ArticleBiochemistry2006
The N-terminal domain of Bcl-xL reversibly binds membranes in a pH-dependent manner.
Article in Biochemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- The pH-Dependent Trigger in Diphtheria Toxin T Domain Comes with a Safety Latch.Biophysical journal · 2016Article
- Type 3 Secretion Translocators Spontaneously Assemble a Hexadecameric Transmembrane Complex.The Journal of biological chemistry · 2016Article
- Comparison of membrane insertion pathways of the apoptotic regulator Bcl-xL and the diphtheria toxin translocation domain.Biochemistry · 2013Article
- The N-terminal helix of Bcl-xL targets mitochondria.Mitochondrion · 2013Article
- Acidic pH promotes oligomerization and membrane insertion of the BclXL apoptotic repressor.Archives of biochemistry and biophysics · 2012Article
- The dynamics of Bax channel formation: influence of ionic strength.Biophysical journal · 2012Article
- Ligand binding and membrane insertion compete with oligomerization of the BclXL apoptotic repressor.Journal of molecular biology · 2012Article
- Protein oligomerization mediated by the transmembrane carboxyl terminal domain of Bcl-XL.FEBS letters · 2011Article
- Efficient isolation of Pseudomonas aeruginosa type III secretion translocators and assembly of heteromeric transmembrane pores in model membranes.Biochemistry · 2011Article
- The C. elegans B-cell lymphoma 2 (Bcl-2) homolog cell death abnormal 9 (CED-9) associates with and remodels LIPID membranes.Protein science : a publication of the Protein Society · 2011Article
- Article
- Membrane promotes tBID interaction with BCL(XL).Nature structural & molecular biology · 2009Article
- Structural dynamics of soluble chloride intracellular channel protein CLIC1 examined by amide hydrogen-deuterium exchange mass spectrometry.Biochemistry · 2009Article
- The annexins: spatial and temporal coordination of signaling events during cellular stress.Cellular and molecular life sciences : CMLS · 2009Review
- Membrane permeabilization by trypanosome lytic factor, a cytolytic human high density lipoprotein.The Journal of biological chemistry · 2009Article
- CED-9 and mitochondrial homeostasis in C. elegans muscle.Journal of cell science · 2008Article
- Unravelling the bcl-2 apoptosis code with a simple model system.PLoS biology · 2008Article
- Anti-apoptotic Bcl-2 Family Proteins Disassemble Ceramide Channels.The Journal of biological chemistry · 2008Article
- Regulation of apoptosis by C. elegans CED-9 in the absence of the C-terminal transmembrane domain.Cell death and differentiation · 2007Article
- Lipid-modulation of membrane insertion and refolding of the apoptotic inhibitor Bcl-xL.Biochimica et biophysica acta. Proteins and proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Bcl-xL regulates apoptosis by maintaining the integrity of the mitochondrial outer membrane by adopting both soluble and membrane-associated forms. The membrane-associated conformation does not require a conserved, C-terminal transmembrane domain and appears to be inserted into the bilayer of synthetic membranes as assessed by membrane permeabilization and critical surface pressure measurements. Membrane association is reversible and is regulated by the cooperative binding of approximately two protons to the protein. Two acidic residues, Glu153 and Asp156, that lie in a conserved hairpin of Bcl-xLDeltaTM appear to be important in this process on the basis of a 16% increase in the level of membrane association of the double mutant E153Q/D156N. Contrary to that for the wild type, membrane permeabilization for the mutant is not correlated with membrane association. Monolayer surface pressure measurements suggest that this effect is primarily due to less membrane penetration. These results suggest that E153 and D156 are important for the Bcl-xLDeltaTM conformational change and that membrane binding can be distinct from membrane permeabilization. Taken together, these studies support a model in which Bcl-xL activity is controlled by reversible insertion of its N-terminal domain into the mitochondrial outer membrane. Future studies with Bcl-xL mutants such as E153Q/D156N should allow determination of the relative contributions of membrane binding, insertion, and permeabilization to the regulation of apoptosis.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.