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Taher, Mohiuddin M.; Lammering, Guido; Hershey, Chad M.; Valerie, Kristoffer

doi:10.1023/a:1027393719610

Cited by 26 publications

(8 citation statements)

References 48 publications

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“…It was found to be a potent inhibitor of the HIV-1 integrase (41). Furthermore, curcumin could also inhibit the HIV-1 Tat-mediated transactivation (42) and the UV induced activation of the HIV-LTR gene expression, presumably through the inhibition of nuclear factor-B activation (43). Although these reports suggest that curcumin may act as a repressor of HIV multiplication, its effect on viral replication was not demonstrated.…”

Section: A Lane 3 Versus Lanes 7 and 8 And B Lane 2 Versus Lanes 4mentioning

confidence: 97%

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Curcumin, a Novel p300/CREB-binding Protein-specific Inhibitor of Acetyltransferase, Represses the Acetylation of Histone/Nonhistone Proteins and Histone Acetyltransferase-dependent Chromatin Transcription

Balasubramanyam

Varier

Altaf

et al. 2004

Journal of Biological Chemistry

741

511

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Acetylation of histones and non-histone proteins is an important post-translational modification involved in the regulation of gene expression in eukaryotes and all viral DNA that integrates into the human genome (e.g. the human immunodeficiency virus). Dysfunction of histone acetyltransferases (HATs) is often associated with the manifestation of several diseases. In this respect, HATs are the new potential targets for the design of therapeutics. In this study, we report that curcumin (diferuloylmethane), a major curcumanoid in the spice turmeric, is a specific inhibitor of the p300/CREB-binding protein (CBP) HAT activity but not of p300/CBPassociated factor, in vitro and in vivo. Furthermore, curcumin could also inhibit the p300-mediated acetylation of p53 in vivo. It specifically represses the p300/CBP HAT activity-dependent transcriptional activation from chromatin but not a DNA template. It is significant that curcumin could inhibit the acetylation of HIV-Tat protein in vitro by p300 as well as proliferation of the virus, as revealed by the repression in syncytia formation upon curcumin treatment in SupT1 cells. Thus, nontoxic curcumin, which targets p300/CBP, may serve as a lead compound in combinatorial HIV therapeutics.

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Section: A Lane 3 Versus Lanes 7 and 8 And B Lane 2 Versus Lanes 4mentioning

confidence: 97%

“…Curcumin is able to inhibit different enzymatic activities that include HIV-1 integrase (41), nuclear factor-B activation (43), and p300-specific HAT/factor acetyltransferase activity. Repression of the HIV replication by curcumin could be caused by any of the above or a combination thereof.…”

Section: A Lane 3 Versus Lanes 7 and 8 And B Lane 2 Versus Lanes 4mentioning

confidence: 99%

Curcumin, a Novel p300/CREB-binding Protein-specific Inhibitor of Acetyltransferase, Represses the Acetylation of Histone/Nonhistone Proteins and Histone Acetyltransferase-dependent Chromatin Transcription

Balasubramanyam

Varier

Altaf

et al. 2004

Journal of Biological Chemistry

741

511

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“…The interaction of curcumin with a variety of cellular molecules is due to its adaptable chemical structure. Such interactions lead to diversified biological effects, including regulation of the cell cycle, growth suppression, the induction of developmental distinction, the scavenge of reactive oxygen species (ROS), chemo-prevention and the up-regulation of pro-apoptotic factors (Surh, 1999; Chauhan, 2002; Miquel et al, 2002; Saleheen et al, 2002; Taher et al, 2003; Itokawa et al, 2008).…”

Section: Epigenetic Modulation By Curcuminmentioning

confidence: 99%

Curcumin as an Alternative Epigenetic Modulator: Mechanism of Action and Potential Effects

et al. 2019

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Curcumin (a polyphenolic compound in turmeric) is famous for its potent anti-inflammatory, anti-oxidant, and anti-cancer properties, and has a great potential to act as an epigenetic modulator. The epigenetic regulatory roles of curcumin include the inhibition of DNA methyltransferases (DNMTs), regulation of histone modifications via the regulation of histone acetyltransferases (HATs) and histone deacetylases (HDACs), regulation of microRNAs (miRNA), action as a DNA binding agent and interaction with transcription factors. These mechanisms are interconnected and play a vital role in tumor progression. The recent research has demonstrated the role of epigenetic inactivation of pivotal genes that regulate human pathologies such as cancers. Epigenetics helps to understand the mechanism of chemoprevention of cancer through different therapeutic agents. In this regard, dietary phytochemicals, such as curcumin, have emerged as a potential source to reverse epigenetic modifications and efficiently regulate the expression of genes and molecular targets that are involved in the promotion of tumorigenesis. The curcumin may also act as an epigenetic regulator in neurological disorders, inflammation, and diabetes. Moreover, curcumin can induce the modifications of histones (acetylation/deacetylation), which are among the most important epigenetic changes responsible for altered expression of genes leading to modulating the risks of cancers. Curcumin is an effective medicinal agent, as it regulates several important molecular signaling pathways that modulate survival, govern anti-oxidative properties like nuclear factor E2-related factor 2 (Nrf2) and inflammation pathways, e.g., nuclear factor kappa B (NF-κB). Curcumin is a potent proteasome inhibitor that increases p-53 level and induces apoptosis through caspase activation. Moreover, the disruption of 26S proteasome activity induced by curcumin through inhibiting DYRK2 in different cancerous cells resulting in the inhibition of cell proliferation opens up a new horizon for using curcumin as a potential preventive and treatment approach in proteasome-linked cancers. This review presents a brief summary of knowledge about the mechanism of epigenetic changes induced by curcumin and the potential effects of curcumin such as anti-oxidant activity, enhancement of wound healing, modulation of angiogenesis and its interaction with inflammatory cytokines. The development of curcumin as a clinical molecule for successful chemo-prevention and alternate therapeutic approach needs further mechanistic insights.

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“…The high levels of intracellular curcumin achieved through nano-curcumin administration may account for this previously unreported observation. Curcumin has been previously demonstrated to inhibit HIV activation and replication [30]–[33]. Mechanisms involved include inhibition of both HIV protease [32] and integrase [34].…”

Section: Discussionmentioning

confidence: 99%

Curcumin-Loaded Apotransferrin Nanoparticles Provide Efficient Cellular Uptake and Effectively Inhibit HIV-1 Replication In Vitro

et al. 2011

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BackgroundCurcumin (diferuloylmethane) shows significant activity across a wide spectrum of conditions, but its usefulness is rather limited because of its low bioavailability. Use of nanoparticle formulations to enhance curcumin bioavailability is an emerging area of research.Methodology/Principal FindingsIn the present study, curcumin-loaded apotransferrin nanoparticles (nano-curcumin) prepared by sol-oil chemistry and were characterized by electron and atomic force microscopy. Confocal studies and fluorimetric analysis revealed that these particles enter T cells through transferrin-mediated endocytosis. Nano-curcumin releases significant quantities of drug gradually over a fairly long period, ∼50% of curcumin still remaining at 6 h of time. In contrast, intracellular soluble curcumin (sol-curcumin) reaches a maximum at 2 h followed by its complete elimination by 4 h. While sol-curcumin (GI50 = 15.6 µM) is twice more toxic than nano-curcumin (GI50 = 32.5 µM), nano-curcumin (IC50<1.75 µM) shows a higher anti-HIV activity compared to sol-curcumin (IC50 = 5.1 µM). Studies in vitro showed that nano-curcumin prominently inhibited the HIV-1 induced expression of Topo II α, IL-1β and COX-2, an effect not seen with sol-curcumin. Nano-curcumin did not affect the expression of Topoisomerase II β and TNF α. This point out that nano-curcumin affects the HIV-1 induced inflammatory responses through pathways downstream or independent of TNF α. Furthermore, nano-curcumin completely blocks the synthesis of viral cDNA in the gag region suggesting that the nano-curcumin mediated inhibition of HIV-1 replication is targeted to viral cDNA synthesis.ConclusionCurcumin-loaded apotransferrin nanoparticles are highly efficacious inhibitors of HIV-1 replication in vitro and promise a high potential for clinical usefulness.

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Untitled

Cited by 26 publications

References 48 publications

Curcumin, a Novel p300/CREB-binding Protein-specific Inhibitor of Acetyltransferase, Represses the Acetylation of Histone/Nonhistone Proteins and Histone Acetyltransferase-dependent Chromatin Transcription

Curcumin, a Novel p300/CREB-binding Protein-specific Inhibitor of Acetyltransferase, Represses the Acetylation of Histone/Nonhistone Proteins and Histone Acetyltransferase-dependent Chromatin Transcription

Curcumin as an Alternative Epigenetic Modulator: Mechanism of Action and Potential Effects

Curcumin-Loaded Apotransferrin Nanoparticles Provide Efficient Cellular Uptake and Effectively Inhibit HIV-1 Replication In Vitro

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