TIPARP, also known as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible Poly-ADP-ribose Polymerase, is a member of the PARP family. It catalyzes mono-ADP-ribosylation, adding a single ADP-ribose moiety to itself or other proteins. This process is involved in various biological pathways, and TIPARP is important in physiological and pathophysiological processes [1,3].

In a study using Tiparp-/-mice, loss of Tiparp led to an aberrant organization of the mouse cortex, with increased cell density in the upper layers, mainly affecting GABAergic neuron distribution and number. Neural progenitor cell proliferation was reduced, and neural stem cells showed slower migration. The reduction of α-tubulin mono-ADP ribosylation (MAR) levels in Tiparp-/-cells suggested Tiparp's role in α-tubulin MAR [3]. Knockdown of Tiparp in ischemic stroke mice reduced brain infarction and promoted motor function recovery. A TIPARP inhibitor, XG-04-B1, also promoted brain injury repair and motor function recovery, increased neuronal plasticity, and inhibited astrocyte activation. EIF3B was identified as a direct target of TIPARP, and TIPARP-EIF3B interaction led to mitochondrial dysfunction, which was restored by Tiparp knockdown or inhibitor treatment [2].

In conclusion, TIPARP plays crucial roles in the development of the cerebral cortex, as revealed by gene knockout mouse models. It is also involved in mitochondrial function and brain injury in ischemic stroke, highlighting its potential as a therapeutic target in stroke. These model-based studies contribute to understanding TIPARP's biological functions and its implications in specific disease areas [2,3].