Ilka Wittig

This study identifies biallelic UQCC1 variants as a cause of early-onset mitochondrial disease by impairing complex III assembly and function.

This study identifies SNHG29 and IGF2BP1 as a lineage-specific oncogenic circuit in AMKL, showing their dependency and therapeutic vulnerability.

The paper shows TMBIM5 and SLC8B1 work together in tissue-specific mitochondrial calcium regulation in zebrafish, with TMBIM5 acting as a calcium efflux pathway.

The paper uses human heart organoids to model mitochondrial disease and identifies a drug that improves mitochondrial function and tissue contractility.

The paper identifies the transaminase-omega-amidase pathway as a redox-sensitive metabolic switch in endothelial glutamine metabolism, showing that NIT2 oxidation inhibits its activity and affects angiogenesis.

This study identifies nuclear eNOS's role in modulating ADAR1 activity and type I interferon signaling, linking NO bioavailability to endothelial function and atherogenesis.

This study identifies QKI as a regulator of splicing fidelity during cardiogenesis by interacting with U6 snRNA to enhance splicing at weak 5' splice sites.

This study shows RTN4IP1 is critical for mitochondrial complex I assembly and coenzyme Q biosynthesis, with mutations causing defects in both processes in patient cells.

This study shows that expressing alternative oxidase (AOX) reduces reverse electron transfer and oxidative stress in ischemia-reperfusion brain injury, preserving complex I function and providing neuroprotection.

The paper identifies a COA5 missense variant causing isolated mitochondrial complex IV assembly impairment in two siblings and validates its role in early CIV assembly using patient-derived cells and CRISPR/Cas9 knockout models.

This study identifies long non-coding RNAs (lncRNAs) as guides for the SWI/SNF complex to cell-specific enhancers, revealing a mechanism for chromatin accessibility and gene expression control.

This paper identifies MIRIAL as an aging-induced lncRNA that regulates endothelial quiescence and mitochondrial function through a novel triplex mechanism.

This study identifies NUDT6 as an antisense transcript of FGF2, showing that its silencing enhances smooth muscle cell survival and limits vascular disease progression.

This study identifies LINC00607 as an endothelial-specific lncRNA that supports angiogenic function by interacting with BRG1 to regulate chromatin accessibility and ERG target gene transcription.

The paper identifies HIF1α-AS1 as a DNA:DNA:RNA triplex-forming lncRNA that interacts with the HUSH complex to repress gene expression and modulates angiogenesis in pulmonary hypertension.

CEDAR provides a database for complexome profiling data with standardized formats, a web interface, and tools for analysis and exploration.