Bcl-xL
Bcl-xL, by Wikipedia https://en.wikipedia.org/wiki?curid=10029222 / CC BY SA 3.0
#Mitochondria
#Cancer_research
#Apoptosis
X-ray crystal structure of Bcl-xL with 1.
76 Å resolution B-cell lymphoma-extra large (Bcl-xL), encoded by the BCL2-like 1 gene, is a transmembrane molecule in the mitochondria.
It is a member of the Bcl-2 family of proteins, and acts as an anti-apoptotic protein by preventing the release of mitochondrial contents such as cytochrome c, which leads to caspase activation and ultimately, programmed cell death.
It is a well-established concept in the field of apoptosis that relative amounts of pro- and anti-survival Bcl-2 family of proteins determine whether the cell will undergo cell death; if more Bcl-xL is present,
then pores are non-permeable to pro-apoptotic molecules and the cell survives.
However, if Bax and Bak become activated, and Bcl-xL is sequestered away by gatekeeper BH3-only factors (e.g. Bim) causing a pore to form, cytochrome c is released leading to initiation of caspase cascade and apoptotic events.
While the exact signaling pathway of Bcl-xL is still not known, it is believed that Bcl-xL differs highly from Bcl-2 in their mechanism of inducing apoptosis.
Bcl-xL is about ten times more functional than Bcl-2 when induced by the chemotherapy drug, Doxorubicin and can specifically bind to cytochrome C residues, preventing apoptosis.
It can also prevent the formation of Apaf-1 and Caspase 9 complex by acting directly upon Apaf-1 rather than Caspase 9, as shown in nematode homologs.
Overview of signal transduction pathways Bcl-xL dysfunction in mice can cause ineffective production of red blood cells, severe anemia, hemolysis, and death.
This protein has also been shown as a requirement for heme production and in erythroid lineage, Bcl-xL is a major survival factor responsible
for an estimated half of the total survival "signal" proerythroblasts must receive in order to survive and become red cells.
Bcl-xL promoter contains GATA-1 and...
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