Hristina Ivanova

Leuven, VLG 3000, Belgium

Last Updated: 09/26/2026

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Found 17 publications

Allosteric cross-talk between the hydrophobic cleft and the BH4 domain of Bcl-2 in control of inositol 1,4,5-trisphosphate receptor activity.

Allosteric cross-talk between the hydrophobic cleft and the BH4 domain of Bcl-2 in control of inositol 1,4,5-trisphosphate receptor activity.

Journal: Exploration of targeted anti-tumor therapy

Published: November 02, 2021

Tracing the evolutionary history of Ca2+-signaling modulation by human Bcl-2: Insights from the Capsaspora owczarzaki IP3 receptor ortholog.

Tracing the evolutionary history of Ca2+-signaling modulation by human Bcl-2: Insights from the Capsaspora owczarzaki IP3 receptor ortholog.

Journal: Biochimica et biophysica acta. Molecular cell research

Published: April 21, 2021

Bcl-xL acts as an inhibitor of IP3R channels, thereby antagonizing Ca2+-driven apoptosis.

Bcl-xL acts as an inhibitor of IP3R channels, thereby antagonizing Ca2+-driven apoptosis.

Journal: Cell death and differentiation

Published: February 25, 2021

Bcl-2-Protein Family as Modulators of IP3 Receptors and Other Organellar Ca2+ Channels.

Bcl-2-Protein Family as Modulators of IP3 Receptors and Other Organellar Ca2+ Channels.

Journal: Cold Spring Harbor perspectives in biology

Published: September 11, 2019

Bcl-2 and IP3 compete for the ligand-binding domain of IP3Rs modulating Ca2+ signaling output.

Bcl-2 and IP3 compete for the ligand-binding domain of IP3Rs modulating Ca2+ signaling output.

Journal: Cellular and molecular life sciences : CMLS

Published: December 21, 2018

Pathophysiological consequences of isoform-specific IP3 receptor mutations.

Pathophysiological consequences of isoform-specific IP3 receptor mutations.

Journal: Biochimica et biophysica acta. Molecular cell research

Published: May 06, 2018

Modulation of Ca2+ Signaling by Anti-apoptotic B-Cell Lymphoma 2 Proteins at the Endoplasmic Reticulum-Mitochondrial Interface.

Modulation of Ca2+ Signaling by Anti-apoptotic B-Cell Lymphoma 2 Proteins at the Endoplasmic Reticulum-Mitochondrial Interface.

Journal: Frontiers in oncology

Published: January 20, 2017

A double point mutation at residues Ile14 and Val15 of Bcl-2 uncovers a role for the BH4 domain in both protein stability and function.

A double point mutation at residues Ile14 and Val15 of Bcl-2 uncovers a role for the BH4 domain in both protein stability and function.

Journal: The FEBS journal

Published: December 19, 2016

Endoplasmic Reticulum-Mitochondrial Ca2+ Fluxes Underlying Cancer Cell Survival.

Endoplasmic Reticulum-Mitochondrial Ca2+ Fluxes Underlying Cancer Cell Survival.

Journal: Frontiers in oncology

Published: December 12, 2016

The BH4 domain of Bcl-2 orthologues from different classes of vertebrates can act as an evolutionary conserved inhibitor of IP3 receptor channels.

The BH4 domain of Bcl-2 orthologues from different classes of vertebrates can act as an evolutionary conserved inhibitor of IP3 receptor channels.

Journal: Cell calcium

Published: November 28, 2016

The selective Bcl-2 inhibitor venetoclax, a BH3 mimetic, does not dysregulate intracellular Ca2+ signaling.

The selective Bcl-2 inhibitor venetoclax, a BH3 mimetic, does not dysregulate intracellular Ca2+ signaling.

Journal: Biochimica et biophysica acta. Molecular cell research

Published: September 23, 2016

The trans-membrane domain of Bcl-2α, but not its hydrophobic cleft, is a critical determinant for efficient IP3 receptor inhibition.

The trans-membrane domain of Bcl-2α, but not its hydrophobic cleft, is a critical determinant for efficient IP3 receptor inhibition.

Journal: Oncotarget

Published: March 03, 2016

Showing 1-12 of 17

Last Updated: 09/26/2026