Abstract：
:Although dephosphorylation of tyrosine containing proteins is considered a necessary step in the induction of leukemia cell differentiation by hybrid polar compounds (HPC), the crucial actors in this step remain unknown. We present evidence that tyrosine phosphorylation of JAK1 and JAK2 is down-regulated in murine erythroleukemia cells (MELC) within the first 6 h of their exposure to the prototype of the HPC family, hexamethylenebisacetamide (HMBA), with full recovery at 14 h. Further evidence that the JAKs-centered signalling pathway is switched off early by HMBA was provided by the demonstration that STAT5, a downstream member of this pathway, turned out to be completely dephosphorylated at 6 h in HMBA-treated cells. This JAKs dephosphorylation did not occur in HMBA-resistant clones, suggesting that JAKs are possible targets of the dephosphorylative process required for leukemia cell commitment to differentiation. These results may have impact on leukemia therapy based on JAKs inhibitors.
journal_name
Leukemiajournal_title
Leukemiaauthors
Arcangeli A,Fontana L,Crociani O,Cherubini A,Hofmann G,Piccini E,Polvani S,D'Amico M,Carlà M,Olivotto Mdoi
10.1038/sj.leu.2401936subject
Has Abstractpub_date
2000-12-01 00:00:00pages
2112-7issue
12eissn
0887-6924issn
1476-5551journal_volume
14pub_type
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