The L2a element is a mouse CD8 silencer that interacts with MAR-binding proteins SATB1 and CDP.
The L2a element is a mouse CD8 silencer that interacts with MAR-binding proteins SATB1 and CDP.
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DOI：
10.1016/j.molimm.2010.08.014
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发表时间：
2010-11
影响因子：
3.6
通讯作者：
Tucker PW
中科院分区：
文献类型：
--
作者：
Yao X;Nie H;Rojas IC;Harriss JV;Maika SD;Gottlieb PD;Rathbun G;Tucker PW
Previous transgenic-reporter and targeted-deletion studies indicate that the subset-specific expression of CD8αβ heterodimers is controlled by multiple enhancer activities, since no silencer elements had been found within the locus. We have identified such a silencer as L2a, a previously characterized ~220 bp nuclear matrix associating region (MAR) located ~4.5 kb upstream of CD8α. L2a transgenes driven by the E8I enhancer showed no reporter expression in thymic subsets or T cells in splenic, inguinal and mesenteric lymph node peripheral T cells. Deletion of L2a resulted in significant reporter de-repression, even in the CD4+CD8+ double positive (DP) thymocyte population. L2a contains binding sites for two MAR-interacting proteins, SATB1 and CDP. We found that that binding of these factors was markedly influenced by the content and spacing of L2a sub-motifs (L and S) and that SATB1 binds preferentially to the L motif both in vitro and in vivo. A small fraction of the transgenic CD8+ single positive (SP) thymocytes and peripheral CD8+ T cells bypassed L2a-silencing to give rise to variegated expression of the transgenic reporter. Crossing the L2a-containing transgene onto a SATB1 knockdown background enhanced variegated expression, suggesting that SATB1 is critical in overcoming L2a-silenced transcription.
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影响因子：
4
作者：
Hart, CM;Laemmli, UK
通讯作者：
Laemmli, UK
影响因子：
64.5
作者：
DICKINSON, LA;JOH, T;KOHWISHIGEMATSU, T
通讯作者：
KOHWISHIGEMATSU, T
影响因子：
14.9
作者：
NAKAUCHI, H;TAGAWA, M;HERZENBERG, LA
通讯作者：
HERZENBERG, LA
DOI：
10.1084/jem.178.3.941
发表时间：
1993-09-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Landry DB;Engel JD;Sen R
通讯作者：
Sen R
影响因子：
32.4
作者：
Hostert, A;Tolaini, M;Kioussis, D
通讯作者：
Kioussis, D