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Bcl-xL regulates apoptosis by heterodimerization-dependent and -independent mechanisms.
A hydrophobic cleft formed by the BH1, BH2 and BH3 domains of Bcl-xL is responsible for interactions between Bcl-xL and BH3-containing death agonists. Mutants were constructed which did not bind to Bax but retained anti-apoptotic activity. Since Bcl-xL can form an ion channel in synthetic lipid memb...
Gorde:
| Egile Nagusiak: | , , , , , , , , |
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| Formatua: | Artigo |
| Hizkuntza: | Inglês |
| Argitaratua: |
1999
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| Gaiak: | |
| Sarrera elektronikoa: | https://ncbi.nlm.nih.gov/pmc/articles/PMC1171156/ https://ncbi.nlm.nih.gov/pubmed/9927423 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1093/emboj/18.3.632 |
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