DNase Hypersensitive Site (HSS/DHS)

2012 ◽  
Keyword(s):  
Hypersensitive Site ◽  
Dnase Hypersensitive Site

scholarly journals Association of Ddx5/p68 protein with the upstream erythroid enhancer element (EHS1) of the Klf1 gene

2019 ◽  
Author(s):  
Xiaoyong Chen ◽  
Felix Lohmann ◽  
James J Bieker
Keyword(s):  
Transcription Factor ◽  
Expression Pattern ◽  
Transcriptional Activation ◽  
Affinity Purification ◽  
Hypersensitive Site ◽  
Enhancer Element ◽  
Restricted Expression Pattern ◽  
Dnase Hypersensitive Site ◽  
Essential Transcription Factor ◽  
Klf1 Gene

AbstractEKLF/KLF1 is an essential transcription factor that plays a global role in erythroid transcriptional activation. It’s own regulation is of interest, as it displays a highly restricted expression pattern, limited to erythroid cells and its progenitors. Here we use biochemical affinity purification to identify the Ddx5/p68 protein as a potential activator of KLF1 by virtue of its interaction with the erythroid-specific DNAse hypersensitive site (EHS1) upstream enhancer element. We postulate that its range of interactions with other proteins known to interact with this element render it part of the enhanseosome complex critical for optimal expression of KLF1.

scholarly journals Enhancer-dependent transcription of the epsilon-globin promoter requires promoter-bound GATA-1 and enhancer-bound AP-1/NF-E2.

1993 ◽  
Vol 13 (2) ◽  
pp. 911-917 ◽  
Author(s):  
Q Gong ◽  
A Dean
Keyword(s):  
Globin Gene ◽  
Gene Mutations ◽  
In Vitro Transcription ◽  
Beta Globin ◽  
Hypersensitive Site ◽  
Dnase Hypersensitive Site ◽  
Globin Promoter ◽  
Distal Promoter

We analyzed epsilon-globin transcription in erythroid cells and in erythroid extracts to determine the requirements for enhancer-dependent expression of this gene. Mutations that abolished GATA-1 binding at a single position in the promoter prevented interaction with enhancers, whereas elimination of a second more distal promoter GATA-1 site had no effect. Deletion or mutation of the GATA-1 sites in either the human beta-globin locus control region DNase-hypersensitive site II enhancer or the chicken beta A/epsilon-globin enhancer did not diminish the ability of the enhancers to interact with the promoter. In contrast, mutation of the AP-1/NF-E2 sites in these enhancers resulted in elimination of enhancement. In vitro transcription of these constructs was promoter dependent and was not sensitive to abolition of GATA-1 binding in the promoter, consistent with the role of GATA-1 solely as a mediator of the enhancer effect. Thus, GATA-1 regulates the response of the epsilon-globin gene to enhancers through a specific site in the promoter and requires enhancer AP-1/NF-E2 binding to transduce the enhancer effect on transcription.

Enhancer-dependent transcription of the epsilon-globin promoter requires promoter-bound GATA-1 and enhancer-bound AP-1/NF-E2

1993 ◽  
Vol 13 (2) ◽  
pp. 911-917
Author(s):  
Q Gong ◽  
A Dean
Keyword(s):  
Globin Gene ◽  
Gene Mutations ◽  
In Vitro Transcription ◽  
Beta Globin ◽  
Hypersensitive Site ◽  
Dnase Hypersensitive Site ◽  
Globin Promoter ◽  
Distal Promoter

We analyzed epsilon-globin transcription in erythroid cells and in erythroid extracts to determine the requirements for enhancer-dependent expression of this gene. Mutations that abolished GATA-1 binding at a single position in the promoter prevented interaction with enhancers, whereas elimination of a second more distal promoter GATA-1 site had no effect. Deletion or mutation of the GATA-1 sites in either the human beta-globin locus control region DNase-hypersensitive site II enhancer or the chicken beta A/epsilon-globin enhancer did not diminish the ability of the enhancers to interact with the promoter. In contrast, mutation of the AP-1/NF-E2 sites in these enhancers resulted in elimination of enhancement. In vitro transcription of these constructs was promoter dependent and was not sensitive to abolition of GATA-1 binding in the promoter, consistent with the role of GATA-1 solely as a mediator of the enhancer effect. Thus, GATA-1 regulates the response of the epsilon-globin gene to enhancers through a specific site in the promoter and requires enhancer AP-1/NF-E2 binding to transduce the enhancer effect on transcription.

A novel lineage-specific hypersensitive site is essential for position independent granzyme B expression in transgenic mice

2008 ◽  
Vol 368 (2) ◽  
pp. 357-363 ◽  
Author(s):  
Brenda L. Duggan ◽  
Nora R. Cabilio ◽  
Peter Dickie ◽  
Jennifer Witmer ◽  
Ing Swie Goping ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Granzyme B ◽  
Hypersensitive Site
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