Structural insights into the degradation of Mcl-1 induced by BH3 domains
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Genome-wide prediction and validation of peptides that bind human prosurvival Bcl-2 proteinsPrevention of cytokine withdrawal-induced apoptosis by Mcl-1 requires interaction between Mcl-1 and BimHuman nuclear clusterin mediates apoptosis by interacting with Bcl-XL through C-terminal coiled coil domainHeterodimerization of BAK and MCL-1 activated by detergent micellesThe hepatitis C virus core protein contains a BH3 domain that regulates apoptosis through specific interaction with human Mcl-1Vaccinia virus anti-apoptotic F1L is a novel Bcl-2-like domain-swapped dimer that binds a highly selective subset of BH3-containing death ligandsMutation to Bax beyond the BH3 domain disrupts interactions with pro-survival proteins and promotes apoptosisDown-regulation of micro-RNA-1 (miR-1) in lung cancer. Suppression of tumorigenic property of lung cancer cells and their sensitization to doxorubicin-induced apoptosis by miR-1Regulation of Bim in Health and DiseaseStapled BH3 peptides against MCL-1: mechanism and design using atomistic simulationsCrystal structure of ABT-737 complexed with Bcl-xL: implications for selectivity of antagonists of the Bcl-2 familyA novel BH3 ligand that selectively targets Mcl-1 reveals that apoptosis can proceed without Mcl-1 degradationStructural and Biochemical Bases for the Inhibition of Autophagy and Apoptosis by Viral BCL-2 of Murine γ-Herpesvirus 68Completing the family portrait of the anti-apoptotic Bcl-2 proteins: crystal structure of human Bfl-1 in complex with BimConformational Changes in Bcl-2 Pro-survival Proteins Determine Their Capacity to Bind LigandsMcl-1-Bim complexes accommodate surprising point mutations via minor structural changesDeterminants of BH3 Binding Specificity for Mcl-1 versus Bcl-xLApoptotic Regulation by MCL-1 through HeterodimerizationStructural Basis for Apoptosis Inhibition by Epstein-Barr Virus BHRF1Discovery and molecular characterization of a Bcl-2-regulated cell death pathway in schistosomesStructural Basis of Bcl-xL Recognition by a BH3-Mimetic α/β-Peptide Generated by Sequence-Based DesignRational Design of Proteolytically Stable, Cell-Permeable Peptide-Based Selective Mcl-1 InhibitorsEvaluation of Diverse α/β-Backbone Patterns for Functional α-Helix Mimicry: Analogues of the Bim BH3 DomainStructure-Guided Rational Design of α/β-Peptide Foldamers with High Affinity for BCL-2 Family Prosurvival ProteinsHigh-quality NMR structure of human anti-apoptotic protein domain Mcl-1(171-327) for cancer drug designDiscovery of 2-Indole-acylsulfonamide Myeloid Cell Leukemia 1 (Mcl-1) Inhibitors Using Fragment-Based MethodsBH3-only proteins: a 20-year stock-takeBuilding blocks of the apoptotic pore: how Bax and Bak are activated and oligomerize during apoptosisUpregulating Noxa by ER stress, celastrol exerts synergistic anti-cancer activity in combination with ABT-737 in human hepatocellular carcinoma cellsProliferating cell nuclear antigen (PCNA) interactions in solution studied by NMRProteasomal degradation of Mcl-1 by maritoclax induces apoptosis and enhances the efficacy of ABT-737 in melanoma cellsPyoluteorin derivatives induce Mcl-1 degradation and apoptosis in hematological cancer cells.The functional differences between pro-survival and pro-apoptotic B cell lymphoma 2 (Bcl-2) proteins depend on structural differences in their Bcl-2 homology 3 (BH3) domains.The NOXA-MCL1-BIM axis defines lifespan on extended mitotic arrestNovel Bcl-2 homology-3 domain-like sequences identified from screening randomized peptide libraries for inhibitors of the pro-survival Bcl-2 proteins.Nitric oxide induces cell death by regulating anti-apoptotic BCL-2 family members.Endogenous Bak inhibitors Mcl-1 and Bcl-xL: differential impact on TRAIL resistance in Bax-deficient carcinoma.Zebrafish Noxa promotes mitosis in early embryonic development and regulates apoptosis in subsequent embryogenesis.3-Substituted-N-(4-hydroxynaphthalen-1-yl)arylsulfonamides as a novel class of selective Mcl-1 inhibitors: structure-based design, synthesis, SAR, and biological evaluation.Vinblastine induces acute, cell cycle phase-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed.
P2860
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P2860
Structural insights into the degradation of Mcl-1 induced by BH3 domains
description
2007 nî lūn-bûn
@nan
2007 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
name
Structural insights into the degradation of Mcl-1 induced by BH3 domains
@ast
Structural insights into the degradation of Mcl-1 induced by BH3 domains
@en
Structural insights into the degradation of Mcl-1 induced by BH3 domains
@nl
type
label
Structural insights into the degradation of Mcl-1 induced by BH3 domains
@ast
Structural insights into the degradation of Mcl-1 induced by BH3 domains
@en
Structural insights into the degradation of Mcl-1 induced by BH3 domains
@nl
prefLabel
Structural insights into the degradation of Mcl-1 induced by BH3 domains
@ast
Structural insights into the degradation of Mcl-1 induced by BH3 domains
@en
Structural insights into the degradation of Mcl-1 induced by BH3 domains
@nl
P2093
P2860
P50
P3181
P356
P1476
Structural insights into the degradation of Mcl-1 induced by BH3 domains
@en
P2093
Mark G Hinds
Peter E Czabotar
Peter M Colman
P2860
P304
P3181
P356
10.1073/PNAS.0701297104
P407
P577
2007-03-27T00:00:00Z