Arid
DOI10.1371/journal.pone.0161468
Arid3b Is Critical for B Lymphocyte Development
Kurkewich, Jeffrey L.1,2; Klopfenstein, Nathan2,4; Hallas, William M.2,5; Wood, Christian1,2; Sattler, Rachel A.2,6; Das, Chhaya3; Tucker, Haley; Dahl, Richard1,2,4; Dahl, Karen D. Cowden2,5,6
通讯作者Dahl, Richard ; Dahl, Karen D. Cowden
来源期刊PLOS ONE
ISSN1932-6203
出版年2016
卷号11期号:8
英文摘要

Arid3a and Arid3b belong to a subfamily of ARID (AT-rich interaction domain) transcription factors. The Arid family is involved in regulating chromatin accessibility, proliferation, and differentiation. Arid3a and Arid3b are closely related and share a unique REKLES domain that mediates their homo- and hetero-multimerization. Arid3a was originally isolated as a B cell transcription factor binding to the AT rich matrix attachment regions (MARS) of the immunoglobulin heavy chain intronic enhancer. Deletion of Arid3a results in a highly penetrant embryonic lethality with severe defects in erythropoiesis and hematopoietic stem cells (HSCs). The few surviving Arid3a(-/-) (<1%) animals have decreased HSCs and early progenitors in the bone marrow, but all mature lineages are normally represented in the bone marrow and periphery except for B cells. Arid3b(-/-) animals die around E7.5 precluding examination of hematopoietic development. So it is unclear whether the phenotype of Arid3a loss on hematopoiesis is dependent or independent of Arid3b. In this study we circumvented this limitation by also examining hematopoiesis in mice with a conditional allele of Arid3b. Bone marrow lacking Arid3b shows decreased common lymphoid progenitors (CLPs) and downstream B cell populations while the T cell and myeloid lineages are unchanged, reminiscent of the adult hematopoietic defect in Arid3a mice. Unlike Arid3a(-/-) mice, HSC populations are unperturbed in Arid3b(-/-) mice. This study demonstrates that HSC development is independent of Arid3b, whereas B cell development requires both Arid3a and Arid3b transcription factors.


类型Article
语种英语
国家USA
收录类别SCI-E
WOS记录号WOS:000381577000109
WOS关键词MOUSE BONE-MARROW ; IN-VITRO ; CELL ; TRANSCRIPTION ; EXPRESSION ; BRIGHT ; RESPONSES ; DEFECTS ; FAMILY ; CANCER
WOS类目Multidisciplinary Sciences
WOS研究方向Science & Technology - Other Topics
来源机构Arizona State University
资源类型期刊论文
条目标识符http://119.78.100.177/qdio/handle/2XILL650/195654
作者单位1.Univ Notre Dame, Dept Biol Sci, Notre Dame, IN 46556 USA;
2.Harper Canc Res Inst, South Bend, IN 46617 USA;
3.Univ Texas Austin, Dept Mol Biosci, Inst Cellular & Mol Biol, Austin, TX 78712 USA;
4.Indiana Univ Sch Med, Dept Microbiol & Immunol, South Bend, IN 46617 USA;
5.Indiana Univ Sch Med, Dept Biochem & Mol Biol, South Bend, IN 46617 USA;
6.Univ Notre Dame, Dept Chem & Biochem, Notre Dame, IN 46556 USA
推荐引用方式
GB/T 7714
Kurkewich, Jeffrey L.,Klopfenstein, Nathan,Hallas, William M.,et al. Arid3b Is Critical for B Lymphocyte Development[J]. Arizona State University,2016,11(8).
APA Kurkewich, Jeffrey L..,Klopfenstein, Nathan.,Hallas, William M..,Wood, Christian.,Sattler, Rachel A..,...&Dahl, Karen D. Cowden.(2016).Arid3b Is Critical for B Lymphocyte Development.PLOS ONE,11(8).
MLA Kurkewich, Jeffrey L.,et al."Arid3b Is Critical for B Lymphocyte Development".PLOS ONE 11.8(2016).
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