Skip to navigation Skip to content
  • Woodruff
  • Business
  • Health Sciences
  • Law
  • MARBL
  • Oxford College
  • Theology
  • Schools
    • Undergraduate

      • Emory College
      • Oxford College
      • Business School
      • School of Nursing

      Community

      • Emory College
      • Oxford College
      • Business School
      • School of Nursing
    • Graduate

      • Business School
      • Graduate School
      • School of Law
      • School of Medicine
      • School of Nursing
      • School of Public Health
      • School of Theology
  • Libraries
    • Libraries

      • Robert W. Woodruff
      • Business
      • Chemistry
      • Health Sciences
      • Law
      • MARBL
      • Music & Media
      • Oxford College
      • Theology
    • Library Tools

      • Course Reserves
      • Databases
      • Digital Scholarship (ECDS)
      • discoverE
      • eJournals
      • Electronic Dissertations
      • EmoryFindingAids
      • EUCLID
      • ILLiad
      • OpenEmory
      • Research Guides
  • Resources
    • Resources

      • Administrative Offices
      • Emory Healthcare
      • Academic Calendars
      • Bookstore
      • Campus Maps
      • Shuttles and Parking
      • Athletics: Emory Eagles
      • Arts at Emory
      • Michael C. Carlos Museum
      • Emory News Center
      • Emory Report
    • Resources

      • Emergency Contacts
      • Information Technology (IT)
      • Outlook Web Access
      • Office 365
      • Blackboard
      • OPUS
      • PeopleSoft Financials: Compass
      • Careers
      • Human Resources
      • Emory Alumni Association
  • Browse
    • Works by Author
    • Works by Journal
    • Works by Subject
    • Works by Dept
    • Faculty by Dept
  • For Authors
    • How to Submit
    • Deposit Advice
    • Author Rights
    • Publishing Your Data
    • FAQ
    • Emory Open Access Policy
    • Open Access Fund
  • About OpenEmory
    • About OpenEmory
    • About Us
    • Citing Articles
    • Contact Us
    • Privacy Policy
    • Terms of Use
 
Contact Us

Filter Results:

Year

  • 2012 (1)
  • 2015 (1)
  • 2016 (1)
  • 2017 (1)

Author

  • An, W. Frank (1)
  • Bliss-Moreau, Meghan (1)
  • Bray, Mark-Anthony (1)
  • Dancik, Vladimir (1)
  • Diebold, Lauren (1)
  • Donnerhak, Christian (1)
  • Eaton, Douglas (1)
  • Finkernagel, Malin (1)
  • Flory, Egbert (1)
  • Gauthier, Theresa (1)
  • Gilles, Laure (1)
  • Goldenson, Benjamin (1)
  • Himmelsbach, Kiyoshi (1)
  • Hoover Jr, Robert (1)
  • Huang, Zan (1)
  • Kettern, Nadja (1)
  • Kim, Baek (1)
  • König, Renate (1)
  • Lewis, Timothy (1)
  • Li, Xiaoyu (1)
  • Liese, Juliane (1)
  • Linck, Valerie (1)
  • Ma, He-Ping (1)
  • Moore, Christopher B. (1)
  • Münk, Carsten (1)
  • Ni, Yi (1)
  • Qu, Bingqian (1)
  • Riess, Maximilian (1)
  • Rivière, Lise (1)
  • Schenone, Monica (1)
  • Schnellbaecher, Esther (1)
  • Schott, Kerstin (1)
  • Shepard, Caitlin (1)
  • Silver, Serena J. (1)
  • Sommer, Andreas F. (1)
  • Thiollier, Clarisse (1)
  • Tolliday, Nicola J. (1)
  • Urban, Stephan (1)
  • VerPlank, Lynn (1)
  • Vokes, Martha S. (1)
  • Wang, Ling-Zhi (1)
  • Welzel, Karin (1)
  • Wen, Qiang (1)
  • Woods, William G (1)
  • Wynne, Brandi (1)
  • Zou, Li (1)

Subject

  • Biology, Physiology (1)
  • Biology, Virology (1)
  • Health Sciences, Human Development (1)
  • Health Sciences, Oncology (1)

Journal

  • Alcohol Research Current Reviews (1)
  • Analytical Cellular Pathology / Cellular Oncology (1)
  • Frontiers in Immunology (1)
  • Scientific Reports (1)

Keyword

  • technolog (4)
  • biomedicin (3)
  • life (3)
  • a (2)
  • acid (2)
  • acut (2)
  • alveolar (2)
  • cell (2)
  • immun (2)
  • inhibit (2)
  • phosphoryl (2)
  • protein (2)
  • 1 (1)
  • 8237 (1)
  • abus (1)
  • activ (1)
  • aicardi (1)
  • aicardigoutier (1)
  • alcohol (1)
  • alcoholrel (1)
  • alpha (1)
  • alphadepend (1)
  • aurora (1)
  • auroraa (1)
  • avail (1)
  • beta (1)
  • bind (1)
  • bindingprotein (1)
  • biochemistri (1)
  • biolog (1)
  • birth (1)
  • birthweight (1)
  • cellcycl (1)
  • channel (1)
  • children (1)
  • clearanc (1)
  • cycl (1)
  • cytokin (1)
  • depend (1)
  • develop (1)
  • disord (1)
  • distress (1)
  • dntpase (1)
  • down (1)
  • downsyndrom (1)
  • edema (1)
  • effect (1)
  • epitheli (1)
  • ester (1)
  • ethanol (1)
  • ethyl (1)
  • ethylest (1)
  • exposur (1)
  • factor (1)
  • factorkappab (1)
  • fetal (1)
  • fluid (1)
  • function (1)
  • glutathion (1)
  • goutier (1)
  • group (1)
  • groupbstreptococcus (1)
  • growth (1)
  • growthfactorbeta (1)
  • hepat (1)
  • hiv (1)
  • immunolog (1)
  • infant (1)
  • infect (1)
  • inflamm (1)
  • inhibitor (1)
  • injuri (1)
  • innat (1)
  • intrauterin (1)
  • ion (1)
  • iontransport (1)
  • kappa (1)
  • kinas (1)
  • leukemia (1)
  • lung (1)
  • macrophag (1)
  • mechan (1)
  • megakaryoblast (1)
  • megakaryocyt (1)
  • megakaryopoiesi (1)
  • mln (1)
  • molecular (1)
  • multidisciplinari (1)
  • necrosi (1)
  • neonat (1)
  • network (1)
  • nitric (1)
  • nitricoxid (1)
  • nucleas (1)
  • oxid (1)
  • physiolog (1)
  • pregnanc (1)

Author department

  • Medicine: Nephrology (1)
  • Neonatology (1)
  • Neuro-Oncology (1)
  • Peds: Emory LOBP (1)
  • Physiology: Admin (1)

Search Results for all work with filters:

  • Health Sciences, General
  • t
  • b
  • syndrom
  • scienc

Work 1-4 of 4

Sorted by relevance

Article

Restrictive influence of SAMHD1 on Hepatitis B Virus life cycle

by Andreas F. Sommer; Lise Rivière; Bingqian Qu; Kerstin Schott; Maximilian Riess; Yi Ni; Caitlin Shepard; Esther Schnellbaecher; Malin Finkernagel; Kiyoshi Himmelsbach; Karin Welzel; Nadja Kettern; Christian Donnerhak; Carsten Münk; Egbert Flory; Juliane Liese; Baek Kim; Stephan Urban; Renate König

2016

Subjects
  • Biology, Virology
  • Health Sciences, General
  • File Download
  • View Abstract

Abstract:Close

Deoxynucleotide triphosphates (dNTPs) are essential for efficient hepatitis B virus (HBV) replication. Here, we investigated the influence of the restriction factor SAMHD1, a dNTP hydrolase (dNTPase) and RNase, on HBV replication. We demonstrated that silencing of SAMHD1 in hepatic cells increased HBV replication, while overexpression had the opposite effect. SAMHD1 significantly affected the levels of extracellular viral DNA as well as intracellular reverse transcription products, without affecting HBV RNAs or cccDNA. SAMHD1 mutations that interfere with the dNTPase activity (D137N) or in the catalytic center of the histidine-aspartate (HD) domain (D311A), and a phospho-mimetic mutation (T592E), abrogated the inhibitory activity. In contrast, a mutation diminishing the potential RNase but not dNTPase activity (Q548A) and a mutation disabling phosphorylation (T592A) did not affect antiviral activity. Moreover, HBV restriction by SAMHD1 was rescued by addition of deoxynucleosides. Although HBV infection did not directly affect protein level or phosphorylation of SAMHD1, the virus upregulated intracellular dATPs. Interestingly, SAMHD1 was dephosphorylated, thus in a potentially antiviral-active state, in primary human hepatocytes. Furthermore, SAMHD1 was upregulated by type I and II interferons in hepatic cells. These results suggest that SAMHD1 is a relevant restriction factor for HBV and restricts reverse transcription through its dNTPase activity.

Article

Prenatal Alcohol Exposure and the Developing Immune System

by Theresa Gauthier

2015

Subjects
  • Health Sciences, Human Development
  • Health Sciences, General
  • File Download
  • View Abstract

Abstract:Close

Evidence from research in humans and animals suggest that ingesting alcohol during pregnancy can disrupt the fetal immune system and result in an increased risk of infections and disease in newborns that may persist throughout life. Alcohol may have indirect effects on the immune system by increasing the risk of premature birth, which itself is a risk factor for immune-related problems. Animal studies suggest that alcohol exposure directly disrupts the developing immune system. A comprehensive knowledge of the mechanisms underlying alcohol's effects on the developing immune system only will become clear once researchers establish improved methods for identifying newborns exposed to alcohol in utero.

Article

Identification of Regulators of Polyploidization Presents Therapeutic Targets for Treatment of AMKL/Post-Print Title: Integrative screening approach identifies regulators of polyploidization and targets for acute megakaryocytic leukemia

by Qiang Wen; Benjamin Goldenson; Serena J. Silver; Monica Schenone; Vladimir Dancik; Zan Huang; Ling-Zhi Wang; Timothy Lewis; W. Frank An; Xiaoyu Li; Mark-Anthony Bray; Clarisse Thiollier; Lauren Diebold; Laure Gilles; Martha S. Vokes; Christopher B. Moore; Meghan Bliss-Moreau; Lynn VerPlank; Nicola J. Tolliday; William G Woods

2012

Subjects
  • Health Sciences, Oncology
  • Health Sciences, General
  • File Download
  • View Abstract

Abstract:Close

The mechanism by which cells decide to skip mitosis to become polyploid is largely undefined. Here we used a high-content image-based screen to identify small-molecule probes that induce polyploidization of megakaryocytic leukemia cells and serve as perturbagens to help understand this process. Our study implicates five networks of kinases that regulate the switch to polyploidy. Moreover, we find that dimethylfasudil (diMF, H-1152P) selectively increased polyploidization, mature cell-surface marker expression, and apoptosis of malignant megakaryocytes. An integrated target identification approach employing proteomic and shRNA screening revealed that a major target of diMF is Aurora kinase A (AURKA). We further find that MLN8237 (Alisertib), a selective inhibitor of AURKA, induced polyploidization and expression of mature megakaryocyte markers in acute megakaryocytic leukemia (AMKL) blasts and displayed potent anti-AMKL activity in vivo. Our findings provide a rationale to support clinical trials of MLN8237 and other inducers of polyploidization and differentiation in AMKL.

Article

Regulation of Lung epithelial Sodium Channels by Cytokines and Chemokines

by Brandi Wynne; Li Zou; Valerie Linck; Robert Hoover Jr; He-Ping Ma; Douglas Eaton

2017

Subjects
  • Biology, Physiology
  • Health Sciences, General
  • File Download
  • View Abstract

Abstract:Close

Acute lung injury leading to acute respiratory distress (ARDS) is a global health concern. ARDS patients have significant pulmonary inflammation leading to flooding of the pulmonary alveoli. This prevents normal gas exchange with consequent hypoxemia and causes mortality. A thin fluid layer in the alveoli is normal. The maintenance of this thin layer results from fluid movement out of the pulmonary capillaries into the alveolar interstitium driven by vascular hydrostatic pressure and then through alveolar tight junctions. This is then balanced by fluid reabsorption from the alveolar space mediated by transepithelial salt and water transport through alveolar cells. Reabsorption is a two-step process: first, sodium enters via sodium-permeable channels in the apical membranes of alveolar type 1 and 2 cells followed by active extrusion of sodium into the interstitium by the basolateral Na + , K + -ATPase. Anions follow the cationic charge gradien t and water follows the salt-induced osmotic gradient. The proximate cause of alveolar flooding is the result of a failure to reabsorb sufficient salt and water or a failure of the tight junctions to prevent excessive movement of fluid from the interstitium to alveolar lumen. Cytokine- and chemokine-induced inflammation can have a particularly profound effect on lung sodium transport since they can alter both ion channel and barrier function. Cytokines and chemokines affect alveolar amiloride-sensitive epithelial sodium channels (ENaCs), which play a crucial role in sodium transport and fluid reabsorption in the lung. This review discusses the regulation of ENaC via local and systemic cytokines during inflammatory disease and the effect on lung fluid balance.
Site Statistics
  • 16,898
  • Total Works
  • 3,656,404
  • Downloads
  • 1,132,315
  • Downloads This Year
  • 6,807
  • Faculty Profiles

Copyright © 2016 Emory University - All Rights Reserved
540 Asbury Circle, Atlanta, GA 30322-2870
(404) 727-6861
Privacy Policy | Terms & Conditions

v2.2.8-dev

Contact Us Recent and Popular Items
Download now