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dc.contributor.authorHansen, N.en
dc.contributor.authorÅgerstam, H.en
dc.contributor.authorWahlestedt, M.en
dc.contributor.authorLandberg, N.en
dc.contributor.authorAskmyr, M.en
dc.contributor.authorEhinger, M.en
dc.contributor.authorRissler, M.en
dc.contributor.authorLilljebjörn, H.en
dc.contributor.authorJohnels, P.en
dc.contributor.authorIshiko, J.en
dc.contributor.authorMelo, J.en
dc.contributor.authorAlexander, W.en
dc.contributor.authorBryder, D.en
dc.contributor.authorJärås, M.en
dc.contributor.authorFioretos, T.en
dc.identifier.citationLeukemia, 2013; 27(1):130-135en
dc.description.abstractSuppressor of cytokine signaling 2 (SOCS2) is known as a feedback inhibitor of cytokine signaling and is highly expressed in primary bone marrow (BM) cells from patients with chronic myeloid leukemia (CML). However, it has not been established whether SOCS2 is involved in CML, caused by the BCR/ABL1 fusion gene, or important for normal hematopoietic stem cell (HSC) function. In this study, we demonstrate that although Socs2 was found to be preferentially expressed in long-term HSCs, Socs2-deficient HSCs were indistinguishable from wild-type HSCs when challenged in competitive BM transplantation experiments. Furthermore, by using a retroviral BCR/ABL1-induced mouse model of CML, we demonstrate that SOCS2 is dispensable for the induction and propagation of the disease, suggesting that the SOCS2-mediated feedback regulation of the JAK/STAT pathway is deficient in BCR/ABL1-induced CML.en
dc.description.statementofresponsibilityN Hansen, H Ågerstam, M Wahlestedt, N Landberg, M Askmyr, M Ehinger, M Rissler, H Lilljebjörn, P Johnels, J Ishiko, J V Melo, W S Alexander, D Bryder, M Järås, and T Fioretosen
dc.publisherNature Publishing Groupen
dc.rights© 2013 Macmillan Publishers Limited. This work is licensed under the Creative Commons Attribution- NonCommercial-No Derivative Works 3.0 Unported License.en
dc.subjectCML; BCR/ABL1; SOCS2; HSC; STAT5 phosphorylationen
dc.titleSOCS2 is dispensable for BCR/ABL1-induced chronic myeloid leukemia-like disease and for normal hematopoietic stem cell functionen
dc.typeJournal articleen
Appears in Collections:Medicine publications

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