| scholarly article | Q13442814 |
| P2093 | author name string | J Marie Hardwick | |
| Gorka Basañez | |||
| P2860 | cites work | Bax-type apoptotic proteins porate pure lipid bilayers through a mechanism sensitive to intrinsic monolayer curvature. | Q54536632 |
| Gossypol induces Bax/Bak-independent activation of apoptosis and cytochrome c release via a conformational change in Bcl-2 | Q58022865 | ||
| Pro-apoptotic cleavage products of Bcl-xL form cytochrome c-conducting pores in pure lipid membranes | Q74001282 | ||
| Hierarchical regulation of mitochondrion-dependent apoptosis by BCL-2 subfamilies | Q79370601 | ||
| Upgrading the BCL-2 network | Q79397659 | ||
| Membrane-insertion fragments of Bcl-xL, Bax, and Bid | Q80478793 | ||
| Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak | Q24296478 | ||
| Interaction with a membrane surface triggers a reversible conformational change in Bax normally associated with induction of apoptosis | Q24296781 | ||
| Inhibition of Bax channel-forming activity by Bcl-2 | Q24317099 | ||
| Evidence that membrane insertion of the cytosolic domain of Bcl-xL is governed by an electrostatic mechanism | Q24681039 | ||
| Cell death: critical control points | Q28240722 | ||
| Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3 | Q28246420 | ||
| The BCL-2 protein family: opposing activities that mediate cell death | Q29547380 | ||
| Bid, Bax, and lipids cooperate to form supramolecular openings in the outer mitochondrial membrane | Q29616354 | ||
| The mechanism of pore formation by bacterial toxins | Q30159862 | ||
| Bcl-XL inhibits membrane permeabilization by competing with Bax. | Q33343021 | ||
| Bax forms multispanning monomers that oligomerize to permeabilize membranes during apoptosis | Q33854131 | ||
| The tail-anchoring domain of Bfl1 and HCCS1 targets mitochondrial membrane permeability to induce apoptosis | Q34658010 | ||
| The N-terminal domain of Bcl-xL reversibly binds membranes in a pH-dependent manner. | Q35574660 | ||
| Structural biology of the Bcl-2 family of proteins | Q35680498 | ||
| Nur77 converts phenotype of Bcl-B, an antiapoptotic protein expressed in plasma cells and myeloma | Q35804409 | ||
| Bax, but not Bcl-xL, decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations | Q36353924 | ||
| The daily job of night killers: alternative roles of the BCL-2 family in organelle physiology | Q37031106 | ||
| Diagnosing and exploiting cancer's addiction to blocks in apoptosis | Q37059647 | ||
| How do BCL-2 proteins induce mitochondrial outer membrane permeabilization? | Q37100016 | ||
| Anti-apoptotic Bcl-2 Family Proteins Disassemble Ceramide Channels | Q37269319 | ||
| Bcl-2 changes conformation to inhibit Bax oligomerization | Q40287064 | ||
| During apoptosis bcl-2 changes membrane topology at both the endoplasmic reticulum and mitochondria | Q40554731 | ||
| To trigger apoptosis, Bak exposes its BH3 domain and homodimerizes via BH3:groove interactions. | Q46142204 | ||
| Mechanism of mitochondrial glutathione-dependent hepatocellular susceptibility to TNF despite NF-kappaB activation. | Q46699956 | ||
| Contributions to Bax insertion and oligomerization of lipids of the mitochondrial outer membrane | Q46765170 | ||
| BIM and tBID are not mechanistically equivalent when assisting BAX to permeabilize bilayer membranes | Q46808299 | ||
| Bax activation and stress-induced apoptosis delayed by the accumulation of cholesterol in mitochondrial membranes | Q46847162 | ||
| A quorum on bacterial programmed cell death | Q46879560 | ||
| Lipidic pore formation by the concerted action of proapoptotic BAX and tBID. | Q47618625 | ||
| P275 | copyright license | Creative Commons Attribution 4.0 International | Q20007257 |
| P6216 | copyright status | copyrighted | Q50423863 |
| P433 | issue | 6 | |
| P407 | language of work or name | English | Q1860 |
| P304 | page(s) | e154 | |
| P577 | publication date | 2008-06-01 | |
| P1433 | published in | PLOS Biology | Q1771695 |
| P1476 | title | Unravelling the bcl-2 apoptosis code with a simple model system | |
| P478 | volume | 6 |
| Q48244299 | A new theory of development: the generation of complexity in ontogenesis |
| Q37796181 | Apoptosis-induced changes in mitochondrial lipids |
| Q37202353 | Bcl-x L increases mitochondrial fission, fusion, and biomass in neurons |
| Q104111083 | Calcium cytotoxicity sensitizes prostate cancer cells to standard-of-care treatments for locally advanced tumors |
| Q33927481 | Cholesterol and peroxidized cardiolipin in mitochondrial membrane properties, permeabilization and cell death |
| Q24324817 | Endophilin B1/Bif-1 stimulates BAX activation independently from its capacity to produce large scale membrane morphological rearrangements |
| Q24323186 | Membrane binding by tBid initiates an ordered series of events culminating in membrane permeabilization by Bax |
| Q47123534 | Membrane insertion of the BAX core, but not latch domain, drives apoptotic pore formation |
| Q34326024 | Multiple functions of BCL-2 family proteins |
| Q41975085 | Reconstitution of proapoptotic BAK function in liposomes reveals a dual role for mitochondrial lipids in the BAK-driven membrane permeabilization process |
| Q33830140 | Redox control of liver function in health and disease |
Search more.