JAK3: A two-faced player in hematological disorders

被引：73

作者：

Cornejo, Melanie G. ^{[2
]}

Boggon, Titus J. ^{[3
]}

Mercher, Thomas ^{[1
]}

机构：

[1] Univ Paris 05, INSERM, E0210, Hop Necker, F-75015 Paris, France

[2] Harvard Univ, Sch Med, Boston, MA 02115 USA

[3] Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06520 USA

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2009年 / 41卷 / 12期

关键词：

Hematopoiesis; Lymphocytes; Tyrosine kinase; Cytokine signaling; ACUTE MEGAKARYOBLASTIC LEUKEMIA; LARGE-CELL LYMPHOMA; TRANSIENT MYELOPROLIFERATIVE DISORDER; DOWN-SYNDROME; JANUS KINASES; NPM-ALK; MUTATIONS; ACTIVATION; FAMILY;

D O I：

10.1016/j.biocel.2009.09.004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

JAK3 is a non-receptor tyrosine kinase, predominantly expressed in hematopoietic cells and that has been implicated in the signal transduction of the common gamma chain subfamily of cytokine receptors. As a result, JAK3 plays an essential role in hematopoieisis during T cell development. JAK3 inactivating mutations result in immunodeficiency syndromes (SCID) in both humans and mice. Recent data indicate that abnormal activation of JAK3 due to activating mutations is also found in human hematological malignancies, including acute megakaryoblastic leukemia (AMKL) and cutaneous T cell lymphoma (CTCL). After a brief summary of the JAK3 structure and function, we will review the evidence on the emerging role of JAK3 activation in hematological malignancies that warrant further studies to test the relevance of specific inhibition of JAK3 as a therapeutic approach to these challenging clinical entities. (C) 2009 Elsevier Ltd. All rights reserved.

引用

页码：2376 / 2379

页数：4

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