Mireya: a Computational Approach to Detect Mirna- Directed Gene Activation [Version 2; Peer Review: 1 Approved, 2 Approved with Reservations]
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Case Report a Fetus with Kabuki Syndrome 2 Detected by Chromosomal Microarray Analysis
Int J Clin Exp Pathol 2020;13(2):302-306 www.ijcep.com /ISSN:1936-2625/IJCEP0104334 Case Report A fetus with Kabuki syndrome 2 detected by chromosomal microarray analysis Chen-Zhao Lin1, Bi-Ru Qi1, Jian-Su Hu2, Xiu-Qiong Huang3 Departments of 1Obstetrics and Gynecology, 2Ultrasound, 3Laboratory Medicine, Fuzhou Municipal First Hospital Affiliated to Fujian Medical University, Fuzhou 350009, Fujian Province, The People’s Republic of China Received November 1, 2019; Accepted January 26, 2020; Epub February 1, 2020; Published February 15, 2020 Abstract: Background: Kabuki syndrome is a rare multiple congenital anomaly syndrome characterized by distinct facial features, intellectual disability, cardiovascular and musculoskeletal abnormalities, persistence of fetal finger- tip pads, and postnatal growth deficiency. Currently, the diagnosis mainly depends on clinical manifestations and genetic testing. To date, there is no report on the identification Kabuki syndrome in fetuses using chromosomal microarray analysis (CMA). Case presentation: A fetus was identified with growth retardation and cardiovascular abnormality on color Doppler ultrasonography; however, non-invasive prenatal testing (NIPT) revealed a low risk and G-banding karyotyping revealed no abnormal karyotype detected. CMA identified a 1.3 Mb deletion on the X chromosome (Xp11.3) containing KDM6A, DUSP21, MIR222, MIR221 and CXorf36 genes. The fetus was diagnosed with Kabuki syndrome 2, and labor was induced. In addition, CMA detected a 1.3 Mb deletion in the chromosome Xp11.3 in the mother, which contains 5 genes namely KDM6A, DUSP21, MIR222, MIR221 and CXorf36, while no chromosomal abnormality was identified in the father. Conclusions: We report a fetus with Kabuki syndrome 2 detected using CMA. -
Abou Alezz, Monah Characterization of the Genomic and Splicing Features of Long 51 Non-Coding Rnas Using Bioinformatics Approaches
Posters A-Z Abou Alezz, Monah Characterization of the genomic and splicing features of long 51 non-coding RNAs using bioinformatics approaches Aguilera-Cortés, Paulina Identification of cellular lncRNAs associated to the HIV-1 genomic RNA 52 by interactome capture Ahram, Mamoun The androgen, dihydrotestosterone, induces chemoresistance of triple 53 negative breast cancer cells independent of ABCG2 and microRNA-328-3p Ahunbay, Esra Watching the self-catalyzed splicing of a group II intron with 54 single-molecule sensitivity Alemu, Endalkachew Integrated Global Mapping of miRNA:target-RNA Interactions 55 Ali, Tamer The lncRNA locus Handsdown regulates cardiac gene programs and is 56 essential for early mouse development Alzahrani, Salma Revisiting the sRNAome Under a Revised MicroRNA Annotation Criteria 57 Amorim, Marcella Dissecting the threshold-based readout of mobile small RNA gradients 58 Arnoldi, Michele SINEUPs technology: a new route to possibly treat 59 haploinsufficiency-induced Epilepsy and Autism Spectrum Disorders (ASDs) Azhikina, Tatyana Small RNA F6 influences Mycobacterium smegmatis entry into 60 dormancy EMBO | EMBL Symposium: The Non-Coding Genome Barasa, Sheila Olendo Long non-coding RNAs in High Grade Serous Ovarian Carcinoma 61 Behera, Alok LIN28 as a new drug target 62 Behrmann, Iris Modulation of the IL-6-Signaling Pathway in Liver Cells by miRNAs 63 Targeting gp130, JAK1, and/or STAT3 Bencurova, Petra Inhibition of miRNA-129-2-3p increases risk and severity of seizures in 64 developing brain Bica, Cecilia The emerging -
The Role of Microrna in Human Leukemia: a Review
Leukemia (2009) 23, 1257–1263 & 2009 Macmillan Publishers Limited All rights reserved 0887-6924/09 $32.00 www.nature.com/leu SPOTLIGHT REVIEW The role of microRNA in human leukemia: a review S Yendamuri1 and GA Calin2 1Department of Thoracic Surgery, Roswell Park Cancer Institute, Buffalo, NY, USA and 2Department of Experimental Therapeutics, University of Texas MD Anderson Cancer Center, Houston, TX, USA MicroRNAs (miRNAs or miRs) are 18–22-nucleotide non-coding target. If the sequence is a perfect match, the final result seems RNAs that have emerged as a new paradigm of epigenetic to be target mRNA degradation in a manner similar to siRNA- regulation in both normal development and cellular function, and in the pathogenesis of human disease including cancer. induced gene expression silencing. This seems to be the This review summarizes the current literature of mechanism of predominant mechanism in plants. A less than perfect match gene regulation by miRNA and their role in hematopoiesis and may result in inefficient translation leading to effective down- leukemogenesis. An understanding of these processes sug- regulation of the gene, a mechanism more common in gests further avenues for research to understand gene regula- animals.7–9 Isolated examples of miRNA leading to upregulation tion and miRNA-based therapeutic approaches. of genes have been reported.10 Leukemia (2009) 23, 1257–1263; doi:10.1038/leu.2008.382; The mechanism of translational repression is known only published online 15 January 2009 11 Keywords: microRNA; non-coding RNA; microarray; partially. The mRNA segments that miRNAs bind seem to be mostly in the 30UTRs of genes. -
Supplementary Materials
Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine -
Development of Novel Therapeutic Agents by Inhibition of Oncogenic Micrornas
International Journal of Molecular Sciences Review Development of Novel Therapeutic Agents by Inhibition of Oncogenic MicroRNAs Dinh-Duc Nguyen and Suhwan Chang * ID Department of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea; [email protected] * Correspondence: [email protected] Received: 21 November 2017; Accepted: 22 December 2017; Published: 27 December 2017 Abstract: MicroRNAs (miRs, miRNAs) are regulatory small noncoding RNAs, with their roles already confirmed to be important for post-transcriptional regulation of gene expression affecting cell physiology and disease development. Upregulation of a cancer-causing miRNA, known as oncogenic miRNA, has been found in many types of cancers and, therefore, represents a potential new class of targets for therapeutic inhibition. Several strategies have been developed in recent years to inhibit oncogenic miRNAs. Among them is a direct approach that targets mature oncogenic miRNA with an antisense sequence known as antimiR, which could be an oligonucleotide or miRNA sponge. In contrast, an indirect approach is to block the biogenesis of miRNA by genome editing using the CRISPR/Cas9 system or a small molecule inhibitor. The development of these inhibitors is straightforward but involves significant scientific and therapeutic challenges that need to be resolved. In this review, we summarize recent relevant studies on the development of miRNA inhibitors against cancer. Keywords: antimiR; antagomiR; miRNA-sponge; oncomiR; CRISPR/Cas9; cancer therapeutics 1. Introduction Cancer has been the leading cause of death and a major health problem worldwide for many years; basically, it results from out-of-control cell proliferation. Traditionally, several key proteins have been identified and found to affect signaling pathways regulating cell cycle progression, apoptosis, and gene transcription in various types of cancers [1,2]. -
Differential Expression of Micrornas in Adipose Tissue After Long-Term High-Fat Diet-Induced Obesity in Mice
Differential Expression of MicroRNAs in Adipose Tissue after Long-Term High-Fat Diet-Induced Obesity in Mice Dionysios V. Chartoumpekis1, Apostolos Zaravinos2, Panos G. Ziros1, Ralitsa P. Iskrenova1, Agathoklis I. Psyrogiannis1, Venetsana E. Kyriazopoulou1, Ioannis G. Habeos1* 1 Department of Internal Medicine, Division of Endocrinology, Medical School, University of Patras, Patras, Greece, 2 Laboratory of Clinical Virology, Medical School, University of Crete, Heraklion, Greece Abstract Obesity is a major health concern worldwide which is associated with increased risk of chronic diseases such as metabolic syndrome, cardiovascular disease and cancer. The elucidation of the molecular mechanisms involved in adipogenesis and obesogenesis is of essential importance as it could lead to the identification of novel biomarkers and therapeutic targets for the development of anti-obesity drugs. MicroRNAs (miRNAs) have been shown to play regulatory roles in several biological processes. They have become a growing research field and consist of promising pharmaceutical targets in various fields such as cancer, metabolism, etc. The present study investigated the possible implication of miRNAs in adipose tissue during the development of obesity using as a model the C57BLJ6 mice fed a high-fat diet. C57BLJ6 wild type male mice were fed either a standard (SD) or a high-fat diet (HFD) for 5 months. Total RNA was prepared from white adipose tissue and was used for microRNA profiling and qPCR. Twenty-two of the most differentially expressed miRNAs, as identified by the microRNA profiling were validated using qPCR. The results of the present study confirmed previous results. The up- regulation of mmu-miR-222 and the down-regulation of mmu-miR-200b, mmu-miR-200c, mmu-miR-204, mmu-miR-30a*, mmu-miR-193, mmu-miR-378 and mmu-miR-30e* after HFD feeding has also been previously reported. -
Enhancer Rnas: Transcriptional Regulators and Workmates of Namirnas in Myogenesis
Odame et al. Cell Mol Biol Lett (2021) 26:4 https://doi.org/10.1186/s11658-021-00248-x Cellular & Molecular Biology Letters REVIEW Open Access Enhancer RNAs: transcriptional regulators and workmates of NamiRNAs in myogenesis Emmanuel Odame , Yuan Chen, Shuailong Zheng, Dinghui Dai, Bismark Kyei, Siyuan Zhan, Jiaxue Cao, Jiazhong Guo, Tao Zhong, Linjie Wang, Li Li* and Hongping Zhang* *Correspondence: [email protected]; zhp@sicau. Abstract edu.cn miRNAs are well known to be gene repressors. A newly identifed class of miRNAs Farm Animal Genetic Resources Exploration termed nuclear activating miRNAs (NamiRNAs), transcribed from miRNA loci that and Innovation Key exhibit enhancer features, promote gene expression via binding to the promoter and Laboratory of Sichuan enhancer marker regions of the target genes. Meanwhile, activated enhancers pro- Province, College of Animal Science and Technology, duce endogenous non-coding RNAs (named enhancer RNAs, eRNAs) to activate gene Sichuan Agricultural expression. During chromatin looping, transcribed eRNAs interact with NamiRNAs University, Chengdu 611130, through enhancer-promoter interaction to perform similar functions. Here, we review China the functional diferences and similarities between eRNAs and NamiRNAs in myogen- esis and disease. We also propose models demonstrating their mutual mechanism and function. We conclude that eRNAs are active molecules, transcriptional regulators, and partners of NamiRNAs, rather than mere RNAs produced during enhancer activation. Keywords: Enhancer RNA, NamiRNAs, MicroRNA, Myogenesis, Transcriptional regulator Introduction Te identifcation of lin-4 miRNA in Caenorhabditis elegans in 1993 [1] triggered research to discover and understand small microRNAs’ (miRNAs) mechanisms. Recently, some miRNAs are reported to activate target genes during transcription via base pairing to the 3ʹ or 5ʹ untranslated regions (3ʹ or 5ʹ UTRs), the promoter [2], and the enhancer regions [3]. -
Supplementary Information.Pdf
Supplementary Information Whole transcriptome profiling reveals major cell types in the cellular immune response against acute and chronic active Epstein‐Barr virus infection Huaqing Zhong1, Xinran Hu2, Andrew B. Janowski2, Gregory A. Storch2, Liyun Su1, Lingfeng Cao1, Jinsheng Yu3, and Jin Xu1 Department of Clinical Laboratory1, Children's Hospital of Fudan University, Minhang District, Shanghai 201102, China; Departments of Pediatrics2 and Genetics3, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Supplementary information includes the following: 1. Supplementary Figure S1: Fold‐change and correlation data for hyperactive and hypoactive genes. 2. Supplementary Table S1: Clinical data and EBV lab results for 110 study subjects. 3. Supplementary Table S2: Differentially expressed genes between AIM vs. Healthy controls. 4. Supplementary Table S3: Differentially expressed genes between CAEBV vs. Healthy controls. 5. Supplementary Table S4: Fold‐change data for 303 immune mediators. 6. Supplementary Table S5: Primers used in qPCR assays. Supplementary Figure S1. Fold‐change (a) and Pearson correlation data (b) for 10 cell markers and 61 hypoactive and hyperactive genes identified in subjects with acute EBV infection (AIM) in the primary cohort. Note: 23 up‐regulated hyperactive genes were highly correlated positively with cytotoxic T cell (Tc) marker CD8A and NK cell marker CD94 (KLRD1), and 38 down‐regulated hypoactive genes were highly correlated positively with B cell, conventional dendritic cell -
Mirna Goes Nuclear
POINT-OF-VIEW RNA Biology 9:3, 1–5; March 2012; G 2012 Landes Bioscience miRNA goes nuclear Vera Huang and Long-Cheng Li Department of Urology and Helen-Diller Comprehensive Cancer Center, University of California—San Francisco; San Francisco, CA USA icroRNAs (miRNAs), defined as to target(s). miRNAs are convention- m 21–24 nucleotide non-coding ally regarded as negative regulators of RNAs, are important regulators of gene gene expression, mostly through post- expression. Initially, the functions of transcriptional events taking place in the miRNAs were recognized as post- cytoplasm. They are known to target transcriptional regulators on mRNAs complementary sequence on the mRNA that result in mRNA degradation and/or at different sites or on many different translational repression. It is becoming mRNAs through base-pairing between evident that miRNAs are not only the miRNA seed region and the 3' restricted to function in the cytoplasm, untranslated region (UTR) in the target they can also regulate gene expression in mRNA. It has been reported that other cellular compartments by a spec- miRNAs can also regulate gene expres- trum of targeting mechanisms via coding sion by targeting the 5' UTR,3 coding © 2012 Landesregions, 5' and 3'untransalated Bioscience. regions regions,4 promoters,5-8 and gene termini.9 (UTRs), promoters, and gene termini. In addition, miRNAs are predicted by In this point-of-view, we will speci- several genome-wide computational ana- fically focus on the nuclear functions lyses to target gene promoters because of miRNAs and discuss examples of potential targets for miRNAs are com- miRNA-directed transcriptional gene monly found based on sequence homo- regulation identified in recent years. -
Induction of Micrornas, Mir-155, Mir-222, Mir-424 and Mir-503, Promotes Monocytic Differentiation Through Combinatorial Regulation
Leukemia (2010) 24, 460–466 & 2010 Macmillan Publishers Limited All rights reserved 0887-6924/10 $32.00 www.nature.com/leu ‘ ORIGINAL ARTICLE Induction of microRNAs, mir-155, mir-222, mir-424 and mir-503, promotes monocytic differentiation through combinatorial regulation ARR Forrest1,2, M Kanamori-Katayama1, Y Tomaru1, T Lassmann1, N Ninomiya1, Y Takahashi1, MJL de Hoon1, A Kubosaki1, A Kaiho1, M Suzuki1, J Yasuda1, J Kawai1, Y Hayashizaki1, DA Hume3 and H Suzuki1 1LSA Technology Development Unit, Omics Science Center, RIKEN Yokohama Institute, Yokohama, Kanagawa, Japan; 2The Eskitis Institute for Cell and Molecular Therapies, Griffith University, Brisbane, Queensland, Australia and 3The Roslin Institute, Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Roslin, UK Acute myeloid leukemia (AML) involves a block in terminal that might promote differentiation. MicroRNAs are short 21–22 differentiation of the myeloid lineage and uncontrolled prolif- nucleotide RNA molecules that cause translational repression eration of a progenitor state. Using phorbol myristate acetate and degradation of multiple mRNAs by binding target sequences (PMA), it is possible to overcome this block in THP-1 cells 0 5 (an M5-AML containing the MLL-MLLT3 fusion), resulting in in their 3 UTRs. Multiple microRNAs are implicated in differentiation to an adherent monocytic phenotype. As part of differentiation of cell lineages including skeletal muscle, FANTOM4, we used microarrays to identify 23 microRNAs that adipocytes and neurons6–8 and in mammals, the microRNA are regulated by PMA. We identify four PMA-induced micro- subsystem is essential for embryonic development. Dicer RNAs (mir-155, mir-222, mir-424 and mir-503) that when over- is required for differentiation of embryonic stem cells,9 Dicer expressed cause cell-cycle arrest and partial differentiation and (À/À) knockouts are embryonic lethal10 and Ago2 (À/À) when used in combination induce additional changes not seen 11 by any individual microRNA. -
Noncoding Rnas As Novel Pancreatic Cancer Targets
NONCODING RNAS AS NOVEL PANCREATIC CANCER TARGETS by Amy Makler A Thesis Submitted to the Faculty of The Charles E. Schmidt College of Science In Partial Fulfillment of the Requirements for the Degree of Master of Science Florida Atlantic University Boca Raton, FL August 2018 Copyright 2018 by Amy Makler ii ACKNOWLEDGEMENTS I would first like to thank Dr. Narayanan for his continuous support, constant encouragement, and his gentle, but sometimes critical, guidance throughout the past two years of my master’s education. His faith in my abilities and his belief in my future success ensured I continue down this path of research. Working in Dr. Narayanan’s lab has truly been an unforgettable experience as well as a critical step in my future endeavors. I would also like to extend my gratitude to my committee members, Dr. Binninger and Dr. Jia, for their support and suggestions regarding my thesis. Their recommendations added a fresh perspective that enriched our initial hypothesis. They have been indispensable as members of my committee, and I thank them for their contributions. My parents have been integral to my successes in life and their support throughout my education has been crucial. They taught me to push through difficulties and encouraged me to pursue my interests. Thank you, mom and dad! I would like to thank my boyfriend, Joshua Disatham, for his assistance in ensuring my writing maintained a logical progression and flow as well as his unwavering support. He was my rock when the stress grew unbearable and his encouraging words kept me pushing along. -
Expression and Change of Mirs 145, 221 and 222 in Hypertensive Subjects Treated with Enalapril, Losartan Or Olmesartan
biomedicines Article Expression and Change of miRs 145, 221 and 222 in Hypertensive Subjects Treated with Enalapril, Losartan or Olmesartan Giuseppe Mandraffino 1,2,3,*,† , Alberto Lo Gullo 4,*,† , Maria Cinquegrani 1, Angela D’Ascola 3, Davide Sinicropi 1, Egidio Imbalzano 1 , Giuseppe Blando 1, Giuseppe Maurizio Campo 3, Carmela Morace 1, Clemente Giuffrida 4, Salvatore Campo 5, Giovanni Squadrito 1,‡ and Michele Scuruchi 2,3,‡ 1 Internal Medicine Unit, Department of Clinical and Experimental Medicine, University of Messina, 98122 Messina, Italy; [email protected] (M.C.); [email protected] (D.S.); [email protected] (E.I.); [email protected] (G.B.); [email protected] (C.M.); [email protected] (G.S.) 2 Lipid Center, Internal Medicine Unit, University of Messina, 98122 Messina, Italy; [email protected] 3 Laboratory of Clinical Biochemistry, Department of Clinical and Experimental Medicine, University of Messina, 98122 Messina, Italy; [email protected] (A.D.); [email protected] (G.M.C.) 4 IRCCS Neurolesi Bonino Pulejo, 98123 Messina, Italy; [email protected] 5 Laboratory of Molecular Biology, Department of Biomedical and Dental Sciences and Morphofunctional Images, University of Messina, 98122 Messina, Italy; [email protected] * Correspondence: gmandraffi[email protected] (G.M.); [email protected] (A.L.G.) † These authors equally contributed to this work: co-first authors. ‡ These authors equally contributed to this work: both senior authors. Citation: Mandraffino, G.; Lo Gullo, Abstract: miR profile could be associated to CV risk, and also to prognosis/outcome in response to A.; Cinquegrani, M.; D’Ascola, A.; Sinicropi, D.; Imbalzano, E.; Blando, therapeutic approach. We aimed to evaluate if anti-hypertensive drugs enalapril, losartan or olmesar- G.; Campo, G.M.; Morace, C.; tan have effects on monocyte miR profile in essential hypertensives without target organ involvement.