ArticleMolecular and cellular biology2001
Histone deacetylase activity represses gamma interferon-inducible HLA-DR gene expression following the establishment of a DNase I-hypersensitive chromatin conformation.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 41 citations in OpenAlex.
- A Ménage à trois: NLRC5, immunity, and metabolism.Frontiers in immunology · 2024Review
- MHC class II associated stomach cancer mutations correlate with lack of subsequent tumor development.Molecular and clinical oncology · 2017Article
- The RB tumor suppressor at the intersection of proliferation and immunity: relevance to disease immune evasion and immunotherapy.Cell cycle (Georgetown, Tex.) · 2015Review
- An Oct-1-based, feed-forward mechanism of apoptosis inhibited by co-culture with Raji B-cells: towards a model of the cancer cell/B-cell microenvironment.Experimental and molecular pathology · 2014Article
- Regulation of HLA-DR peptide occupancy by histone deacetylase inhibitors.Human vaccines & immunotherapeutics · 2013Article
- Article
- The Yin and Yang of YY1 in the nervous system.Journal of neurochemistry · 2008Review
- Histone deacetylase inhibitors induce TAP, LMP, Tapasin genes and MHC class I antigen presentation by melanoma cells.Cancer immunology, immunotherapy : CII · 2008Article
- The histone deacetylase inhibitor trichostatin A induces GADD45 gamma expression via Oct and NF-Y binding sites.Oncogene · 2008Article
- Transcription factor YY1: structure, function, and therapeutic implications in cancer biology.Oncogene · 2006Review
- The POU transcription factor Oct-1 represses virus-induced interferon A gene expression.Molecular and cellular biology · 2005Article
- Mutations and regulatory anomalies effecting tumor cell immune functions.Cancer immunology, immunotherapy : CII · 2004Review
- Histone deacetylase 1/mSin3A disrupts gamma interferon-induced CIITA function and major histocompatibility complex class II enhanceosome formation.Molecular and cellular biology · 2003Article
- Phorbol myristate acetate and Bryostatin 1 rescue IFN-gamma inducibility of MHC class II molecules in LS1034 colorectal carcinoma cell line.Cancer cell international · 2003Article
- Human cytomegalovirus gene expression during infection of primary hematopoietic progenitor cells: a model for latency.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- The class II transactivator requires brahma-related gene 1 to activate transcription of major histocompatibility complex class II genes.Molecular and cellular biology · 2002Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Expression of the retinoblastoma tumor suppressor protein (Rb) is required for gamma interferon (IFN-gamma)-inducible major histocompatibility complex class II gene expression and transcriptionally productive HLA-DRA promoter occupancy in several human tumor cell lines. Treatment of these Rb-defective tumor cell lines with histone deacetylase (HDAC) inhibitors rescued IFN-gamma-inducible HLA-DRA and -DRB mRNA and cell surface protein expression, demonstrating repression of these genes by endogenous cellular HDAC activity. Additionally, Rb-defective, transcriptionally incompetent tumor cells retained the HLA-DRA promoter DNase I-hypersensitive site. Thus, HDAC-mediated repression of the HLA-DRA promoter occurs following the establishment of an apparent nucleosome-free promoter region and before transcriptionally productive occupancy of the promoter by the required transactivators. Repression of HLA-DRA promoter activation by HDAC activity likely involves a YY1 binding element located in the first exon of the HLA-DRA gene. Chromatin immunoprecipitation experiments localized YY1 to the HLA-DRA gene in Rb-defective tumor cells. Additionally, mutation of the YY1 binding site prevented repression of the promoter by HDAC1 and partially prevented activation of the promoter by trichostatin A. Mutation of the octamer element also significantly reduced the ability of HDAC1 to confer repression of inducible HLA-DRA promoter activation. Treatment of Rb-defective tumor cells with HDAC inhibitors greatly reduced the DNA binding activity of Oct-1, a repressor of inducible HLA-DRA promoter activation. These findings represent the first evidence that HDAC activity can repress IFN-gamma-inducible HLA class II gene expression and also demonstrate that HDAC activity can contribute to promoter repression following the establishment of a DNase I-hypersensitive chromatin conformation.
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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.