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Double immunostaining for PAR and NeuN or OX-42 revealed that PAR formation in neurons was an early process as compared to that observed in microglial cells.
Low to moderate levels of PAR may be beneficial for important cellular functions, whereas extensive PAR formation can be detrimental and lead to various forms of cell death.
Given that PARP protein levels remained constant while PAR formation increased, as verified by western blot against PARP and PAR, we concluded that PARP was activated within 15 min of stimulation with GO.
PAR western blots were also used to evaluate the time course of PAR formation.
Given that PARP-1 can be inhibited by PAR auto-modification [2], it is possible that the reduced peak PAR level observed in the PARG antisense-treated cultures is due to increased or prolonged PAR formation on PARP-1 with resultant reduced PARP-1 activity in these cultures.
These comprise basal arenaceous Par formation overlain by volcano-sedimentary sequences of Morar formation consisting of ferruginous shale with bands of chert, jasper and limestone.
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These data indicate that NEIL1 stimulates PAR polymer formation both in vitro and in vivo.
To detect PAR polymer formation by immunoblotting, wild-type and NEIL1−/− MEFs were untreated or treated with 500 mM H2O2 for 30 min and lysed in RIPA buffer.
In conclusion, these data suggest Ang II causes nNOS/Nox4 to co-localize at the peri-nuclear region of A549 cells, where superoxide produced by Nox4, and NO produced by nNOS immediately react to form peroxynitrite, which leads to subsequent nuclear oxidative damage as evidenced by increased PAR polymer formation.
A greater number of iron-positive cells were evident along the entire substantia nigra pars compacta formation (Fig. 5A F).
In addition to heterodimerization there are now data demonstrating PAR-PAR homodimer complex formation.
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