Anton Gartner

This paper characterizes the C. elegans Shu complex as an ATPase that remodels RAD51 filaments during homologous recombination.

This study identifies MUL-1 proteins as redox-responsive modulators of oxidative stress signaling in C. elegans, showing their role in buffering oxidative stress and preventing germ cell apoptosis.

This study shows that LEM-3/ANKLE1 nuclease cleaves branched DNA substrates and requires both LEM-like and GIY-YIG domains for DNA bridge processing in C. elegans.

The paper analyzes whole-genome sequencing data from DNA repair-deficient cell lines to identify mutational signatures linked to aging and temozolomide chemotherapy.

This study investigates the distinct roles of RAD-54.L and RAD-54.B in C. elegans meiotic prophase, showing RAD-54.L facilitates RAD-51 removal while RAD-54.B prevents excessive RAD-51 accumulation.

This study identifies the role of SPT2 in chromatin structure and function across Metazoa, showing its importance in germline development and chromatin accessibility.

The paper analyzes mutational spectra in C. elegans DNA repair mutants to identify how different repair pathways affect mutagenesis in germ cells.

This study shows that mutation spectra in C. elegans are shaped by both DNA damage and repair processes, with repair deficiencies altering mutation rates and spectra in many experimental conditions.

The paper shows that NEDP1 regulates the NEDD8 cycle upon DNA damage, modulating HSP70 ATPase activity to promote apoptosis and identifies this as relevant in hepatocellular carcinoma.

The paper identifies mutational signatures linked to DNA mismatch repair deficiency in C. elegans and human cancers, revealing similarities and differences between species.

This study identifies genes that protect C. elegans dopaminergic neurons from oxidative stress, showing that glit-1, tsp-17, the apoptosis pathway, and crt-1 are required to prevent 6-OHDA-induced neurodegeneration.

The paper identifies TTR-33 as a neuroprotective factor against 6-OHDA-induced dopaminergic neurodegeneration in C. elegans, showing its role in oxidative stress resistance and interaction with MAPK pathways.