Single-point mutations of a lysine residue change function of Bax and Bcl-xL expressed in Bax- and Bak-less mouse embryonic fibroblasts: novel insights into the molecular mechanisms of Bax-induced apoptosis. [electronic resource]
Producer: 20110531Description: 427-38 p. digitalISSN:- 1476-5403
- Amino Acid Sequence
- Animals
- Apoptosis -- genetics
- Cytochromes c -- metabolism
- Embryo, Mammalian -- cytology
- Fibroblasts -- cytology
- Humans
- Ion Channel Gating
- Jurkat Cells
- Kv1.3 Potassium Channel -- metabolism
- Lipid Bilayers -- metabolism
- Lysine -- genetics
- Membrane Potential, Mitochondrial
- Mice
- Molecular Sequence Data
- Mutant Proteins -- chemistry
- Point Mutation -- genetics
- Protein Structure, Quaternary
- Sequence Homology, Amino Acid
- bcl-2 Homologous Antagonist-Killer Protein -- chemistry
- bcl-2-Associated X Protein -- chemistry
- bcl-X Protein -- chemistry
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't
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