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JAK2V617F promotes replication fork stalling with disease-restricted impairment of the intra-S checkpoint response.

Abstract:

Cancers result from the accumulation of genetic lesions, but the cellular consequences of driver mutations remain unclear, especially during the earliest stages of malignancy. The V617F mutation in the JAK2 non-receptor tyrosine kinase (JAK2V617F) is present as an early somatic event in most patients with myeloproliferative neoplasms (MPNs), and the study of these chronic myeloid malignancies provides an experimentally tractable approach to understanding early tumorigenesis. Introduction of e...

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Publication status:
Published

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Publisher copy:
10.1073/pnas.1401873111

Authors


Publisher:
National Academy of Sciences
Journal:
Proceedings of the National Academy of Sciences of the United States of America
Volume:
111
Issue:
42
Pages:
15190-15195
Publication date:
2014-10-01
DOI:
EISSN:
1091-6490
ISSN:
0027-8424
Language:
English
Keywords:
Pubs id:
pubs:486160
UUID:
uuid:3ad70471-b6be-4872-bc3e-d6fbcf03f2aa
Local pid:
pubs:486160
Source identifiers:
486160
Deposit date:
2014-10-13

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