NMNAT is genetically required for glioma development and promotes glioma growth by allowing a higher tolerance to DNA damage and inhibiting DNA damage-p53-caspase-3 apoptosis signaling pathway by enhancing NAD⁺-dependent posttranslational modifications (PTMs) poly(ADP-ribosyl)ation (PARylation) and deacetylation of p53.

PARP-7 is a mono(ADP-ribosyl) transferase that directs an extensive ADP-ribosylated proteome to control microtubule stability, and regulate ovarian cancer cell growth and motility.

A technology to produce homogenously poly-ADP-ribosylated proteins reveals key molecular mechanisms that govern ATP-dependent chromatin remodeling activity at DNA damage sites.

The first-in-class cell-permeant fluorescent probe provides direct and visual evidence of SARM1 activation in axonal degeneration and identified the first covalent, allosteric inhibitor of SARM1 acting on the NAD-binding pocket in the ARM domain.

The pseudokinase-like Legionella effector SidJ catalyzes the glutamylation of bacterial ubiquitin ligases in a calmodulin-dependent manner.

Legionella pneumophila modulates host energy metabolism by targeting the ADP/ATP translocase carrier proteins with an effector of ADP-ribosyltransferase activity.

The nuclear protein Sam68 plays a role in the genotoxic stress-initiated "nuclear to cytoplasmic" activation of NF-κB and is involved in the development and survival of colon cancer.

By moving between DNA segments like a child swinging on monkey bars, poly(ADP-ribose) polymerase 1 explores possible DNA damage sites more effectively.

DePARylation is essential for cell survival and thus poly(ADP-ribose) glycohydrolase (PARG) expression correlates with cytotoxicity induced by PARG inhibition, which will benefit the development of PARG inhibitors for cancer treatment.