Abstract:
:JAK2 V617F, identified in the majority of patients with myeloproliferative neoplasms, tyrosine phosphorylates SOCS3 and escapes its inhibition. Here, we demonstrate that the JAK2 exon 12 mutants described in a subset of V617F-negative MPN cases, also stabilize tyrosine phosphorylated SOCS3. SOCS3 tyrosine phosphorylation was also observed in peripheral blood mononuclear cells and granulocytes isolated from patients with JAK2 H538QK539L or JAK2 F537-K539delinsL mutations. JAK kinase inhibitors, which effectively inhibited the proliferation of cells expressing V617F or K539L, also caused a dose-dependent reduction in both mutant JAK2 and SOCS3 tyrosine phosphorylation. We propose, therefore, that SOCS3 tyrosine phosphorylation may be a novel bio-marker of myeloproliferative neoplasms resulting from a JAK2 mutation and a potential reporter of effective JAK2 inhibitor therapy currently in clinical development.
journal_name
Haematologicajournal_title
Haematologicaauthors
Elliott J,Suessmuth Y,Scott LM,Nahlik K,McMullin MF,Constantinescu SN,Green AR,Johnston JAdoi
10.3324/haematol.2008.002352subject
Has Abstractpub_date
2009-04-01 00:00:00pages
576-80issue
4eissn
0390-6078issn
1592-8721pii
haematol.2008.002352journal_volume
94pub_type
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