Many players in BCL-2 family affairs.

No abstract is available for this paper.

• Publication year

  2014

• Venue

  TIBS -Trends in Biochemical Sciences. Regular ed

• Publication date

  2014-03-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/j.tibs.2013.12.006PMID 24503222PMCID PMC4005919
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Cell Death

  2014cited by this paper
• Bax crystal structures reveal how BH3 domains activate Bax and nucleate its oligomerization to induce apoptosis.

  2013influential reference
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  2013cited by this paper
• Structure-guided design of a selective BCL-X(L) inhibitor.

  2013cited by this paper
• Mechanisms of action of Bcl-2 family proteins.

  2013cited by this paper
• Targeting BCL-2 with the BH3 mimetic ABT-199 in estrogen receptor-positive breast cancer.

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• Bcl-2 antagonists: a proof of concept for CLL therapy

  2013cited by this paper
• Deletion of MCL-1 causes lethal cardiac failure and mitochondrial dysfunction.

  2013cited by this paper
• Protein-protein interactions as druggable targets: recent technological advances.

  2013cited by this paper
• Assembly of the Bak Apoptotic Pore

  2013cited by this paper
• ABT‐199 selectively inhibits BCL2 but not BCL2L1 and efficiently induces apoptosis of chronic lymphocytic leukaemic cells but not platelets

  2013cited by this paper
• Mitochondria: gatekeepers of response to chemotherapy.

  2013cited by this paper
• The Bcl-2 specific BH3 mimetic ABT-199: a promising targeted therapy for t(11;14) multiple myeloma

  2013cited by this paper
• Discovery of potent myeloid cell leukemia 1 (Mcl-1) inhibitors using fragment-based methods and structure-based design.

  2013cited by this paper
• Evaluation and critical assessment of putative MCL-1 inhibitors

  2013cited by this paper
• ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets

  2013cited by this paper
• Evaluation of the BH3-only Protein Puma as a Direct Bak Activator*

  2013cited by this paper
• Direct BAKtivation

  2013cited by this paper
• Structural biology of the Bcl-2 family and its mimicry by viral proteins

  2013cited by this paper
• Dual-site Interactions of p53 Protein Transactivation Domain with Anti-apoptotic Bcl-2 Family Proteins Reveal a Highly Convergent Mechanism of Divergent p53 Pathways*

  2013cited by this paper
• Direct activation of full-length proapoptotic BAK

  2013cited by this paper
• Viral Inhibition of BAK Promotes Murine Cytomegalovirus Dissemination to Salivary Glands

  2013cited by this paper
• Xk-Related Protein 8 and CED-8 Promote Phosphatidylserine Exposure in Apoptotic Cells

  2013cited by this paper
• BID-induced structural changes in BAK promote apoptosis

  2013cited by this paper
• Organization of the Mitochondrial Apoptotic BAK Pore

  2013cited by this paper
• A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer

  2012cited by this paper
• Live or let die: manipulation of cellular suicide programs by murine cytomegalovirus

  2012cited by this paper
• Shedding light on apoptosis at subcellular membranes.

  2012cited by this paper
• BH3-only proteins in apoptosis at a glance

  2012cited by this paper
• Navitoclax (ABT‐263) and bendamustine ± rituximab induce enhanced killing of non‐Hodgkin's lymphoma tumours in vivo

  2012cited by this paper
• PUMA Binding Induces Partial Unfolding within BCL-xL to Disrupt p53 Binding and Promote Apoptosis

  2012cited by this paper
• A stapled BIM peptide overcomes apoptotic resistance in hematologic cancers.

  2012cited by this paper
• Direct and selective small-molecule activation of proapoptotic BAX.

  2012cited by this paper
• Structural mechanism of Bax inhibition by cytomegalovirus protein vMIA

  2012cited by this paper
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  2011cited by this paper
• BH3-only proteins: Orchestrators of apoptosis.

  2011cited by this paper
• Bcl-x(L) retrotranslocates Bax from the mitochondria into the cytosol.

  2011cited by this paper
• Molecular Basis of Bcl-XL-p53 Interaction: Insights from Molecular Dynamics Simulations

  2011cited by this paper
• Bax dimerizes via a symmetric BH3:groove interface during apoptosis

  2011cited by this paper
• A unified model of mammalian BCL-2 protein family interactions at the mitochondria.

  2011cited by this paper
• Evidence that inhibition of BAX activation by BCL-2 involves its tight and preferential interaction with the BH3 domain of BAX

  2011cited by this paper
• Transient binding of an activator BH3 domain to the Bak BH3-binding groove initiates Bak oligomerization

  2011cited by this paper
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  2010cited by this paper
• Apoptotic Regulation by MCL-1 through Heterodimerization*

  2010cited by this paper
• BH3-triggered structural reorganization drives the activation of proapoptotic BAX.

  2010influential reference
• BID, BIM, and PUMA Are Essential for Activation of the BAX- and BAK-Dependent Cell Death Program

  2010cited by this paper
• The landscape of somatic copy-number alteration across human cancers

  2010cited by this paper
• Cytomegaloviruses inhibit Bak- and Bax-mediated apoptosis with two separate viral proteins

  2010cited by this paper
• Cell Death

  2010cited by this paper
• BH3 Domains other than Bim and Bid Can Directly Activate Bax/Bak*

  2010cited by this paper
• Conformational Changes in BAK, a Pore-forming Proapoptotic Bcl-2 Family Member, upon Membrane Insertion and Direct Evidence for the Existence of BH3-BH3 Contact Interface in BAK Homo-oligomers*

  2010cited by this paper
• The BCL-2 family reunion.

  2010cited by this paper
• Heterodimerization of BAK and MCL-1 Activated by Detergent Micelles*

  2010cited by this paper
• Bax activation by the BH3-only protein Puma promotes cell dependence on antiapoptotic Bcl-2 family members

  2009cited by this paper
• Molecular Details of Bax Activation, Oligomerization, and Membrane Insertion*

  2009cited by this paper
• BclxL Changes Conformation upon Binding to Wild-type but Not Mutant p53 DNA Binding Domain*

  2009cited by this paper
• Bak activation for apoptosis involves oligomerization of dimers via their alpha6 helices.

  2009cited by this paper
• Cytoplasmic functions of the tumour suppressor p53

  2009cited by this paper
• The MDM2-binding region in the transactivation domain of p53 also acts as a Bcl-X(L)-binding motif.

  2009cited by this paper
• Cell death.

  2009cited by this paper
• Stepwise activation of BAX and BAK by tBID, BIM, and PUMA initiates mitochondrial apoptosis.

  2009cited by this paper
• Targeting post-mitochondrial effectors of apoptosis for neuroprotection.

  2009cited by this paper
• Dynamics and structure of the Bax-Bak complex responsible for releasing mitochondrial proteins during apoptosis

  2008cited by this paper
• ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor.

  2008cited by this paper
• BAX Activation is Initiated at a Novel Interaction Site

  2008influential reference
• The BCL-2 protein family: opposing activities that mediate cell death

  2008cited by this paper
• BCL-2 family antagonists for cancer therapy

  2008cited by this paper
• How do BCL-2 proteins induce mitochondrial outer membrane permeabilization?

  2008cited by this paper
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  2008cited by this paper
• Structure of the BH3 domains from the p53-inducible BH3-only proteins Noxa and Puma in complex with Mcl-1.

  2008cited by this paper
• Oligomerization of BAK by p53 Utilizes Conserved Residues of the p53 DNA Binding Domain*

  2008cited by this paper
• To trigger apoptosis, Bak exposes its BH3 domain and homodimerizes via BH3:groove interactions.

  2008cited by this paper
• [Discovering high-affinity ligands for proteins: SAR by NMR].

  2007cited by this paper
• Bim, Bad and Bmf: intrinsically unstructured BH3-only proteins that undergo a localized conformational change upon binding to prosurvival Bcl-2 targets

  2007cited by this paper
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  2007cited by this paper
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  2007cited by this paper
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  2007cited by this paper
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  2006cited by this paper
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  2006cited by this paper
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  2005cited by this paper
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  2005cited by this paper
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  2005cited by this paper
• Bax forms multispanning monomers that oligomerize to permeabilize membranes during apoptosis

  2005cited by this paper
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  2005cited by this paper
• Transcription, apoptosis and p53: catch-22.

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  2004cited by this paper
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  2004cited by this paper
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  2004cited by this paper
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  2004cited by this paper
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  2004cited by this paper
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  2004cited by this paper
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  2003cited by this paper
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  2003cited by this paper
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  2000cited by this paper
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  2000cited by this paper
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