ArticleMolecular and cellular biology2007
The locus control region activates serpin gene expression through recruitment of liver-specific transcription factors and RNA polymerase II.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 29 citations in OpenAlex.
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- Review
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- Effect of Interaction between Chromatin Loops on Cell-to-Cell Variability in Gene Expression.PLoS computational biology · 2016Article
- CNTF Gene Therapy Confers Lifelong Neuroprotection in a Mouse Model of Human Retinitis Pigmentosa.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Article
- Uncovering enhancer functions using the α-globin locus.PLoS genetics · 2014Review
- Function of GATA factors in the adult mouse liver.PloS one · 2013Article
- Recruitment of transcription complexes to enhancers and the role of enhancer transcription.Biology · 2012Article
- Growth hormone-activated STAT5 may indirectly stimulate IGF-I gene transcription through HNF-3{gamma}.Molecular endocrinology (Baltimore, Md.) · 2009Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The human serine protease inhibitor (serpin) gene cluster at 14q32.1 comprises 11 serpin genes, many of which are expressed specifically in hepatic cells. Previous studies identified a locus control region (LCR) upstream of the human alpha1-antitrypsin (alpha1AT) gene that is required for gene activation, chromatin remodeling, and histone acetylation throughout the proximal serpin subcluster. Here we show that the LCR interacts with multiple liver-specific transcription factors, including hepatocyte nuclear factor 3beta (HNF-3beta), HNF-6alpha, CCAAT/enhancer binding protein alpha (C/EBPalpha), and C/EBPbeta. RNA polymerase II is also recruited to the locus through the LCR. Nongenic transcription at both the LCR and an upstream regulatory region was detected, but the deletion of the LCR abolished transcription at both sites. The deletion of HNF-3 and HNF-6 binding sites within the LCR reduced histone acetylation at both the LCR and the upstream regulatory region and decreased the transcription of the alpha1AT, corticosteroid binding globulin, and protein Z-dependent protease inhibitor genes. These results suggest that the LCR activates genes in the proximal serpin subcluster by recruiting liver-specific transcription factors and components of the general transcription machinery to regulatory regions upstream of the alpha1AT gene.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.