Targets for human encoded microRNAs in HIV genes

Hariharan, Manoj; Scaria, Vinod; Pillai, Beena; Brahmachari, Samir K.

doi:10.1016/j.bbrc.2005.09.183

Cited by 198 publications

(174 citation statements)

References 22 publications

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“…23 We were particularly interested in miRNA-28, miRNA-125b, miRNA-150, miRNA-223, and miR-382 because these miRNAs can target a highly conserved region of HIV, present in all HIV clades. 25 These miRNAs are highly expressed in resting CD4 ϩ T cells 28 and monocytes. 23 The levels of these miRNAs correlate with the susceptibility of monocytes/macrophages to HIV infection.…”

Section: Discussionmentioning

confidence: 99%

“…Several cellular miRNAs (miRNA-28, miRNA-29a, miRNA125b, miRNA-150, miRNA-198, miRNA-223, and miRNA-382) target a set of accessory genes of HIV. [23][24][25][26][27] For example, these miRNAs can target the 3=-UTR of HIV transcripts, 28 potentially rendering productive infection of HIV into latency in resting CD4 ϩ T lymphocytes. Recently, it was reported that monocytes express significantly higher levels of anti-HIV miRNAs than donormatched macrophages, thereby unraveling the refractory nature of monocytes to HIV infection.…”

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confidence: 99%

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Inhibition of Anti-HIV MicroRNA Expression

Wang

Zhou

et al. 2011

The American Journal of Pathology

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Several micro RNAs (miRNAs) have the ability to inhibit HIV replication in target cells. Thus, we investigated the impact of opioids (morphine and heroin), widely abused drugs among people infected with HIV, on the expression of cellular anti-HIV miRNAs in monocytes. We found that morphine-treated monocytes expressed lower levels of cellular anti-HIV miRNAs than untreated cells. In addition, morphine treatment of monocytes compromised type I interferon (IFN)-induced anti-HIV miRNA expression. These findings paralleled the observation that morphine treatment of monocytes enhanced HIV replication. These morphine-mediated actions on the anti-HIV miRNAs and HIV could be antagonized by the opioid receptor antagonists (naltrexone or Cys2, Tyr3, Arg5, Pen7-amide). Furthermore, the in vitro impact of morphine on miRNA expression was confirmed by the in vivo observation that heroin-dependent subjects had significantly lower levels of anti-HIV miRNAs (miRNA-28, 125b, 150, and 382) in peripheral blood mononuclear cells than the healthy subjects. These in vitro and in vivo findings indicate that opioid use impairs intracellular innate anti-HIV mechanism(s) in monocytes, contributing to cell susceptibility to HIV infection. (Am J

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Inhibition of Anti-HIV MicroRNA Expression

Wang

Zhou

et al. 2011

The American Journal of Pathology

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“…(64) The procedure followed was according to Hariharan et al and is detailed under methods. (65) We found that amongst the 128 genes of the IP-VE set for which the 3 0 UTR sequences were retrieved, 70% of the genes (88 of 128) contained miRNA binding site(s) ( Table 2, Supporting Information Table 2). These 88 IP-VE genes were targeted by 167 human encoded miRNAs giving rise to 233 target gene-miRNA pairs, which indicated that some genes are targeted by multiple miRNA; 66% of the genes (58 of 88) contained multiple nonoverlapping miRNA binding sites in their 3 0 UTR.…”

Section: Molecular Basis Of Ip-vementioning

confidence: 95%

“…Mature miRNA sequences were downloaded for the 470 miRNAs available at miRBase release 9.0 (http://microrna.sanger.ac.uk/). (77) miRNA target predictions were carried out by taking a consensus (65) of miRanda, (61) TargetScan, (62) and RNAhybrid. (63) Redundant target gene-miRNA pairs generated due to alternate transcripts of gene were removed to obtain unique pairs.…”

Section: Dataset Sourcementioning

confidence: 99%

Incomplete penetrance and variable expressivity: is there a microRNA connection?

et al. 2009

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Incomplete penetrance and variable expressivity are non‐Mendelian phenomena resulting in the lack of correlation between genotype and phenotype. Not withstanding the diversity in mechanisms, differential expression of homologous alleles within cells manifests as variations in penetrance and expressivity of mutations between individuals of the same genotype. These phenomena are seen most often in dominantly inherited diseases, implying that they are sensitive to concentration of the gene product. In this framework and the advances in understanding the role of microRNA (miRNA) in fine‐tuning gene expression at translational level, we propose miRNA‐mediated regulation as a mechanism for incomplete penetrance and variable expressivity. The presence of miRNA binding sites at 3′ UTR, co‐expression of target gene–miRNA pairs for genes showing incomplete penetrance and variable expressivity derived from available data lend support to our hypothesis. Single nucleotide polymorphisms in the miRNA target site facilitate the implied differential targeting of the transcripts from homologous alleles.

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“…Altered miR expressions during virus infection include host miRs that target virus sequences and host genes to modulate and influence viral replication. 60,61 Hepatitis B…”

Section: Viral Hepatitismentioning

confidence: 99%

MicroRNAs in Liver Disease: Bench to Bedside

Shah

Nelson

Kowdley

2013

Journal of Clinical and Experimental Hepatology

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MicroRNAs (miRs) are small non-coding RNAs that negatively regulate gene expression by pairing with partially complementary target sequences in the 3 0 UTRs of mRNAs to promote degradation and/or block translation. Aberrant miR expression is associated with development of multiple diseases including hepatic diseases. The role of miRs in the regulation of gene expression and rapid progress in the field of microRNA research are resulting in momentum toward development of diagnostic markers and novel therapeutic strategies for human liver diseases. Recent studies provide clear evidence that miRs are abundant in the liver and modulate a diverse spectrum of biological functions, thereby supporting an association between alterations of miR homeostasis and pathological liver diseases. Here we review the role of miRs in liver as their physiological and pathological importance has been demonstrated in metabolism, immunity, viral hepatitis, oncogenesis, fatty liver diseases (alcoholic and non-alcoholic), drug-induced liver injury, fibrosis as well as acute liver failure. ( J CLIN EXP HEPATOL 2013;3:231-242)

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Targets for human encoded microRNAs in HIV genes

Cited by 198 publications

References 22 publications

Inhibition of Anti-HIV MicroRNA Expression

Inhibition of Anti-HIV MicroRNA Expression

Incomplete penetrance and variable expressivity: is there a microRNA connection?

MicroRNAs in Liver Disease: Bench to Bedside

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