ArticleMolecular and cellular biology1997
Efficient repression of endogenous major histocompatibility complex class II expression through dominant negative CIITA mutants isolated by a functional selection strategy.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 69 citations in OpenAlex.
- Hazara orthonairovirus nucleoprotein facilitates viral cell-to-cell spread by modulating tight junction protein, claudin-1.Frontiers in microbiology · 2023Article
- The MHC Class II Transactivator CIITA: Not (Quite) the Odd-One-Out Anymore among NLR Proteins.International journal of molecular sciences · 2021Review
- MHC class II transactivator CIITA induces cell resistance to Ebola virus and SARS-like coronaviruses.Science (New York, N.Y.) · 2020Article
- Development of potent class II transactivator gene delivery systems capable of inducing de novo MHC II expression in human cells, in vitro and ex vivo.Gene therapy · 2017Article
- Evidence that Receptor Destruction by the Sendai Virus Hemagglutinin-Neuraminidase Protein Is Responsible for Homologous Interference.Journal of virology · 2016Article
- Enhanced growth of influenza A virus by coinfection with human parainfluenza virus type 2.Medical microbiology and immunology · 2016Article
- Article
- Antipsychotic treatment modulates glutamate transport and NMDA receptor expression.European archives of psychiatry and clinical neuroscience · 2014Review
- PML promotes MHC class II gene expression by stabilizing the class II transactivator.The Journal of cell biology · 2012Article
- Activation of the beta interferon promoter by unnatural Sendai virus infection requires RIG-I and is inhibited by viral C proteins.Journal of virology · 2007Article
- Targeting of the Sendai virus C protein to the plasma membrane via a peptide-only membrane anchor.Journal of virology · 2007Article
- New functions of the major histocompatibility complex class II-specific transcription factor RFXANK revealed by a high-resolution mutagenesis study.Molecular and cellular biology · 2005Article
- A short peptide at the amino terminus of the Sendai virus C protein acts as an independent element that induces STAT1 instability.Journal of virology · 2004Article
- Persistence of MHC DR nonexpression on swine cells by introduction of a mutated MHC class II transactivator gene: a comparison with the effect induced by antisense RNA.Journal of clinical immunology · 2004Article
- The amino-terminal extensions of the longer Sendai virus C proteins modulate pY701-Stat1 and bulk Stat1 levels independently of interferon signaling.Journal of virology · 2003Article
- Novel mechanisms of class II major histocompatibility complex gene regulation.Immunologic research · 2003Review
- Sendai virus trailer RNA binds TIAR, a cellular protein involved in virus-induced apoptosis.The EMBO journal · 2002Article
- Promoter-specific functions of CIITA and the MHC class II enhanceosome in transcriptional activation.The EMBO journal · 2002Article
- Expression of the three human major histocompatibility complex class II isotypes exhibits a differential dependence on the transcription factor RFXAP.Molecular and cellular biology · 2001Article
- Maturation of dendritic cells is accompanied by rapid transcriptional silencing of class II transactivator (CIITA) expression.The Journal of experimental medicine · 2001Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Major histocompatibility complex class II (MHC-II) molecules present peptide antigens to CD4-positive T cells and are of critical importance for the immune response. The MHC-II transactivator CIITA is essential for all aspects of MHC-II gene expression examined so far and thus constitutes a master regulator of MHC-II expression. In this study, we generated and analyzed mutant CIITA molecules which are able to suppress endogenous MHC-II expression in a dominant negative manner for both constitutive and inducible MHC-II expression. Dominant negative CIITA mutants were generated via specific restriction sites and by functional selection from a library of random N-terminal CIITA deletions. This functional selection strategy was very effective, leading to strong dominant negative CIITA mutants in which the N-terminal acidic and proline/serine/threonine-rich regions were completely deleted. Dominant negative activity is dependent on an intact C terminus. Efficient repression of endogenous MHC-II mRNA levels was quantified by RNase protection analysis. The quantitative effects of various dominant negative CIITA mutants on mRNA expression levels of the different MHC-II isotypes are very similar. The optimized dominant negative CIITA mutants isolated by functional selection should be useful for in vivo repression of MHC-II expression.
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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.