Area of research
Molecular Biology · Physiology
Research interest
Research focused on Cell biology and Autophagy, with related work in Endoplasmic reticulum, Mitochondrion, Apoptosis. Notable publications include 'The regulation of autophagy by calcium signals: Do we have a consensus?', 'Intracellular Ca2+ signaling and Ca2+ microdomains in the control of cell survival, apoptosis and autophagy', and 'Regulation of the Autophagic Bcl-2/Beclin 1 Interaction'.
The ER-mitochondria interface, where Ca2+ and cell death meet
TRPC3 shapes the ER-mitochondria Ca2+ transfer characterizing tumour-promoting senescence
TMBIM5 loss of function alters mitochondrial matrix ion homeostasis and causes a skeletal myopathy
Sec61 complex/translocon: The role of an atypical ER Ca2+-leak channel in health and disease
Balancing ER-Mitochondrial Ca2+ Fluxes in Health and Disease
Bcl-xL acts as an inhibitor of IP3R channels, thereby antagonizing Ca2+-driven apoptosis
A comprehensive overview of the complex world of the endo- and sarcoplasmic reticulum Ca2+-leak channels
Necroptosis in Immuno-Oncology and Cancer Immunotherapy
Transmembrane BAX Inhibitor-1 Motif Containing Protein 5 (TMBIM5) Sustains Mitochondrial Structure, Shape, and Function by Impacting the Mitochondrial Protein Synthesis Machinery
New Insights in the IP3 Receptor and Its Regulation
Bcl-2 and IP3 compete for the ligand-binding domain of IP3Rs modulating Ca2+ signaling output
Emerging molecular mechanisms in chemotherapy: Ca2+ signaling at the mitochondria-associated endoplasmic reticulum membranes
Constitutive IP3 signaling underlies the sensitivity of B-cell cancers to the Bcl-2/IP3 receptor disruptor BIRD-2
Pathophysiological consequences of isoform-specific IP3 receptor mutations
The regulation of autophagy by calcium signals: Do we have a consensus?
IP3 Receptor-Mediated Calcium Signaling and Its Role in Autophagy in Cancer
Endoplasmic Reticulum-Mitochondria Communication Through Ca2+ Signaling: The Importance of Mitochondria-Associated Membranes (MAMs)
Downregulation of type 3 inositol (1,4,5)-trisphosphate receptor decreases breast cancer cell migration through an oscillatory Ca2+ signal
Resveratrol-induced autophagy is dependent on IP3Rs and on cytosolic Ca2+
Bcl-2 inhibitors as anti-cancer therapeutics: The impact of and on calcium signaling
Alterations in Ca2+ Signalling via ER-Mitochondria Contact Site Remodelling in Cancer
Intracellular Ca2+ signaling and Ca2+ microdomains in the control of cell survival, apoptosis and autophagy
Bcl-2 proteins and calcium signaling: complexity beneath the surface
ER functions of oncogenes and tumor suppressors: Modulators of intracellular Ca2+ signaling
The selective Bcl-2 inhibitor venetoclax, a BH3 mimetic, does not dysregulate intracellular Ca 2+ signaling
The trans-membrane domain of Bcl-2α, but not its hydrophobic cleft, is a critical determinant for efficient IP3 receptor inhibition
The BH4 Domain of Anti-apoptotic Bcl-XL, but Not That of the Related Bcl-2, Limits the Voltage-dependent Anion Channel 1 (VDAC1)-mediated Transfer of Pro-apoptotic Ca2+ Signals to Mitochondria
Endoplasmic reticulum Ca2+ content decrease by PKA-dependent hyperphosphorylation of type 1 IP3 receptor contributes to prostate cancer cell resistance to androgen deprivation
BAX inhibitor-1 is a Ca2+ channel critically important for immune cell function and survival
A dual role for the anti-apoptotic Bcl-2 protein in cancer: Mitochondria versus endoplasmic reticulum