Nadine Hempel

The paper compares the ability of different Orai isoforms to promote NFAT activation and transcription, finding Orai1α and Orai1β are more potent than Orai2 and Orai3.

This study shows that chemotherapy-induced senescence-associated secretome promotes metastasis in ovarian cancer by reprogramming metabolism and increasing cell detachment.

This study shows that αKG-mediated carnitine synthesis supports HR proficiency by promoting histone acetylation, which enhances DNA repair.

This study identifies RHOV as a detachment-sensitive Rho GTPase critical for ovarian cancer peritoneal metastasis by enhancing anoikis resistance and cytoskeletal remodeling.

This study shows CDK8/19 inhibition can reverse anoikis resistance and metastasis in ovarian cancer by altering transcriptional programs.

This study shows that loss of MPZL3 promotes EMT and chemoresistance in ovarian cancer by reducing adhesion and increasing drug resistance.

This study shows that loss of STIM2 in colorectal cancer promotes tumor growth and metastasis through metabolic reprogramming and activation of the PERK-ATF4 ER stress pathway.

This study shows ATR enhances mTORC1 activity through cholesterol synthesis via LSS, independent of CHK1 and TSC, and this effect is amplified in p16-deficient cells.

This study identifies high-risk mesenchymal stem cells (hrMSCs) that drive DNA damage and promote high-grade serous ovarian cancer initiation in fallopian tube epithelium.

This study shows that zinc availability in the tumor microenvironment affects anti-PD1 therapy response in CDKN2A-low tumors through macrophage phagocytosis.

This paper uses CRISPR-edited human iPSCs with hypomorphic NOTCH1 to model hypoplastic left heart syndrome, identifying auranofin as a potential therapeutic.

This study shows that ACSS2-mediated acetate conversion to acetyl-CoA promotes quiescence in ovarian cancer cells, linking metabolic reprogramming to therapeutic resistance.

This study identifies an alternative splice variant of Drp1 in ovarian cancer that promotes metastasis and chemoresistance by altering mitochondrial dynamics.

This study shows GPX3 is necessary for ovarian cancer growth in vivo and promotes GDF15 expression, linking it to immune checkpoint inhibitor response.