| pubmed-article:20404132 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C0027022 | lld:lifeskim |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C0013126 | lld:lifeskim |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C1822705 | lld:lifeskim |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C1135629 | lld:lifeskim |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:20404132 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:20404132 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:20404132 | pubmed:dateCreated | 2010-8-13 | lld:pubmed |
| pubmed-article:20404132 | pubmed:abstractText | Dysregulated Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling due to activation of tyrosine kinases is a common feature of myeloid malignancies. Here we report the first human disease-related mutations in the adaptor protein LNK, a negative regulator of JAK-STAT signaling, in 2 patients with JAK2 V617F-negative myeloproliferative neoplasms (MPNs). One patient exhibited a 5 base-pair deletion and missense mutation leading to a premature stop codon and loss of the pleckstrin homology (PH) and Src homology 2 (SH2) domains. A second patient had a missense mutation (E208Q) in the PH domain. BaF3-MPL cells transduced with these LNK mutants displayed augmented and sustained thrombopoietin-dependent growth and signaling. Primary samples from MPN patients bearing LNK mutations exhibited aberrant JAK-STAT activation, and cytokine-responsive CD34(+) early progenitors were abnormally abundant in both patients. These findings indicate that JAK-STAT activation due to loss of LNK negative feedback regulation is a novel mechanism of MPN pathogenesis. | lld:pubmed |
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| pubmed-article:20404132 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20404132 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20404132 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20404132 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20404132 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20404132 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20404132 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:20404132 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20404132 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20404132 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:20404132 | pubmed:issn | 1528-0020 | lld:pubmed |
| pubmed-article:20404132 | pubmed:author | pubmed-author:NolanGarry... | lld:pubmed |
| pubmed-article:20404132 | pubmed:author | pubmed-author:ZehnderJames... | lld:pubmed |
| pubmed-article:20404132 | pubmed:author | pubmed-author:JonesCarolC | lld:pubmed |
| pubmed-article:20404132 | pubmed:author | pubmed-author:MerkerJason... | lld:pubmed |
| pubmed-article:20404132 | pubmed:author | pubmed-author:GotlibJasonJ | lld:pubmed |
| pubmed-article:20404132 | pubmed:author | pubmed-author:GibbsKenneth... | lld:pubmed |
| pubmed-article:20404132 | pubmed:author | pubmed-author:OhStephen TST | lld:pubmed |
| pubmed-article:20404132 | pubmed:author | pubmed-author:GoltsevYuryY | lld:pubmed |
| pubmed-article:20404132 | pubmed:author | pubmed-author:HaleMatthew... | lld:pubmed |
| pubmed-article:20404132 | pubmed:author | pubmed-author:SimondsErin... | lld:pubmed |
| pubmed-article:20404132 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20404132 | pubmed:day | 12 | lld:pubmed |
| pubmed-article:20404132 | pubmed:volume | 116 | lld:pubmed |
| pubmed-article:20404132 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20404132 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20404132 | pubmed:pagination | 988-92 | lld:pubmed |
| pubmed-article:20404132 | pubmed:dateRevised | 2011-8-25 | lld:pubmed |
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| pubmed-article:20404132 | pubmed:meshHeading | pubmed-meshheading:20404132... | lld:pubmed |
| pubmed-article:20404132 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20404132 | pubmed:articleTitle | Novel mutations in the inhibitory adaptor protein LNK drive JAK-STAT signaling in patients with myeloproliferative neoplasms. | lld:pubmed |
| pubmed-article:20404132 | pubmed:affiliation | Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford Cancer Center, 875 Blake Wilbur Dr., Stanford, CA 94305-5821, USA. | lld:pubmed |
| pubmed-article:20404132 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20404132 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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