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Barlow et al. BMC Biology (2018) 16:27 https://doi.org/10.1186/s12915-018-0492-9 RESEARCHARTICLE Open Access A sophisticated, differentiated Golgi in the ancestor of eukaryotes Lael D. Barlow1, Eva Nývltová2,3, Maria Aguilar1, Jan Tachezy2 and Joel B. Dacks1,4* Abstract Background: The Golgi apparatus is a central meeting point for the endocytic and exocytic systems in eukaryotic cells, and the organelle’s dysfunction results in human disease. Its characteristic morphology of multiple differentiated compartments organized into stacked flattened cisternae is one of the most recognizable features of modern eukaryotic cells, and yet how this is maintained is not well understood. The Golgi is also an ancient aspect of eukaryotes, but the extent and nature of its complexity in the ancestor of eukaryotes is unclear. Various proteins have roles in organizing the Golgi, chief among them being the golgins. Results: We address Golgi evolution by analyzing genome sequences from organisms which have lost stacked cisternae as a feature of their Golgi and those that have not. Using genomics and immunomicroscopy, we first identify Golgi in the anaerobic amoeba Mastigamoeba balamuthi. We then searched 87 genomes spanning eukaryotic diversity for presence of the most prominent proteins implicated in Golgi structure, focusing on golgins. We show some candidates as animal specific and others as ancestral to eukaryotes. Conclusions: None of the proteins examined show a phyletic distribution that correlates with the morphology of stacked cisternae, suggesting the possibility of stacking as an emergent property. Strikingly, however, the combination of golgins conserved among diverse eukaryotes allows for the most detailed reconstruction of the organelle to date, showing a sophisticated Golgi with differentiated compartments and trafficking pathways in the common eukaryotic ancestor. -
The Role and Mechanisms of Action of Micrornas in Cancer Drug Resistance Wengong Si1,2,3, Jiaying Shen4, Huilin Zheng1,5 and Weimin Fan1,6*
Si et al. Clinical Epigenetics (2019) 11:25 https://doi.org/10.1186/s13148-018-0587-8 REVIEW Open Access The role and mechanisms of action of microRNAs in cancer drug resistance Wengong Si1,2,3, Jiaying Shen4, Huilin Zheng1,5 and Weimin Fan1,6* Abstract MicroRNAs (miRNAs) are small non-coding RNAs with a length of about 19–25 nt, which can regulate various target genes and are thus involved in the regulation of a variety of biological and pathological processes, including the formation and development of cancer. Drug resistance in cancer chemotherapy is one of the main obstacles to curing this malignant disease. Statistical data indicate that over 90% of the mortality of patients with cancer is related to drug resistance. Drug resistance of cancer chemotherapy can be caused by many mechanisms, such as decreased antitumor drug uptake, modified drug targets, altered cell cycle checkpoints, or increased DNA damage repair, among others. In recent years, many studies have shown that miRNAs are involved in the drug resistance of tumor cells by targeting drug-resistance-related genes or influencing genes related to cell proliferation, cell cycle, and apoptosis. A single miRNA often targets a number of genes, and its regulatory effect is tissue-specific. In this review, we emphasize the miRNAs that are involved in the regulation of drug resistance among different cancers and probe the mechanisms of the deregulated expression of miRNAs. The molecular targets of miRNAs and their underlying signaling pathways are also explored comprehensively. A holistic understanding of the functions of miRNAs in drug resistance will help us develop better strategies to regulate them efficiently and will finally pave the way toward better translation of miRNAs into clinics, developing them into a promising approach in cancer therapy. -
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. -
Principles and Applications of Rabbit Models for Atherosclerosis Research
J Atheroscler Thromb, 2018; 25: 213-220. http://doi.org/10.5551/jat.RV17018 Review Principles and Applications of Rabbit Models for Atherosclerosis Research Jianglin Fan1, Yajie Chen1, Haizhao Yan1, Manabu Niimi1, Yanli Wang2 and Jingyan Liang3 1Department of Molecular Pathology, Faculty of Medicine, Graduate School of Medical Sciences, University of Yamanashi, Yamanashi, Japan 2Department of Pathology, Xi’an Medical University, Xi’an, China 3Research Center for Vascular Biology, Yangzhou University School of Medicine, Yangzhou, China Rabbits are one of the most used experimental animals for biomedical research, particularly as a bio- reactor for the production of antibodies. However, many unique features of the rabbit have also made it as an excellent species for examining a number of aspects of human diseases such as atherosclerosis. Rabbits are phylogenetically closer to humans than rodents, in addition to their relatively proper size, tame disposition, and ease of use and maintenance in the laboratory facility. Due to their short life spans, short gestation periods, high numbers of progeny, low cost (compared with other large ani- mals) and availability of genomics and proteomics, rabbits usually serve to bridge the gap between smaller rodents (mice and rats) and larger animals, such as dogs, pigs and monkeys, and play an important role in many translational research activities such as pre-clinical testing of drugs and diag- nostic methods for patients. The principle of using rabbits rather than other animals as an experi- mental model is very simple: rabbits should be used for research, such as translational research, that is difficult to accomplish with other species. Recently, rabbit genome sequencing and transcriptomic profiling of atherosclerosis have been successfully completed, which has paved a new way for researchers to use this model in the future. -
GOLGA2/GM130 Is a Novel Target for Neuroprotection Therapy in Intracerebral Hemorrhage
GOLGA2/GM130 is a Novel Target for Neuroprotection Therapy in Intracerebral Hemorrhage Shuwen Deng Second Xiangya Hospital Qing Hu Second Xiangya Hospital Qiang He Second Xiangya Hospital Xiqian Chen Second Xiangya Hospital Wei Lu ( [email protected] ) Second Xiangya Hospital, central south university https://orcid.org/0000-0002-3760-1550 Research Article Keywords: Golgi apparatus, therapy, intracerebral hemorrhage, autophagy, blood–brain barrier Posted Date: June 1st, 2021 DOI: https://doi.org/10.21203/rs.3.rs-547422/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/25 Abstract Blood–brain barrier (BBB) impairment after intracerebral hemorrhage (ICH) can lead to secondary brain injury and aggravate neurological decits. Currently, there are no effective methods for its prevention or treatment partly because of to our lack of understanding of the mechanism of ICH injury to the BBB. Here, we explored the role of Golgi apparatus protein GM130 in the BBB and neurological function after ICH. The levels of the tight junction-associated proteins ZO-1 and occludin decreased, whereas those of LC3-II, an autophagosome marker, increased in hemin-treated Bend.3 cells (p < 0.05). Additionally, GM130 overexpression increased ZO-1 and occludin levels, while decreasing LC3-II levels (p < 0.05). GM130 silencing reversed these effects and mimicked the effect of hemin treatment (p < 0.05). Moreover, tight junctions were disrupted after hemin treatment or GM130 silencing and repaired by GM130 overexpression. GM130 silencing in Bend.3 cells increased autophagic ux, whereas GM130 overexpression downregulated this activity. Furthermore, GM130 silencing-induced tight junction disruption was partially restored by 3-methyladenine (an autophagy inhibitor) administration. -
WO 2017/147196 Al 31 August 2017 (31.08.2017) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2017/147196 Al 31 August 2017 (31.08.2017) P O P C T (51) International Patent Classification: Kellie, E. [US/US]; 70 Lanark Road, Maiden, MA 02148 C12Q 1/68 (2006.01) (US). COLE, Michael, B. [US/US]; 233 1 Eunice Street, Berkeley, CA 94708 (US). YOSEF, Nir [IL/US]; 1520 (21) International Application Number: Laurel Ave., Richmond, CA 94805 (US). GAYO, En¬ PCT/US20 17/0 18963 rique, Martin [ES/US]; 115 Peterborough Street, Boston, (22) International Filing Date: MA 022 15 (US). OUYANG, Zhengyu [CN/US]; 15 Vas- 22 February 2017 (22.02.2017) sar Street, Medford, MA 02155 (US). YU, Xu [CN/US]; 6 Whittier Place, Apt. 16j, Boston, MA 02 114 (US). (25) Filing Language: English (74) Agents: KOWALSKI, Thomas, J. et al; Vedder Price English (26) Publication Language: P.C., 1633 Broadway, New York, NY 1001 9 (US). (30) Priority Data: (81) Designated States (unless otherwise indicated, for every 62/298,349 22 February 2016 (22.02.2016) US kind of national protection available): AE, AG, AL, AM, (71) Applicants: MASSACHUSETTS INSTITUTE OF AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, TECHNOLOGY [US/US]; 77 Massachusetts Ave., Cam BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DJ, DK, DM, bridge, MA 02139 (US). THE REGENTS OF THE UNI¬ DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, VERSITY OF CALIFORNIA [US/US]; 1111 Franklin HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KH, KN, Street, 12th Floor, Oakland, CA 94607 (US). -
S41467-020-18249-3.Pdf
ARTICLE https://doi.org/10.1038/s41467-020-18249-3 OPEN Pharmacologically reversible zonation-dependent endothelial cell transcriptomic changes with neurodegenerative disease associations in the aged brain Lei Zhao1,2,17, Zhongqi Li 1,2,17, Joaquim S. L. Vong2,3,17, Xinyi Chen1,2, Hei-Ming Lai1,2,4,5,6, Leo Y. C. Yan1,2, Junzhe Huang1,2, Samuel K. H. Sy1,2,7, Xiaoyu Tian 8, Yu Huang 8, Ho Yin Edwin Chan5,9, Hon-Cheong So6,8, ✉ ✉ Wai-Lung Ng 10, Yamei Tang11, Wei-Jye Lin12,13, Vincent C. T. Mok1,5,6,14,15 &HoKo 1,2,4,5,6,8,14,16 1234567890():,; The molecular signatures of cells in the brain have been revealed in unprecedented detail, yet the ageing-associated genome-wide expression changes that may contribute to neurovas- cular dysfunction in neurodegenerative diseases remain elusive. Here, we report zonation- dependent transcriptomic changes in aged mouse brain endothelial cells (ECs), which pro- minently implicate altered immune/cytokine signaling in ECs of all vascular segments, and functional changes impacting the blood–brain barrier (BBB) and glucose/energy metabolism especially in capillary ECs (capECs). An overrepresentation of Alzheimer disease (AD) GWAS genes is evident among the human orthologs of the differentially expressed genes of aged capECs, while comparative analysis revealed a subset of concordantly downregulated, functionally important genes in human AD brains. Treatment with exenatide, a glucagon-like peptide-1 receptor agonist, strongly reverses aged mouse brain EC transcriptomic changes and BBB leakage, with associated attenuation of microglial priming. We thus revealed tran- scriptomic alterations underlying brain EC ageing that are complex yet pharmacologically reversible. -
PGRMC1 and PGRMC2 in Uterine Physiology and Disease
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Frontiers - Publisher Connector PERSPECTIVE ARTICLE published: 19 September 2013 doi: 10.3389/fnins.2013.00168 PGRMC1 and PGRMC2 in uterine physiology and disease James K. Pru* and Nicole C. Clark Department of Animal Sciences, School of Molecular Biosciences, Center for Reproductive Biology, Washington State University, Pullman, WA, USA Edited by: It is clear from studies using progesterone receptor (PGR) mutant mice that not all of Sandra L. Petersen, University of the actions of progesterone (P4) are mediated by this receptor. Indeed, many rapid, Massachusetts Amherst, USA non-classical P4 actions have been reported throughout the female reproductive tract. Reviewed by: Progesterone treatment of Pgr null mice results in behavioral changes and in differential Cecily V. Bishop, Oregon National Primate Research Center, USA regulation of genes in the endometrium. Progesterone receptor membrane component Christopher S. Keator, Ross (PGRMC) 1 and PGRMC2 belong to the heme-binding protein family and may serve as University School of Medicine, P4 receptors. Evidence to support this derives chiefly from in vitro culture work using Dominica primary or transformed cell lines that lack the classical PGR. Endometrial expression of *Correspondence: PGRMC1 in menstrual cycling mammals is most abundant during the proliferative phase James K. Pru, Department of Animal Sciences, School of Molecular of the cycle. Because PGRMC2 expression shows the most consistent cross-species Biosciences, Center for expression, with highest levels during the secretory phase, PGRMC2 may serve as a Reproductive Biology, Washington universal non-classical P4 receptor in the uterus. -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
Progesterone – Friend Or Foe?
Frontiers in Neuroendocrinology 59 (2020) 100856 Contents lists available at ScienceDirect Frontiers in Neuroendocrinology journal homepage: www.elsevier.com/locate/yfrne Progesterone – Friend or foe? T ⁎ Inger Sundström-Poromaaa, , Erika Comascob, Rachael Sumnerc, Eileen Ludersd,e a Department of Women’s and Children’s Health, Uppsala University, Sweden b Department of Neuroscience, Science for Life Laboratory, Uppsala University, Uppsala, Sweden c School of Pharmacy, University of Auckland, New Zealand d School of Psychology, University of Auckland, New Zealand e Laboratory of Neuro Imaging, School of Medicine, University of Southern California, Los Angeles, USA ARTICLE INFO ABSTRACT Keywords: Estradiol is the “prototypic” sex hormone of women. Yet, women have another sex hormone, which is often Allopregnanolone disregarded: Progesterone. The goal of this article is to provide a comprehensive review on progesterone, and its Emotion metabolite allopregnanolone, emphasizing three key areas: biological properties, main functions, and effects on Hormonal contraceptives mood in women. Recent years of intensive research on progesterone and allopregnanolone have paved the way Postpartum depression for new treatment of postpartum depression. However, treatment for premenstrual syndrome and premenstrual Premenstrual dysphoric disorder dysphoric disorder as well as contraception that women can use without risking mental health problems are still Progesterone needed. As far as progesterone is concerned, we might be dealing with a two-edged sword: while its metabolite allopregnanolone has been proven useful for treatment of PPD, it may trigger negative symptoms in women with PMS and PMDD. Overall, our current knowledge on the beneficial and harmful effects of progesterone is limited and further research is imperative. Introduction 1. -
Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement. -
The Princeton Journal of East Asian Studies
THE PRINCETON JOURNAL OF EAST ASIAN STUDIES VOLUME IV SPRING 2013 PRINCETON JOURNAL OF EAST ASIAN STUDIES EDITORS-IN-CHIEF Anji Shin ’13 Jenna Song ’14 COPY EDITORS Gavin Cook ’15 Charles Fortin ’15 Kevin Liaw ’15 LAYOUT EDITOR Jiweon Kim ’15 FINANCE & OPERATIONS TEAM Ben Chang ’14 Ryan T. Kang ’14 Kevin Liaw ’15 Jay Park ’16 Samantha Wu ’16 IT TEAM IT MANAGER Pavel Shibayev ’15 STAFF Jenny Nan Jiang ’16 CHINA EDITORIAL TEAM JAPAN EDITORIAL TEAM KOREA EDITORIAL TEAM ASSOCIATE EDITOR ASSOCIATE EDITOR ASSOCIATE EDITOR Charles Fortin ’15 Ben Chang ’14 Ryan T. Kang ’14 EDITORS EDITORS EDITORS Ben Chang ’14 Charles Fortin ’15 Jennifer Cho ’15 Gavin Cook ’15 Tzu-Yung Huang ’15 Jisoo Han ’14 Adrienne Fung ’14 Marina Kaneko ’15 Jee Eun Lee ’15 Rebecca Haynes ’15 Ryan T. Kang ’14 Jay Park ’16 Tzu-Yung Huang ’15 Christian Edwards van Alicia Huaze Li ’16! Muijen ’15 Cameron White ’14 ! ! TABLE OF CONTENTS ! ! 1. PRETTIER IN PINK: IDENTITY RECONSTRUCTION AMONG RURAL MIGRANT WOMEN IN MARY KAY CHINA | JAMNAH MORTON | COLUMBIA UNIVERSITY 1 2. THE PARADOX OF CONSCIOUSNESS AND OTHER CHALLENGES: LABOR RESISTANCE IN CONTEMPORARY BEIJING | RUODI DUAN | AMHERST COLLEGE 26 3. THE INTERSECTION OF CHRISTIANITY AND SUICIDE IN SOUTH KOREA| KRISTEN KIM | PRINCETON UNIVERSITY 39 4. EURASIANS IN EARLY COLONIAL HONG KONG | KIM DENG | THE CHINESE UNIVERSITY OF HONG KONG 53 5. THE EXOTIC WOMEN OF THE WEST: DEPICTIONS OF NANBAN WOMEN IN THE MOMOYAMA PERIOD | AMANDA TSAO | COLUMBIA UNIVERSITY 73 6. KOREAN COMFORT WOMEN: NATIONALIST DISCOURSE IN CONTEMPORARY SOUTH KOREA | JUDY PARK |HARVARD UNIVERSITY 83 7.