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Bcl-XL and Bax are structurally similar members of the Bcl-2 family of cell-death-related proteins, and they compete for binding to membranes, as well as to Bcl-2 family member tBid and activated Bax. Unlike Bax, Bcl-XL is unable to oligomerize and form pores in membranes, so it inhibits membrane permeabilization--a key step during commitment to apoptosis--by functioning like a dominant-negative Bax.
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Keywords {🔍}
bclxl, bax, tbid, membrane, binding, figure, membranes, liposomes, permeabilization, proteins, membranebound, article, view, google, scholar, apoptosis, protein, bcl, function, change, bak, incubated, mitochondria, cell, interaction, conformational, results, tbidmt, interactions, biol, panel, inhibits, mitochondrial, addition, soluble, cells, experiments, similar, inhibition, antiapoptotic, family, bid, insertion, activated, step, immunoblotting, antibody, mutant, inhibited, release,
Topics {✒️}
health research cell biology plos biol 6 cookies plos health membrane systems [39 bcl-xl/bim fragment complex bax-binding-deficient bcl-xl y101k bcl-xl–bak peptide complex inactive g138e/r139l/i140n mutant open-access article distributed membrane-bound bcl-xl increases membrane-bound bcl-xl correlates sepharose cl-2b resin membrane-bound bcl-xl inhibits tbid/bax-mediated liposome permeabilization tbid-mt1/bcl-xl y101k combination bid-induced open conformer membrane-bound bcl-xl prevents membrane-bound bcl-xl affected bcl-xl y101k decreased bcl-xl-binding mutant m1bid p-xylene-bis-pyridinium /p-xylene-bis-pyridinium c-terminal membrane anchor detergent-resistant bax cross-links full-length bcl-xl full-length recombinant proteins multiple bcl-xl molecules similar cross-linking pattern liposome-induced conformational change require bcl-xl–tbid binding tbid-mt1/bcl-xl y101k pro-survival molecule bcl bak-mediated mitochondrial apoptosis c-terminal insertion sequence tbid/bax-induced dye release phenyl-sepharose chromatography step membrane-bound tbid increases membrane-targeted death ligand generate membrane-spanning pores liposome-induced conformation change stable bcl-xl–tbid binding gel filtration chromatography bcl-xl-mediated inhibition δtm bcl-xl showed original author larger encapsulated fluorophores bcl-xl–bax binding contribute excess bcl-xl bound
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