The Human Factors YY1 and LSF Repress the Human Immunodeficiency Virus Type 1 Long Terminal Repeat via Recruitment of Histone Deacetylase 1

Coull, Jason J.; Romerio, Fabio; Sun, Jian; Völker, J; Galvin, Katherine; Davie, James R.; Shi, Yang; Hansen, Ulla; Margolis, David M.

doi:10.1128/jvi.74.15.6790-6799.2000

Cited by 319 publications

(326 citation statements)

References 80 publications

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“…These are as follows: (1) CP-2 (Lim et al, 1992(Lim et al, , 1993Shirra et al, 1994), also referred to as UBP-1, LSF, LBP-1c, and LBP-1d (alternatively spliced form), a widely expressed transcription factor that has been implicated in activation of the ␣-globin gene (Chodosh et al, 1988;Kim et al, 1990), the HIV-1 long terminal repeat (LTR; Jones et al, 1988;Wu et al, 1988;Malim et al, 1989;Kato et al, 1991), and the SV40 major late promoter (Kim et al, 1987;Huang et al, 1990). This factor can also, depending on context, repress transcription and was shown to cooperate with YY1 to repress HIV-1 LTR activity (Coull et al, 2000); (2) LBP-1a (Sueyoshi et al, 1995), also referred to as LBP-1b (alternatively spliced form) and NF2d9 (Yoon et al, 1994), a widely expressed factor implicated in regulation of the HIV-1 LTR (Yoon et al, 1994) and a P450 gene (Sueyoshi et al, 1995); (3) LBP-9 (Huang and Miller, 2000), also referred to as CP2-related transcriptional Repressor-1 (CRTR-1; Rodda et al, 2001), implicated in regulation of the P450 scc promoter; (4) LBP-32 (Huang and Miller, 2000), also refer- . Grainyhead-like epithelial transactivator 1 (GET-1) transcripts are highly expressed in epithelial cells of the mouse embryo and persist in adult mice.…”

Section: Sequence Homology Of Mammalian Grainyhead-like Proteinsmentioning

confidence: 99%

Identification and characterization of Grainyhead‐like epithelial transactivator (GET‐1), a novel mammalian Grainyhead‐like factor

Kudryavtseva¹,

Sugihara²,

Wang³

et al. 2003

Developmental Dynamics

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LMO-4 is an LIM-only factor that is highly expressed in many epithelial cells, including those of the epidermis and hair follicles. Because LMOs may function by interacting with DNA-binding proteins, we have used the yeast two-hybrid system to screen mouse skin libraries for LMO-4 -interacting DNA-binding proteins. In this screen, we isolated a novel LMO-4 -interacting factor highly related to the Drosophila gene Grainyhead. Grainyhead is epidermally expressed and carries out important functions in cuticular formation in the fly embryo. With the identification of this novel mammalian Grainyhead-like gene, referred to as Grainyhead-like epithelial transactivator 1 (GET-1), the known members of the mammalian Grainyhead-like gene family are extended to six, falling into two classes based on sequence homology. Of interest, the expression pattern of GET-1 is similar to that of Drosophila Grainyhead with highest expression in the somatic ectoderm/epidermis, but GET-1 is additionally expressed in epithelial cells of gastrointestinal, genitourinary, and respiratory tracks. The GET-1 protein localizes to the nucleus and binds to at least one Grainyhead DNA-binding site. The GET-1 DNA-binding domain maps to a region containing homology to the Drosophila Grainyhead DNA-binding domain. GET-1 homodimerizes in solution by means of a short C-terminally located domain that is homologous to other Grainyhead-like genes. A short domain located between amino acids 100 and 190, which bears no homology to known transactivation domains, is sufficient to confer transactivation to the heterologous GAL4 DNA-binding domain. In addition, GET-1 appears to contain repression domains consistent with the observation that Grainyhead and other mammalian Grainyhead-like genes can act both as activators and repressors. These data suggest that GET-1 is a transcriptional regulator that may perform important functions in epithelial tissues of mammals. Developmental Dynamics 226:604 -617, 2003.

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Section: Sequence Homology Of Mammalian Grainyhead-like Proteinsmentioning

confidence: 99%

Identification and characterization of Grainyhead‐like epithelial transactivator (GET‐1), a novel mammalian Grainyhead‐like factor

Kudryavtseva¹,

Sugihara²,

Wang³

et al. 2003

Developmental Dynamics

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“…7C), formed by ESRRB, KLF2, and SOX2, KLF2 plays a central role, being simultaneously targeted by two methylationresistant CpGMMs. On the other side, YY1, targeting ESRRB may direct histone deacetylases and histone acetyltransferases to the promoter in order to activate or repress them (Coull et al 2000;He and Margolis 2002). The other network (Fig.…”

Section: A Pluripotent Network Arises From the Crosstalk Between Methmentioning

confidence: 99%

Disclosing the crosstalk among DNA methylation, transcription factors, and histone marks in human pluripotent cells through discovery of DNA methylation motifs

2013

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Gene expression regulation is gated by promoter methylation states modulating transcription factor binding. The known DNA methylation/unmethylation mechanisms are sequence unspecific, but different cells with the same genome have different methylomes. Thus, additional processes bringing specificity to the methylation/unmethylation mechanisms are required. Searching for such processes, we demonstrated that CpG methylation states are influenced by the sequence context surrounding the CpGs. We used such a property to develop a CpG methylation motif discovery algorithm. The newly discovered motifs reveal ''methylation/unmethylation factors'' that could recruit the ''methylation/unmethylation machinery'' to the loci specified by the motifs. Our methylation motif discovery algorithm provides a synergistic approach to the differently methylated region algorithms. Since our algorithm searches for commonly methylated regions inside the same sample, it requires only a single sample to operate. The motifs that were found discriminate between hypomethylated and hypermethylated regions. The hypomethylation-associated motifs have a high CG content, their targets appear in conserved regions near transcription start sites, they tend to co-occur within transcription factor binding sites, they are involved in breaking the H3K4me3/H3K27me3 bivalent balance, and they transit the enhancers from repressive H3K27me3 to active H3K27ac during ES cell differentiation. The new methylation motifs characterize the pluripotent state shared between ES and iPS cells. Additionally, we found a collection of motifs associated with the somatic memory inherited by the iPS from the initial fibroblast cells, thus revealing the existence of epigenetic somatic memory on a fine methylation scale.

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“…Thus, class 1 HDACs are recruited to the proviral DNA, in proximity to nuc-1, through the action of DNA binding proteins. Nuclear factor (NF)-κB p50 homodimer, activating enhancer binding protein 4 (AP-4), retinoblastoma-family protein 2 (RBF2), as well as c-Myc and specificity protein 1 (SP-1) recruit class I HDACs to the LTR, which in turn results in deacetylation of local histones, compaction of the chromatin and prevention of RNA polymerase II binding (25,(27)(28)(29)(30)(31).…”

Section: Which Hdac Is Best For Hiv-1 Expression?mentioning

confidence: 99%

Histone Deacetylase Inhibitors for Purging HIV-1 from the Latent Reservoir

Matalon

Rasmussen

Dinarello

2011

Mol Med

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A reservoir of latently infected memory CD4 + T cells is believed to be the source of HIV-1 reemergence after discontinuation of antiretroviral therapy. HIV-1 eradication may depend on depletion of this reservoir. Integrated HIV-1 is inaccessible for expression, in part because of histone deacetylases (HDACs). One approach is to exploit the ability of HDAC inhibitors to induce HIV-1 expression from an integrated virus. With effective antiretroviral therapy, newly expressed HIV-1 is incapable of reinfecting naive cells.With HIV-1 expression, one assumes the infected cell dies and there is a progressive reduction in the size of the reservoir. The concept was tested using the HDAC inhibitor valproic acid. However, valproic acid is weak in inducing HIV-1 from latency in vitro. As such, clinical trials revealed a small or no effect on reducing the number of latently infected T cells in the peripheral blood. However, the new HDAC inhibitors vorinostat, belinostat and givinostat are more effective at targeting specific HDACs for HIV-1 expression than valproic acid. Here, we review studies on HDAC inhibitor-induced expression of latent HIV-1, with an emphasis on new and specific HDAC inhibitors. With increased potency for HIV-1 expression as well as safety and ease of oral administration, new HDAC inhibitors offer a unique opportunity to deplete the latent reservoir. An additional benefit is the antiinflammatory properties of HDAC inhibitors, including downregulation of HIV-1 coreceptor expression.

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The Human Factors YY1 and LSF Repress the Human Immunodeficiency Virus Type 1 Long Terminal Repeat via Recruitment of Histone Deacetylase 1

Cited by 319 publications

References 80 publications

Identification and characterization of Grainyhead‐like epithelial transactivator (GET‐1), a novel mammalian Grainyhead‐like factor

Identification and characterization of Grainyhead‐like epithelial transactivator (GET‐1), a novel mammalian Grainyhead‐like factor

Disclosing the crosstalk among DNA methylation, transcription factors, and histone marks in human pluripotent cells through discovery of DNA methylation motifs

Histone Deacetylase Inhibitors for Purging HIV-1 from the Latent Reservoir

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