Title : CD38 Knockout Mice Show Significant Protection Against Ischemic Brain Damage Despite High Level Poly-ADP-Ribosylation.

Pub. Date : 2017 Jan

PMID : 27518087






5 Functional Relationships(s)
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1 NAD+ depletion following ischemic insult can result in cell death and has been associated with over-activation of poly-ADP-ribose polymerase PARP1 as well as an increase in NAD+ consuming enzyme CD38. NAD CD38 antigen Mus musculus
2 NAD+ depletion following ischemic insult can result in cell death and has been associated with over-activation of poly-ADP-ribose polymerase PARP1 as well as an increase in NAD+ consuming enzyme CD38. NAD CD38 antigen Mus musculus
3 Decrease of hippocampal NAD+ levels detected during reperfusion in WT mice was only transient in CD38KO animals, suggesting that CD38 contributes to post-ischemic NAD+ catabolism. NAD CD38 antigen Mus musculus
4 Decrease of hippocampal NAD+ levels detected during reperfusion in WT mice was only transient in CD38KO animals, suggesting that CD38 contributes to post-ischemic NAD+ catabolism. NAD CD38 antigen Mus musculus
5 Thus, the absence of CD38 activity can not only directly affect inflammatory response, but also result in unpredicted alterations in the expression levels of enzymes participating in NAD+ metabolism. NAD CD38 antigen Mus musculus