Title : Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression. A prominent role in neuroprotection against excitotoxicity.

Pub. Date : 1999 Mar 5

PMID : 10037682






2 Functional Relationships(s)
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1 Long term, but not acute, treatment of cultured cerebellar granule cells with LiCl induces a concentration-dependent decrease in mRNA and protein levels of proapoptotic p53 and Bax; conversely, mRNA and protein levels of cytoprotective Bcl-2 are remarkably increased. Lithium Chloride BCL2 associated X, apoptosis regulator Homo sapiens
2 Pretreatment with LiCl for 7 days prevents glutamate-induced increase in p53 and Bax expression and maintains Bcl-2 in an elevated state. Lithium Chloride BCL2 associated X, apoptosis regulator Homo sapiens