A Nuclear Matrix Attachment Region Upstream of the T Cell Receptor β Gene Enhancer Binds Cux/CDP and SATB1 and Modulates Enhancer-dependent Reporter Gene Expression but Not Endogenous Gene Expression *
Journal of Biological Chemistry, ISSN: 0021-9258, Vol: 273, Issue: 45, Page: 29838-29846
1998
- 62Citations
- 28Captures
- 1Mentions
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Metrics Details
- Citations62
- Citation Indexes62
- 62
- CrossRef49
- Captures28
- Readers28
- 28
- Mentions1
- References1
- Wikipedia1
Article Description
We have previously identified a DNase I-hypersensitive site in the T cell receptor β locus, designated HS1, that is located 400 base pairs upstream of the transcriptional enhancer E β and is induced during CD4 − CD8 − to CD4 + CD8 + thymocyte differentiation. Using electrophoretic mobility shift assays, we show that HS1 induction correlates with increased binding of two nuclear factors, Cux/CDP and SATB1, to a 170-base pair DNA sequence within HS1. Furthermore, we demonstrate that HS1 is a nuclear matrix attachment region, referred to as MAR β. These findings demonstrate that an analogous organization of cis-regulatory elements in which a nuclear matrix attachment region is in close proximity to an enhancer is conserved in the immunoglobulin and T cell receptor loci. In addition, we show that MAR β represses E β -dependent reporter gene expression in transient transfection assays. However, the targeted deletion of MAR β from the endogenous locus does not change T cell receptor β gene transcription in developing T cells. These contrasting results suggest a potential pitfall of functional studies of nuclear matrix attachment regions outside of their natural chromosomal context.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0021925819593899; http://dx.doi.org/10.1074/jbc.273.45.29838; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0032491508&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/9792700; https://linkinghub.elsevier.com/retrieve/pii/S0021925819593899; https://dx.doi.org/10.1074/jbc.273.45.29838
Elsevier BV
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