ArticleBritish journal of haematology2013
SH2B3 (LNK) mutations from myeloproliferative neoplasms patients have mild loss of function against wild type JAK2 and JAK2 V617F.
Article in British journal of haematology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Diagnostic relevance of SH2B3 mutations in suspected myeloid malignancies and acute leukemia: insights from a large-scale NGS-based screening study.Blood cancer journal · 2025Article
- A Single Nucleotide Polymorphism inCirculation research · 2022Article
- Immune dysregulation associated with co-occurring germline CBL and SH2B3 variants.Human genomics · 2022Article
- The Role of LNK (SH2B3) in the Regulation of JAK-STAT Signalling in Haematopoiesis.Pharmaceuticals (Basel, Switzerland) · 2021Review
- The role of LNK/SH2B3 genetic alterations in myeloproliferative neoplasms and other hematological disorders.Leukemia · 2017Review
- Genetic Alterations of the Thrombopoietin/MPL/JAK2 Axis Impacting Megakaryopoiesis.Frontiers in endocrinology · 2017Review
- Idiopathic hypereosinophilia is clonal disorder? Clonality identified by targeted sequencing.PloS one · 2017Article
- Cytogenetic and molecular abnormalities in chronic myelomonocytic leukemia.Blood cancer journal · 2016Review
- Mutational analysis of SH2B3 in Korean patients with BCR-ABL1 negative myeloproliferative neoplasm.Annals of laboratory medicine · 2016Article
- Protein kinase Cɛ inhibition restores megakaryocytic differentiation of hematopoietic progenitors from primary myelofibrosis patients.Leukemia · 2015Article
- 12q24 locus association with type 1 diabetes: SH2B3 or ATXN2?World journal of diabetes · 2014Review
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
Abstract
Somatic point mutations in the PH domain of SH2B3 (LNK), an adaptor protein that is highly expressed in haematopoietic cells, were recently described in patients with myeloproliferative neoplasms. We studied the effect of these mutations on the JAK2 signalling pathway in cells expressing either wild type JAK2 or the JAK2 V617F mutation. Compared to wild type SH2B3, PH domain mutants have mild loss of function, with no evidence for a dominant-negative effect. Mutants retain binding capacity for JAK2, an established SH2B3 target, as well as for the adaptor proteins 14-3-3 and CBL. Our data suggest that the loss of SH2B3 inhibitory function conferred by the PH domain mutations is mild and may collaborate with JAK2 V617F and CBL mutations in order to promote either the development or the progression of myeloproliferative neoplasms.
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