in this study indicated that BCL2L1 and DLC1 may be regarded as potential druggable targets for specific subsets of gastric cancer cases.
The investigation implicated that the BCL2L1-PGAM5-FUNDC1 axis is involved in receptor-mediated mitophagy in response to hypoxia.
The study indicated that BCL2L1 is not likely to be a driver of chromosome 20q gain associated adenoma-to-carcinoma progression.
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