Corina T. Madreiter-Sokolowski

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Associate Professor

Medical University of Graz

Austria

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About

Corina T. Madreiter-Sokolowski is an Associate Professor at the Medical University of Graz, Austria. Her research areas encompass mitochondrial dysfunction, cellular calcium modulation in cancer, and placental endothelial function, as evidenced by her recent articles. She also explores the implications of aging on cardiovascular health and the application of advanced microscopy techniques in cellular studies.

Recent Grants

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Studying the impact of mitochondrial Ca2+ modulation on aging in yeast

Open Date: 2023-05-01

Close Date: 2023-06-01

Grant: Close

T3-induced rewiring of mitochondrial Ca2+ in cancer cells

Open Date: 2023-03-01

Close Date:

Grant: Close

Promotion of lifespan by mitochondrial Ca2+-induced ROS

Open Date: 2022-12-01

Close Date:

Grant: Close

Analysis of reactive oxygen species and ion homeostasis in Dravet syndrome

Open Date: 2022-10-01

Close Date:

Grant: Close

Investigating novel anti-aging strategies

Open Date: 2022-06-01

Close Date:

Articles (22)

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2021

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2021

Collaborators (17)

ANDREAS PROKESCH

Assoc. Prof. and Group leader

Medical University of Graz

AUSTRIA

Corina T. Madreiter-Sokolowski

Research Interests

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About

Recent Grants

Articles (22)

FXR adapts hepatic mitochondrial function to increased substrate oxidation in patients with obesity

A novel super-resolution STED microscopy analysis approach to observe spatial MCU and MICU1 distribution dynamics in cells.

In vitro examination of Piezo1-TRPV4 dynamics: implications for placental endothelial function in normal and preeclamptic pregnancies

Is ageing a modifiable risk factor for atrial fibrillation?

Evaluation of two printing techniques for maxillary removable partial denture frameworks

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells

Breast cancer cells utilize T3 to trigger proliferation through cellular Ca&lt;sup&gt;2+&lt;/sup&gt; modulation.

Targeting organ-specific mitochondrial dysfunction to improve biological aging.

STEADY-STATE REGULATION OF COPII-DEPENDENT SECRETORY CARGO SORTING BY INOSITOL TRISPHOSPHATE RECEPTORS, CALCIUM, AND PENTA EF HAND PROTEINS.

Exendin-4 protects against high glucose-induced mitochondrial dysfunction and oxidative stress in SH-SY5Y neuroblastoma cells through GLP-1 receptor/Epac/Akt signaling

Investigation of novel Mn(ii) fenamato complexes with neocuproine and their effects on endometrial cell lines

Adipose Triglyceride Lipase Deficiency Attenuates In Vitro Thrombus Formation without Affecting Platelet Activation and Bleeding In Vivo

High Glucose-Induced Cardiomyocyte Damage Involves Interplay between Endothelin ET-1/ETA/ETB Receptor and mTOR Pathway

EGCG Promotes FUS Condensate Formation in a Methylation-Dependent Manner

Cristae junction as a fundamental switchboard for mitochondrial ion signaling and bioenergetics

ALG-2 and peflin regulate COPII targeting and secretion in response to calcium signaling

PCK2 opposes mitochondrial respiration and maintains the redox balance in starved lung cancer cells

Near-UV Light Induced ROS Production Initiates Spatial Ca2+ Spiking to Fire NFATc3 Translocation

Sigma-1 Receptor Promotes Mitochondrial Bioenergetics by Orchestrating ER Ca2+ Leak during Early ER Stress

Green tea catechins EGCG and ECG enhance the fitness and lifespan of Caenorhabditis elegans by complex I inhibition

Targeting cellular senescence based on interorganelle communication, multilevel proteostasis, and metabolic control

Targeting the Mitochondria-Proteostasis Axis to Delay Aging

Collaborators (17)

ANDREAS PROKESCH

Yusuf Ceyhun Erdoğan

Melanie Korbelius

Ursula Hiden

Andrew Peden

Zhanat Koshenov

Katharina Leithner

Wolfgang Graier

Marion Mussbacher

Furkan Enes Oflaz

Sarah Stryeck

Alice Assinger

Axel Schlagenhauf

Dagmar Kratky

Pidder Jansen‐Duerr

David Gordon

Roland Malli

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Breast cancer cells utilize T3 to trigger proliferation through cellular Ca<sup>2+</sup> modulation.