Abstract:
:The critical role of Janus kinase-2 (JAK2) in regulation of myelopoiesis was established 2 decades ago, but identification of mutations in the pseudokinase domain of JAK2 in myeloproliferative neoplasms (MPNs) and in other hematologic malignancies highlighted the role of JAK2 in human disease. These findings have revolutionized the diagnostics of MPNs and led to development of novel JAK2 therapeutics. However, the molecular mechanisms by which mutations in the pseudokinase domain lead to hyperactivation of JAK2 and clinical disease have been unclear. Here, we describe recent advances in the molecular characterization of the JAK2 pseudokinase domain and how pathogenic mutations lead to constitutive activation of JAK2.
journal_name
Bloodjournal_title
Bloodauthors
Silvennoinen O,Hubbard SRdoi
10.1182/blood-2015-01-621110subject
Has Abstractpub_date
2015-05-28 00:00:00pages
3388-92issue
22eissn
0006-4971issn
1528-0020pii
blood-2015-01-621110journal_volume
125pub_type
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