Title : Reactivating PP2A by FTY720 as a novel therapy for AML with C-KIT tyrosine kinase domain mutation.

Pub. Date : 2012 Apr

PMID : 22109829






3 Functional Relationships(s)
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1 Furthermore, FTY720-induced toxicity in AML leukemic cells was mediated by restoration of PP2A activity, via down-regulation of PP2A inhibitor SET, dephosporylation of PP2A-C(TYR307), and up-regulation of relevant PP2A subunit A and B55alpha. Fingolimod Hydrochloride protein phosphatase 2 phosphatase activator Homo sapiens
2 Furthermore, FTY720-induced toxicity in AML leukemic cells was mediated by restoration of PP2A activity, via down-regulation of PP2A inhibitor SET, dephosporylation of PP2A-C(TYR307), and up-regulation of relevant PP2A subunit A and B55alpha. Fingolimod Hydrochloride protein phosphatase 2 phosphatase activator Homo sapiens
3 Furthermore, FTY720-induced toxicity in AML leukemic cells was mediated by restoration of PP2A activity, via down-regulation of PP2A inhibitor SET, dephosporylation of PP2A-C(TYR307), and up-regulation of relevant PP2A subunit A and B55alpha. Fingolimod Hydrochloride protein phosphatase 2 phosphatase activator Homo sapiens