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tale of two mitochondrial channels, MAC and PTP, in apoptosis

Apoptosis (London), 2007-05, Vol.12 (5), p.857-868

2007

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Differences in the glycosylation of recombinant proteins expressed in HEK and CHO cells

Journal of biotechnology, 2012-10, Vol.161 (3), p.336-348

2012

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Bad Targets the Permeability Transition Pore Independent of Bax or Bak to Switch between Ca2+-Dependent Cell Survival and Death

Molecular cell, 2009-02, Vol.33 (3), p.377-388

2009

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Bax Is Present as a High Molecular Weight Oligomer/Complex in the Mitochondrial Membrane of Apoptotic Cells

The Journal of biological chemistry, 2001-04, Vol.276 (15), p.11615-11623

2001

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Bid Induces the Oligomerization and Insertion of Bax into the Outer Mitochondrial Membrane

Molecular and Cellular Biology, 2000-02, Vol.20 (3), p.929-935

2000

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Mitochondrial Cholesterol Contributes to Chemotherapy Resistance in Hepatocellular Carcinoma

Cancer research (Chicago, Ill.), 2008-07, Vol.68 (13), p.5246-5256

2008

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Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria

Biochemical journal, 2000-01, Vol.345 Pt 2 (2), p.271-278

2000

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Lipidic Pore Formation by the Concerted Action of Proapoptotic BAX and tBID

The Journal of biological chemistry, 2004-07, Vol.279 (29), p.30081-30091

2004

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Bax oligomerization in mitochondrial membranes requires tBid (caspase-8-cleaved Bid) and a mitochondrial protein

Biochemical journal, 2002-12, Vol.368 (Pt 3), p.915-921

2002

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Cytochrome c release from mitochondria: all or nothing

Nature cell biology, 2000-03, Vol.2 (3), p.E41-E43

2000

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Bid-Induced Conformational Change of Bax Is Responsible for Mitochondrial Cytochrome c Release during Apoptosis

The Journal of cell biology, 1999-03, Vol.144 (5), p.891-901

1999

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Phosphorylation of Bid by Casein Kinases I and II Regulates Its Cleavage by Caspase 8

Molecular cell, 2001-09, Vol.8 (3), p.601-611

2001

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Bid, but Not Bax, Regulates VDAC Channels

The Journal of biological chemistry, 2004-04, Vol.279 (14), p.13575-13583

2004

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Bax Channel Inhibitors Prevent Mitochondrion-mediated Apoptosis and Protect Neurons in a Model of Global Brain Ischemia

The Journal of biological chemistry, 2005-12, Vol.280 (52), p.42960-42970

2005

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Endophilin B1/Bif-1 Stimulates BAX Activation Independently from Its Capacity to Produce Large Scale Membrane Morphological Rearrangements

The Journal of biological chemistry, 2009-02, Vol.284 (7), p.4200-4212

2009

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Bax-Induced Cytochrome C Release from Mitochondria Is Independent of the Permeability Transition Pore but Highly Dependent on Mg2+Ions

The Journal of cell biology, 1998-10, Vol.143 (1), p.217-224

1998

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A sandwich ELISA for the conformation-specific quantification of the activated form of human Bax

Analytical biochemistry, 2016-03, Vol.497, p.90-94

2016

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Mitochondria and the Bcl-2 family proteins in apoptosis signaling pathways

Molecular and cellular biochemistry, 2004-01, Vol.256-257 (1-2), p.141-155

Antonsson, Bruno

2004

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Catalytic Activation of the Phosphatase MKP-3 by ERK2 Mitogen-Activated Protein Kinase

Science (American Association for the Advancement of Science), 1998-05, Vol.280 (5367), p.1262-1265

1998

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Bax and other pro-apoptotic Bcl-2 family "killer-proteins" and their victim the mitochondrion

Cell and tissue research, 2001-12, Vol.306 (3), p.347-361

Antonsson, B

2001

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Rapid Kinetics of tBid-induced Cytochrome c and Smac/DIABLO Release and Mitochondrial Depolarization

The Journal of biological chemistry, 2002-02, Vol.277 (7), p.5651-5659

2002

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BIM and tBID Are Not Mechanistically Equivalent When Assisting BAX to Permeabilize Bilayer Membranes

The Journal of biological chemistry, 2008-03, Vol.283 (12), p.7790-7803

2008

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Inhibition of Bax Channel-Forming Activity by Bcl-2

Science (American Association for the Advancement of Science), 1997-07, Vol.277 (5324), p.370-372

1997

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The Release of Cytochrome c from Mitochondria during Apoptosis of NGF-Deprived Sympathetic Neurons Is a Reversible Event

The Journal of cell biology, 1999-03, Vol.144 (5), p.883-889

1999

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Bcl-2 Undergoes Phosphorylation by c-Jun N-terminal Kinase/Stress-activated Protein Kinases in the Presence of the Constitutively Active GTP-binding Protein Rac1

The Journal of biological chemistry, 1997-10, Vol.272 (40), p.25238-25242

1997

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tale of two mitochondrial channels, MAC and PTP, in apoptosis

Differences in the glycosylation of recombinant proteins expressed in HEK and CHO cells

Bad Targets the Permeability Transition Pore Independent of Bax or Bak to Switch between Ca2+-Dependent Cell Survival and Death

Bax Is Present as a High Molecular Weight Oligomer/Complex in the Mitochondrial Membrane of Apoptotic Cells

Bid Induces the Oligomerization and Insertion of Bax into the Outer Mitochondrial Membrane

Mitochondrial Cholesterol Contributes to Chemotherapy Resistance in Hepatocellular Carcinoma

Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria

Lipidic Pore Formation by the Concerted Action of Proapoptotic BAX and tBID

Bax oligomerization in mitochondrial membranes requires tBid (caspase-8-cleaved Bid) and a mitochondrial protein

Cytochrome c release from mitochondria: all or nothing

Bid-Induced Conformational Change of Bax Is Responsible for Mitochondrial Cytochrome c Release during Apoptosis

Phosphorylation of Bid by Casein Kinases I and II Regulates Its Cleavage by Caspase 8

Bid, but Not Bax, Regulates VDAC Channels

Bax Channel Inhibitors Prevent Mitochondrion-mediated Apoptosis and Protect Neurons in a Model of Global Brain Ischemia

Endophilin B1/Bif-1 Stimulates BAX Activation Independently from Its Capacity to Produce Large Scale Membrane Morphological Rearrangements

Bax-Induced Cytochrome C Release from Mitochondria Is Independent of the Permeability Transition Pore but Highly Dependent on Mg2+Ions

A sandwich ELISA for the conformation-specific quantification of the activated form of human Bax

Mitochondria and the Bcl-2 family proteins in apoptosis signaling pathways

Catalytic Activation of the Phosphatase MKP-3 by ERK2 Mitogen-Activated Protein Kinase

Bax and other pro-apoptotic Bcl-2 family "killer-proteins" and their victim the mitochondrion

Rapid Kinetics of tBid-induced Cytochrome c and Smac/DIABLO Release and Mitochondrial Depolarization

BIM and tBID Are Not Mechanistically Equivalent When Assisting BAX to Permeabilize Bilayer Membranes

Inhibition of Bax Channel-Forming Activity by Bcl-2

The Release of Cytochrome c from Mitochondria during Apoptosis of NGF-Deprived Sympathetic Neurons Is a Reversible Event

Bcl-2 Undergoes Phosphorylation by c-Jun N-terminal Kinase/Stress-activated Protein Kinases in the Presence of the Constitutively Active GTP-binding Protein Rac1

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