Exploring the Key Genes and Pathways of Side Population Cells In
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Supplementary Materials: Evaluation of Cytotoxicity and Α-Glucosidase Inhibitory Activity of Amide and Polyamino-Derivatives of Lupane Triterpenoids
Supplementary Materials: Evaluation of cytotoxicity and α-glucosidase inhibitory activity of amide and polyamino-derivatives of lupane triterpenoids Oxana B. Kazakova1*, Gul'nara V. Giniyatullina1, Akhat G. Mustafin1, Denis A. Babkov2, Elena V. Sokolova2, Alexander A. Spasov2* 1Ufa Institute of Chemistry of the Ufa Federal Research Centre of the Russian Academy of Sciences, 71, pr. Oktyabrya, 450054 Ufa, Russian Federation 2Scientific Center for Innovative Drugs, Volgograd State Medical University, Novorossiyskaya st. 39, Volgograd 400087, Russian Federation Correspondence Prof. Dr. Oxana B. Kazakova Ufa Institute of Chemistry of the Ufa Federal Research Centre of the Russian Academy of Sciences 71 Prospeсt Oktyabrya Ufa, 450054 Russian Federation E-mail: [email protected] Prof. Dr. Alexander A. Spasov Scientific Center for Innovative Drugs of the Volgograd State Medical University 39 Novorossiyskaya st. Volgograd, 400087 Russian Federation E-mail: [email protected] Figure S1. 1H and 13C of compound 2. H NH N H O H O H 2 2 Figure S2. 1H and 13C of compound 4. NH2 O H O H CH3 O O H H3C O H 4 3 Figure S3. Anticancer screening data of compound 2 at single dose assay 4 Figure S4. Anticancer screening data of compound 7 at single dose assay 5 Figure S5. Anticancer screening data of compound 8 at single dose assay 6 Figure S6. Anticancer screening data of compound 9 at single dose assay 7 Figure S7. Anticancer screening data of compound 12 at single dose assay 8 Figure S8. Anticancer screening data of compound 13 at single dose assay 9 Figure S9. Anticancer screening data of compound 14 at single dose assay 10 Figure S10. -
Effects of Stressors on Differential Gene Expression And
EFFECTS OF STRESSORS ON DIFFERENTIAL GENE EXPRESSION AND SECONDARY METABOLITES BY AXINELLA CORRUGATA by Jennifer Grima A Thesis Submitted to the Faculty of Charles E. Schmidt College of Science in Partial Fulfillment of the Requirements for the Degree of Master of Science Florida Atlantic University Boca Raton, Florida May 2013 ACKNOWLEDGEMENTS This thesis was made possible by the help and support of my mentors and friends. Without their guidance and expertise, I would not have been able to accomplish all that I have. Their belief and encouragement in my efforts have motivated and inspired me along through this journey and into a new era in my life. First and foremost, I am grateful to Dr. Shirley Pomponi for taking on the role as my advisor and giving me the opportunity to experience life as a researcher. Not only has she guided me in my scientific studies, she has become a wonderful, lifelong friend. Dr. Pomponi and Dr. Amy Wright have also provided financial support that enabled me to conduct the research and complete this thesis. I would also like to acknowledge Dr. Amy Wright for her willingness to tender advice on all things chemistry related as well as providing me with the space, equipment, and supplies to conduct the chemical analyses. I am grateful to Dr. Esther Guzman who not only served as a committee member, but has also been readily available to help me in any endeavor, whether it be research or personal related. She is truly one of kind with her breadth of knowledge in research and her loyal and caring character. -
Protein Interaction Network of Alternatively Spliced Isoforms from Brain Links Genetic Risk Factors for Autism
ARTICLE Received 24 Aug 2013 | Accepted 14 Mar 2014 | Published 11 Apr 2014 DOI: 10.1038/ncomms4650 OPEN Protein interaction network of alternatively spliced isoforms from brain links genetic risk factors for autism Roser Corominas1,*, Xinping Yang2,3,*, Guan Ning Lin1,*, Shuli Kang1,*, Yun Shen2,3, Lila Ghamsari2,3,w, Martin Broly2,3, Maria Rodriguez2,3, Stanley Tam2,3, Shelly A. Trigg2,3,w, Changyu Fan2,3, Song Yi2,3, Murat Tasan4, Irma Lemmens5, Xingyan Kuang6, Nan Zhao6, Dheeraj Malhotra7, Jacob J. Michaelson7,w, Vladimir Vacic8, Michael A. Calderwood2,3, Frederick P. Roth2,3,4, Jan Tavernier5, Steve Horvath9, Kourosh Salehi-Ashtiani2,3,w, Dmitry Korkin6, Jonathan Sebat7, David E. Hill2,3, Tong Hao2,3, Marc Vidal2,3 & Lilia M. Iakoucheva1 Increased risk for autism spectrum disorders (ASD) is attributed to hundreds of genetic loci. The convergence of ASD variants have been investigated using various approaches, including protein interactions extracted from the published literature. However, these datasets are frequently incomplete, carry biases and are limited to interactions of a single splicing isoform, which may not be expressed in the disease-relevant tissue. Here we introduce a new interactome mapping approach by experimentally identifying interactions between brain-expressed alternatively spliced variants of ASD risk factors. The Autism Spliceform Interaction Network reveals that almost half of the detected interactions and about 30% of the newly identified interacting partners represent contribution from splicing variants, emphasizing the importance of isoform networks. Isoform interactions greatly contribute to establishing direct physical connections between proteins from the de novo autism CNVs. Our findings demonstrate the critical role of spliceform networks for translating genetic knowledge into a better understanding of human diseases. -
Isoforms, Structures, and Functions of Versatile Spectraplakin MACF1
BMB Rep. 2016; 49(1): 37-44 BMB www.bmbreports.org Reports Contiributed Mini Review Isoforms, structures, and functions of versatile spectraplakin MACF1 Lifang Hu1, Peihong Su1, Runzhi Li1, Chong Yin1, Yan Zhang1, Peng Shang1, Tuanmin Yang2 & Airong Qian1,* 1Key Laboratory for Space Bioscience and Biotechnology, Institute of Special Environmental Biophysics, School of Life Sciences, Northwestern Polytechnical University, Xi’an, Shaanxi 710072, 2Honghui Hospital, Xi’an Jiaotong University College of Medicine, Xi’an, Shaanxi 710054, P. R. China Spectraplakins are crucially important communicators, linking ability of interacting with all three types of cytoskeletal fila- cytoskeletal components to each other and cellular junctions. ments, i.e., F-actin, MTs, and IFs (1). Microtubule actin crosslinking factor 1 (MACF1), also known Spectraplakins are exceptionally long and gigantic with mo- as actin crosslinking family 7 (ACF7), is a member of the spec- lecular weight of >500 kD. They are multi-domain cytoskele- traplakin family. It is expressed in numerous tissues and cells tal proteins and master orchestrators for coordinating cytoske- as one extensively studied spectraplakin. MACF1 has several letal elements by binding to F-actin, MTs, and IFs (1, 2). isoforms with unique structures and well-known function to be Spectraplakins are evolutionarily conserved. They belong to able to crosslink F-actin and microtubules. MACF1 is one ver- both spectrin and plakin superfamilies (3). “Spectraplakins” are satile spectraplakin with various functions in cell processes, named as combinations of “spectrin” and “plakin” because embryo development, tissue-specific functions, and human they share features of both spectrins and plakins (3, 4). So far, diseases. The importance of MACF1 has become more appa- mammalian spectraplakins have two members: microtubule rent in recent years. -
DNA·RNA Triple Helix Formation Can Function As a Cis-Acting Regulatory
DNA·RNA triple helix formation can function as a cis-acting regulatory mechanism at the human β-globin locus Zhuo Zhoua, Keith E. Gilesa,b,c, and Gary Felsenfelda,1 aLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892; bUniversity of Alabama at Birmingham Stem Cell Institute, University of Alabama at Birmingham, Birmingham, AL 35294; and cDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35294 Contributed by Gary Felsenfeld, February 4, 2019 (sent for review January 4, 2019; reviewed by James Douglas Engel and Sergei M. Mirkin) We have identified regulatory mechanisms in which an RNA tran- of the criteria necessary to establish the presence of a triplex script forms a DNA duplex·RNA triple helix with a gene or one of its structure, we first describe and characterize triplex formation at regulatory elements, suggesting potential auto-regulatory mecha- the FAU gene in human erythroid K562 cells. FAU encodes a nisms in vivo. We describe an interaction at the human β-globin protein that is a fusion containing fubi, a ubiquitin-like protein, locus, in which an RNA segment embedded in the second intron of and ribosomal protein S30. Although fubi function is unknown, the β-globin gene forms a DNA·RNA triplex with the HS2 sequence posttranslational processing produces S30, a component of the within the β-globin locus control region, a major regulator of glo- 40S ribosome. We used this system to refine methods necessary bin expression. We show in human K562 cells that the triplex is to detect triplex formation and to distinguish it from R-loop stable in vivo. -
Nuclear Organization and the Epigenetic Landscape of the Mus Musculus X-Chromosome Alicia Liu University of Connecticut - Storrs, [email protected]
University of Connecticut OpenCommons@UConn Doctoral Dissertations University of Connecticut Graduate School 8-9-2019 Nuclear Organization and the Epigenetic Landscape of the Mus musculus X-Chromosome Alicia Liu University of Connecticut - Storrs, [email protected] Follow this and additional works at: https://opencommons.uconn.edu/dissertations Recommended Citation Liu, Alicia, "Nuclear Organization and the Epigenetic Landscape of the Mus musculus X-Chromosome" (2019). Doctoral Dissertations. 2273. https://opencommons.uconn.edu/dissertations/2273 Nuclear Organization and the Epigenetic Landscape of the Mus musculus X-Chromosome Alicia J. Liu, Ph.D. University of Connecticut, 2019 ABSTRACT X-linked imprinted genes have been hypothesized to contribute parent-of-origin influences on social cognition. A cluster of imprinted genes Xlr3b, Xlr4b, and Xlr4c, implicated in cognitive defects, are maternally expressed and paternally silent in the murine brain. These genes defy classic mechanisms of autosomal imprinting, suggesting a novel method of imprinted gene regulation. Using Xlr3b and Xlr4c as bait, this study uses 4C-Seq on neonatal whole brain of a 39,XO mouse model, to provide the first in-depth analysis of chromatin dynamics surrounding an imprinted locus on the X-chromosome. Significant differences in long-range contacts exist be- tween XM and XP monosomic samples. In addition, XM interaction profiles contact a greater number of genes linked to cognitive impairment, abnormality of the nervous system, and abnormality of higher mental function. This is not a pattern that is unique to the imprinted Xlr3/4 locus. Additional Alicia J. Liu - University of Connecticut - 2019 4C-Seq experiments show that other genes on the X-chromosome, implicated in intellectual disability and/or ASD, also produce more maternal contacts to other X-linked genes linked to cognitive impairment. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Identification of Novel Biomarkers and Candidate Small Molecule Drugs in Non-Small-Cell Lung Cancer by Integrated Microarray Analysis
OncoTargets and Therapy Dovepress open access to scientific and medical research Open Access Full Text Article ORIGINAL RESEARCH Identification of novel biomarkers and candidate small molecule drugs in non-small-cell lung cancer by integrated microarray analysis This article was published in the following Dove Press journal: OncoTargets and Therapy Qiong Wu1,2,* Background: Non-small-cell lung cancer (NSCLC) remains the leading cause of cancer Bo Zhang1,2,* morbidity and mortality worldwide. In the present study, we identified novel biomarkers Yidan Sun3 associated with the pathogenesis of NSCLC aiming to provide new diagnostic and therapeu- Ran Xu1 tic approaches for NSCLC. Xinyi Hu4 Methods: The microarray datasets of GSE18842, GSE30219, GSE31210, GSE32863 and Shiqi Ren4 GSE40791 from Gene Expression Omnibus database were downloaded. The differential Qianqian Ma5 expressed genes (DEGs) between NSCLC and normal samples were identified by limma Chen Chen6 package. The construction of protein–protein interaction (PPI) network, module analysis and Jian Shu7 enrichment analysis were performed using bioinformatics tools. The expression and prog- Fuwei Qi7 nostic values of hub genes were validated by GEPIA database and real-time quantitative fi Ting He7 PCR. Based on these DEGs, the candidate small molecules for NSCLC were identi ed by the CMap database. Wei Wang2 Results: A total of 408 overlapping DEGs including 109 up-regulated and 296 down- Ziheng Wang2 regulated genes were identified; 300 nodes and 1283 interactions were obtained from the 1 Medical School of Nantong University, PPI network. The most significant biological process and pathway enrichment of DEGs were Nantong 226001, People’s Republic of China; 2The Hand Surgery Research Center, response to wounding and cell adhesion molecules, respectively. -
Multi-Targeted Mechanisms Underlying the Endothelial Protective Effects of the Diabetic-Safe Sweetener Erythritol
Multi-Targeted Mechanisms Underlying the Endothelial Protective Effects of the Diabetic-Safe Sweetener Erythritol Danie¨lle M. P. H. J. Boesten1*., Alvin Berger2.¤, Peter de Cock3, Hua Dong4, Bruce D. Hammock4, Gertjan J. M. den Hartog1, Aalt Bast1 1 Department of Toxicology, Maastricht University, Maastricht, The Netherlands, 2 Global Food Research, Cargill, Wayzata, Minnesota, United States of America, 3 Cargill RandD Center Europe, Vilvoorde, Belgium, 4 Department of Entomology and UCD Comprehensive Cancer Center, University of California Davis, Davis, California, United States of America Abstract Diabetes is characterized by hyperglycemia and development of vascular pathology. Endothelial cell dysfunction is a starting point for pathogenesis of vascular complications in diabetes. We previously showed the polyol erythritol to be a hydroxyl radical scavenger preventing endothelial cell dysfunction onset in diabetic rats. To unravel mechanisms, other than scavenging of radicals, by which erythritol mediates this protective effect, we evaluated effects of erythritol in endothelial cells exposed to normal (7 mM) and high glucose (30 mM) or diabetic stressors (e.g. SIN-1) using targeted and transcriptomic approaches. This study demonstrates that erythritol (i.e. under non-diabetic conditions) has minimal effects on endothelial cells. However, under hyperglycemic conditions erythritol protected endothelial cells against cell death induced by diabetic stressors (i.e. high glucose and peroxynitrite). Also a number of harmful effects caused by high glucose, e.g. increased nitric oxide release, are reversed. Additionally, total transcriptome analysis indicated that biological processes which are differentially regulated due to high glucose are corrected by erythritol. We conclude that erythritol protects endothelial cells during high glucose conditions via effects on multiple targets. -
Characterization of MAGED1 As a Component of E3 Ubiquitin Ligase Complexes
Characterization of MAGED1 as a component of E3 ubiquitin ligase complexes Nora Riems Student number: 01206813 Promoter: Prof. Dr. Mathieu Bertrand Scientific supervisor: Dario Priem Master’s dissertation submitted to Ghent University to obtain the degree of Master of Science in Biochemistry and Biotechnology. Major Biomedical Biotechnology. Academic year: 2016 - 2017 Ghent University – Department of Biomedical Molecular Biology VIB – Center for Inflammation Research Research Group: Molecular Signalling and Cell Death Acknowledgments Many people have contributed to the realization of this master dissertation and I would like to give a well-deserved thank you to everybody. First of all, I would like to thank my promotor Mathieu Bertrand and scientific supervisor Dario Priem for giving me the opportunity to work on this project. I would like to express my sincere appreciation for your constant guidance and the immense amount of feedback. Without it, this project would have remained uncompleted. Thank you. I would also like to thank Ria Roelandt and Inge Bruggeman for the help and guidance throughout my project. You have not only helped met with practical work but you were also the persons I could turn to with all my questions. Next, I would like to warmly thank all the people of the research group for the fun moments in the lab. In particular Wannes, you have supported me in an emotional way and never failed to make me smile. Finally, I would like to thank my parents. Although the last couple of years have not always been the easiest, you never failed to continuously encourage and support me. -
Genes with 5' Terminal Oligopyrimidine Tracts Preferentially Escape Global Suppression of Translation by the SARS-Cov-2 NSP1 Protein
Downloaded from rnajournal.cshlp.org on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press Genes with 5′ terminal oligopyrimidine tracts preferentially escape global suppression of translation by the SARS-CoV-2 Nsp1 protein Shilpa Raoa, Ian Hoskinsa, Tori Tonna, P. Daniela Garciaa, Hakan Ozadama, Elif Sarinay Cenika, Can Cenika,1 a Department of Molecular Biosciences, University of Texas at Austin, Austin, TX 78712, USA 1Corresponding author: [email protected] Key words: SARS-CoV-2, Nsp1, MeTAFlow, translation, ribosome profiling, RNA-Seq, 5′ TOP, Ribo-Seq, gene expression 1 Downloaded from rnajournal.cshlp.org on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press Abstract Viruses rely on the host translation machinery to synthesize their own proteins. Consequently, they have evolved varied mechanisms to co-opt host translation for their survival. SARS-CoV-2 relies on a non-structural protein, Nsp1, for shutting down host translation. However, it is currently unknown how viral proteins and host factors critical for viral replication can escape a global shutdown of host translation. Here, using a novel FACS-based assay called MeTAFlow, we report a dose-dependent reduction in both nascent protein synthesis and mRNA abundance in cells expressing Nsp1. We perform RNA-Seq and matched ribosome profiling experiments to identify gene-specific changes both at the mRNA expression and translation level. We discover that a functionally-coherent subset of human genes are preferentially translated in the context of Nsp1 expression. These genes include the translation machinery components, RNA binding proteins, and others important for viral pathogenicity. Importantly, we uncovered a remarkable enrichment of 5′ terminal oligo-pyrimidine (TOP) tracts among preferentially translated genes. -
Accepted Version
Article A catalog of genetic loci associated with kidney function from analyses of a million individuals WUTTKE, Matthias, et al. Abstract Chronic kidney disease (CKD) is responsible for a public health burden with multi-systemic complications. Through trans-ancestry meta-analysis of genome-wide association studies of estimated glomerular filtration rate (eGFR) and independent replication (n?=?1,046,070), we identified 264 associated loci (166 new). Of these, 147 were likely to be relevant for kidney function on the basis of associations with the alternative kidney function marker blood urea nitrogen (n?=?416,178). Pathway and enrichment analyses, including mouse models with renal phenotypes, support the kidney as the main target organ. A genetic risk score for lower eGFR was associated with clinically diagnosed CKD in 452,264 independent individuals. Colocalization analyses of associations with eGFR among 783,978 European-ancestry individuals and gene expression across 46 human tissues, including tubulo-interstitial and glomerular kidney compartments, identified 17 genes differentially expressed in kidney. Fine-mapping highlighted missense driver variants in 11 genes and kidney-specific regulatory variants. These results provide a comprehensive priority [...] Reference WUTTKE, Matthias, et al. A catalog of genetic loci associated with kidney function from analyses of a million individuals. Nature Genetics, 2019, vol. 51, no. 6, p. 957-972 DOI : 10.1038/s41588-019-0407-x PMID : 31152163 Available at: http://archive-ouverte.unige.ch/unige:147447 Disclaimer: layout of this document may differ from the published version. 1 / 1 HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Nat Genet Manuscript Author . Author manuscript; Manuscript Author available in PMC 2019 August 19.