ArticleJournal of virology1995
Interactions of the transcription factor AP-1 with the long terminal repeat of different human immunodeficiency virus type 1 strains in Jurkat, glial, and neuronal cells.
Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 65 citations in OpenAlex.
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- Involvement of Human Cellular Proteins and Structures in Realization of the HIV Life Cycle: A Comprehensive Review, 2024.Viruses · 2024Review
- HIV Expression in Infected T Cell Clones.Viruses · 2024Review
- Genome-wide CRISPR/Cas9 screen reveals JunB downmodulation of HIV co-receptor CXCR4.Frontiers in microbiology · 2024Article
- Breaking the Silence: Regulation of HIV Transcription and Latency on the Road to a Cure.Viruses · 2023Review
- Th17 cell master transcription factor RORC2 regulates HIV-1 gene expression and viral outgrowth.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Interactions with Commensal and Pathogenic Bacteria Induce HIV-1 Latency in Macrophages through Altered Transcription Factor Recruitment to the LTR.Journal of virology · 2021Article
- Balance between Retroviral Latency and Transcription: Based on HIV Model.Pathogens (Basel, Switzerland) · 2020Review
- Serum deprivation/starvation leads to reactivation of HIV-1 in latently infected monocytes via activating ERK/JNK pathway.Scientific reports · 2018Article
- The transcriptome of HIV-1 infected intestinal CD4+ T cells exposed to enteric bacteria.PLoS pathogens · 2017Article
- CNS-specific regulatory elements in brain-derived HIV-1 strains affect responses to latency-reversing agents with implications for cure strategies.Molecular psychiatry · 2016Article
- HIV-1 Promoter Single Nucleotide Polymorphisms Are Associated with Clinical Disease Severity.PloS one · 2016Article
- Defining differential genetic signatures in CXCR4- and the CCR5-utilizing HIV-1 co-linear sequences.PloS one · 2014Article
- Article
- Human serum protein enhances HIV-1 replication and up-regulates the transcription factor AP-1.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Latent HIV-1 infection occurs in multiple subsets of hematopoietic progenitor cells and is reversed by NF-κB activation.Journal of virology · 2012Article
- Kinase control prevents HIV-1 reactivation in spite of high levels of induced NF-κB activity.Journal of virology · 2012Article
- Exon level transcriptomic profiling of HIV-1-infected CD4(+) T cells reveals virus-induced genes and host environment favorable for viral replication.PLoS pathogens · 2012Article
- Mechanisms of HIV Transcriptional Regulation and Their Contribution to Latency.Molecular biology international · 2012Article
- The AP-1 binding sites located in the pol gene intragenic regulatory region of HIV-1 are important for viral replication.PloS one · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human immunodeficiency virus type 1 (HIV-1) infection of the neuronal and astroglial cells of the central nervous system has been proposed to contribute to HIV-1-associated dementia. Recently it was shown that differences in the nucleotide sequence of the long terminal repeat (LTR) of different HIV-1 strains govern the tissue-specific pattern of viral expression. The LTR from central nervous system-derived HIV-1 strains JR-FL and JR-CSF directs expression in the neurons of transgenic mice, in contrast with the lymphotropic LAI strain. By in vitro footprinting, gel retardation, and methylation interference experiments, we have studied the interactions of host cell proteins from human neuronal, glial, HeLa, and Jurkat T cells with the LTRs from the neurotropic JR-FL and JR-CSF strains, compared with the LAI strain. Proteins belonging to the nuclear receptor family bind with different affinities to variant -352 to -324 sites. Gel supershift assays with Jun and Fos antibodies showed that the AP-1 transcription factor present in the various cell types was unable to recognize the -352 to -324 and -306 to -285 AP-1 putative binding sites. Interestingly, Jun and Fos components of AP-1 interact with the variant TGGCTCA sequence located in the -247 to -222 region of both neurotropic strains. These interactions were cell type specific, since they were detected only with extracts from glial and HeLa cells and not from neuronal or Jurkat cells. Cotransfection experiments further revealed that the -247 to -222 sequence is able to mediate AP-1-induced transcriptional activation in glial and not neuronal cells.
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