miR-320a regulates erythroid differentiation through MAR binding protein SMAR1

Mittal, Smriti; Mathai, Jinumary; Kulkarni, Abhijeet; Pal, Jayanta K.; Chattopadhyay, Samit

doi:10.1016/j.biocel.2013.07.006

Cited by 23 publications

(11 citation statements)

References 42 publications

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“…Notably, miR-222, miR-34a, miR-371a, Bax, Cyclin D1, NFκB, CD40, FN1 and PDGFRB genes showed presence of S/MAR within 1 Kb region upstream to their transcription start sites (TSS). Presence of S/MARs in the promoters of these genes has already been demonstrated experimentally (21,43–49). Further, 35.57% of the total S/MARs were found to be located in the intergenic region (Figure 4A).…”

Section: Resultsmentioning

confidence: 66%

Mapping of scaffold/matrix attachment regions in human genome: a data mining exercise

Narwade

Patel

Alam

et al. 2019

Nucleic Acids Research

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Scaffold/matrix attachment regions (S/MARs) are DNA elements that serve to compartmentalize the chromatin into structural and functional domains. These elements are involved in control of gene expression which governs the phenotype and also plays role in disease biology. Therefore, genome-wide understanding of these elements holds great therapeutic promise. Several attempts have been made toward identification of S/MARs in genomes of various organisms including human. However, a comprehensive genome-wide map of human S/MARs is yet not available. Toward this objective, ChIP-Seq data of 14 S/MAR binding proteins were analyzed and the binding site coordinates of these proteins were used to prepare a non-redundant S/MAR dataset of human genome. Along with co-ordinate (location) details of S/MARs, the dataset also revealed details of S/MAR features, namely, length, inter-SMAR length (the chromatin loop size), nucleotide repeats, motif abundance, chromosomal distribution and genomic context. S/MARs identified in present study and their subsequent analysis also suggests that these elements act as hotspots for integration of retroviruses. Therefore, these data will help toward better understanding of genome functioning and designing effective anti-viral therapeutics. In order to facilitate user friendly browsing and retrieval of the data obtained in present study, a web interface, MARome (http://bioinfo.net.in/MARome), has been developed.

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Section: Resultsmentioning

confidence: 66%

Mapping of scaffold/matrix attachment regions in human genome: a data mining exercise

Narwade

Patel

Alam

et al. 2019

Nucleic Acids Research

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“…A number of microRNAs, viz., miR-205, miR-383, miR-572, miR-371-373, miR-100, miR-32, miR-206, miR-147, miR-221/222, etc. playing diverse roles in cancer cell proliferation and metastasis, differentiation, epithelial to mesenchymal transition (EMT), inflammation and many other vital cellular functions have been predicted to be SMAR1 targets by ChIP-seq analysis 16 17 18 19 20 21 22 23 24 . Thus, our data suggests multi-faceted role of SMAR1 and projects new and unexplored pathways that SMAR1 might orchestrate globally.…”

Section: Resultsmentioning

confidence: 99%

SMAR1 binds to T(C/G) repeat and inhibits tumor progression by regulating miR-371-373 cluster

Mathai

Mittal

Alam

et al. 2016

Sci Rep

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Chromatin architecture and dynamics are regulated by various histone and non-histone proteins. The matrix attachment region binding proteins (MARBPs) play a central role in chromatin organization and function through numerous regulatory proteins. In the present study, we demonstrate that nuclear matrix protein SMAR1 orchestrates global gene regulation as determined by massively parallel ChIP-sequencing. The study revealed that SMAR1 binds to T(C/G) repeat and targets genes involved in diverse biological pathways. We observe that SMAR1 binds and targets distinctly different genes based on the availability of p53. Our data suggest that SMAR1 binds and regulates one of the imperative microRNA clusters in cancer and metastasis, miR-371-373. It negatively regulates miR-371-373 transcription as confirmed by SMAR1 overexpression and knockdown studies. Further, deletion studies indicate that a ~200 bp region in the miR-371-373 promoter is necessary for SMAR1 binding and transcriptional repression. Recruitment of HDAC1/mSin3A complex by SMAR1, concomitant with alteration of histone marks results in downregulation of the miRNA cluster. The regulation of miR-371-373 by SMAR1 inhibits breast cancer tumorigenesis and metastasis as determined by in vivo experiments. Overall, our study highlights the binding of SMAR1 to T(C/G) repeat and its role in cancer through miR-371-373.

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“…We selected miRNAs that were highly expressed (within the top 10%, except for hsa-miR-320a). We selected miRNAs involved in different cell processes such as cancer (hsa-miR-17-92 cluster 52 , 53 and hsa-miR-21 53 – 55 ) and K562 differentiation (hsa-miR-223 56 , hsa-miR-103 57 , and hsa-miR-320a 57 , 58 ). The selected miRNAs were as follows: hsa-miR-20a (MIMAT0000075), hsa-miR-17 (MIMAT0000070), hsa-miR-19b (MIMAT0000074), hsa-miR-21 (MIMAT0000076), hsa-miR-92a (MIMAT0000092), hsa-miR-223 (MIMAT0000280), hsa-miR-25 (MIMAT0000081), hsa-miR-130b (MIMAT0000691), hsa-miR-103 (MIMAT0000101), and hsa-miR-320a (MIMAT0000510).…”

Section: Methodsmentioning

confidence: 99%

Unraveling the determinants of microRNA mediated regulation using a massively parallel reporter assay

et al. 2018

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Despite extensive research, the sequence features affecting microRNA-mediated regulation are not well understood, limiting our ability to predict gene expression levels in both native and synthetic sequences. Here we employed a massively parallel reporter assay to investigate the effect of over 14,000 rationally designed 3′ UTR sequences on reporter construct repression. We found that multiple factors, including microRNA identity, hybridization energy, target accessibility, and target multiplicity, can be manipulated to achieve a predictable, up to 57-fold, change in protein repression. Moreover, we predict protein repression and RNA levels with high accuracy (R = 0.84 and R = 0.80, respectively) using only 3′ UTR sequence, as well as the effect of mutation in native 3′ UTRs on protein repression (R = 0.63). Taken together, our results elucidate the effect of different sequence features on miRNA-mediated regulation and demonstrate the predictability of their effect on gene expression with applications in regulatory genomics and synthetic biology.

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miR-320a regulates erythroid differentiation through MAR binding protein SMAR1

Cited by 23 publications

References 42 publications

Mapping of scaffold/matrix attachment regions in human genome: a data mining exercise

Mapping of scaffold/matrix attachment regions in human genome: a data mining exercise

SMAR1 binds to T(C/G) repeat and inhibits tumor progression by regulating miR-371-373 cluster

Unraveling the determinants of microRNA mediated regulation using a massively parallel reporter assay

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