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Ana J. García-Sáez

Biochemikerin

Name	Ana J. García-Sáez
Place	Deutschland
Academic degree	Prof. Dr.
Profession	Biochemikerin (characteristic profession)
Variant	A. J. García-Sáez Ana J. García- Sáez Anna J. García-Sáez (falsche Namensform)
Related	Deutsches Krebsforschungszentrum Max-Planck-Institut für Molekulare Zellbiologie und Genetik BioQuant
Record type	Person
GND-Identifier	1156240433
Record ID	1156240433
Involved in show all Lipid unsaturation promotes BAX and BAK pore activity during apoptosis Novel meriolin derivatives activate the mitochondrial apoptosis pathway in the presence of antiapoptotic Bcl-2 A guideline on the molecular ecosystem regulating ferroptosis Dying in self-defense: cell death signaling in animals and plants Reversible Markierung in lebenden Zellen mit retro‐konstruierten HaloTags ermöglicht hoch‐ und superauflösende Langzeitbildgebung Reversible Live‐Cell Labeling with Retro‐engineered HaloTags Enables Long‐Term High‐ and Super‐Resolution Imaging Visualization of BOK pores independent of BAX and BAK reveals a similar mechanism with differing regulation Curcumin and NCLX inhibitors share anti-tumoral mechanisms in microsatellite-instability-driven colorectal cancer DRP1 interacts directly with BAX to induce its activation and apoptosis BCL‐2‐family protein tBID can act as a BAX‐like effector of apoptosis Correction: Drp1 modulates mitochondrial stress responses to mitotic arrest Correction: MLKL promotes cellular differentiation in myeloid leukemia by facilitating the release of G-CSF Mitochondrial outer membrane permeabilization at the single molecule level Ferroptotic pores induce Ca2+ fluxes and ESCRT-III activation to modulate cell death kinetics Lipids glue BAK dimers together Drp1 modulates mitochondrial stress responses to mitotic arrest Pore formation in regulated cell death Apoptotic stress induces Bax-dependent, caspase-independent redistribution of LINC complex nesprins Dynein light chain binding determines complex formation and posttranslational stability of the Bcl-2 family members Bmf and Bim Untersuchung von Proteinbindung an Liposomen mittels Fluoreszenzmikroskopie und dcFCCS BFL1 modulates apoptosis at the membrane level through a bifunctional and multimodal mechanism showing key differences with BCLXL Bax retrotranslocation potentiates Bcl-xL’s antiapoptotic activity and is essential for switch-like transitions between MOMP competency and resistance The mycotoxin phomoxanthone A disturbs the form and function of the inner mitochondrial membrane Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 MIM through MOM: the awakening of Bax and Bak pores Bax retrotranslocation potentiates Bcl-xL's antiapoptotic activity and is essential for switch-like transitions between MOMP competency and resistance Quantitative interactome of a membrane Bcl-2 network identifies a hierarchy of complexes for apoptosis regulation Quantitative interactome of a membrane Bcl-2 network identifies a hierarchy of complexes for apoptosis regulation Transient apoptosis inhibition in donor stem cells improves hematopoietic stem cell transplantation Quaternary structure of a G-protein-coupled receptor heterotetramer in complex with Gi and Gs Membrane promotes tBID interaction with BCLXL

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Ana J. García-Sáez

Lipid unsaturation promotes BAX and BAK pore activity during apoptosis

Novel meriolin derivatives activate the mitochondrial apoptosis pathway in the presence of antiapoptotic Bcl-2

A guideline on the molecular ecosystem regulating ferroptosis

Dying in self-defense: cell death signaling in animals and plants

Reversible Markierung in lebenden Zellen mit retro‐konstruierten HaloTags ermöglicht hoch‐ und superauflösende Langzeitbildgebung

Reversible Live‐Cell Labeling with Retro‐engineered HaloTags Enables Long‐Term High‐ and Super‐Resolution Imaging

Visualization of BOK pores independent of BAX and BAK reveals a similar mechanism with differing regulation

Curcumin and NCLX inhibitors share anti-tumoral mechanisms in microsatellite-instability-driven colorectal cancer

DRP1 interacts directly with BAX to induce its activation and apoptosis

BCL‐2‐family protein tBID can act as a BAX‐like effector of apoptosis

Correction: Drp1 modulates mitochondrial stress responses to mitotic arrest

Correction: MLKL promotes cellular differentiation in myeloid leukemia by facilitating the release of G-CSF

Mitochondrial outer membrane permeabilization at the single molecule level

Ferroptotic pores induce Ca2+ fluxes and ESCRT-III activation to modulate cell death kinetics

Lipids glue BAK dimers together

Drp1 modulates mitochondrial stress responses to mitotic arrest

Pore formation in regulated cell death

Apoptotic stress induces Bax-dependent, caspase-independent redistribution of LINC complex nesprins

Dynein light chain binding determines complex formation and posttranslational stability of the Bcl-2 family members Bmf and Bim

Untersuchung von Proteinbindung an Liposomen mittels Fluoreszenzmikroskopie und dcFCCS

BFL1 modulates apoptosis at the membrane level through a bifunctional and multimodal mechanism showing key differences with BCLXL

Bax retrotranslocation potentiates Bcl-xL’s antiapoptotic activity and is essential for switch-like transitions between MOMP competency and resistance

The mycotoxin phomoxanthone A disturbs the form and function of the inner mitochondrial membrane

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

MIM through MOM: the awakening of Bax and Bak pores

Bax retrotranslocation potentiates Bcl-xL's antiapoptotic activity and is essential for switch-like transitions between MOMP competency and resistance

Quantitative interactome of a membrane Bcl-2 network identifies a hierarchy of complexes for apoptosis regulation

Quantitative interactome of a membrane Bcl-2 network identifies a hierarchy of complexes for apoptosis regulation

Transient apoptosis inhibition in donor stem cells improves hematopoietic stem cell transplantation

Quaternary structure of a G-protein-coupled receptor heterotetramer in complex with Gi and Gs

Membrane promotes tBID interaction with BCLXL