Upregulation of endogenous thrombopoietin receptor (MPL) with in vivo passage of calreticulin (CALR) mutant Ba/F3 cells, highlighting MPL as the requisite cytokine receptor for CALR mediated transformation.
作者信息
Brooks Stefan A, Kim Daniel M, Morse Sarah J, Nguyen Quy H, Craver Brianna M, Lai Hew Yeng, Fleischman Angela G
机构信息
Department of Biological Chemistry, University of California, Irvine, United States.
Department of Medicine, Division of Hematology/Oncology, University of California, Irvine, United States.
出版信息
Leuk Res. 2019 Jul;82:11-14. doi: 10.1016/j.leukres.2019.05.003. Epub 2019 May 9.
Abstract
摘要
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Upregulation of endogenous thrombopoietin receptor (MPL) with in vivo passage of calreticulin (CALR) mutant Ba/F3 cells, highlighting MPL as the requisite cytokine receptor for CALR mediated transformation.随着钙网蛋白（CALR）突变型Ba/F3细胞在体内传代，内源性血小板生成素受体（MPL）上调，突出了MPL作为CALR介导转化所必需的细胞因子受体的作用。
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本文引用的文献
1
Pathologic activation of thrombopoietin receptor and JAK2-STAT5 pathway by frameshift mutants of mouse calreticulin.小鼠钙网蛋白移码突变体对血小板生成素受体及JAK2-STAT5通路的病理性激活
Leukemia. 2016 Aug;30(8):1775-8. doi: 10.1038/leu.2016.47. Epub 2016 Feb 29.
2
Thrombopoietin receptor activation by myeloproliferative neoplasm associated calreticulin mutants.骨髓增殖性肿瘤相关钙网蛋白突变体对血小板生成素受体的激活作用。
Blood. 2016 Mar 10;127(10):1325-35. doi: 10.1182/blood-2015-11-681932. Epub 2015 Dec 14.
3
Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2.伴有未突变 JAK2 的骨髓增殖性肿瘤中的体细胞 CALR 突变。
N Engl J Med. 2013 Dec 19;369(25):2391-2405. doi: 10.1056/NEJMoa1312542. Epub 2013 Dec 10.
4
Somatic mutations of calreticulin in myeloproliferative neoplasms.髓系增殖性肿瘤中的钙网织蛋白体细胞突变。
N Engl J Med. 2013 Dec 19;369(25):2379-90. doi: 10.1056/NEJMoa1311347. Epub 2013 Dec 10.
5
Novel mutations in the inhibitory adaptor protein LNK drive JAK-STAT signaling in patients with myeloproliferative neoplasms.新型抑制衔接蛋白 LNK 突变驱动骨髓增殖性肿瘤患者的 JAK-STAT 信号通路。
Blood. 2010 Aug 12;116(6):988-92. doi: 10.1182/blood-2010-02-270108. Epub 2010 Apr 19.
6
MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia.MPLW515L是骨髓纤维化伴髓外化生中的一种新型体细胞激活突变。
PLoS Med. 2006 Jul;3(7):e270. doi: 10.1371/journal.pmed.0030270.
7
Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation.JAK2V617F介导的细胞转化需要同源二聚体型I细胞因子受体的表达。
Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18962-7. doi: 10.1073/pnas.0509714102. Epub 2005 Dec 19.
8
A gain-of-function mutation of JAK2 in myeloproliferative disorders.骨髓增殖性疾病中JAK2的功能获得性突变。
N Engl J Med. 2005 Apr 28;352(17):1779-90. doi: 10.1056/NEJMoa051113.
9
Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.真性红细胞增多症、原发性血小板增多症和伴有骨髓纤维化的骨髓化生中酪氨酸激酶JAK2的激活突变。
Cancer Cell. 2005 Apr;7(4):387-97. doi: 10.1016/j.ccr.2005.03.023.
10
A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera.一种导致持续性信号传导的独特克隆性JAK2突变会引发真性红细胞增多症。
Nature. 2005 Apr 28;434(7037):1144-8. doi: 10.1038/nature03546.
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