Investigation of Peptidyl-Prolyl Cis/Trans Isomerases in the Virulence of Staphylococcus
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The Ligand-Specific Co-Receptor Function of CD44 for Receptor
The ligand-specific co-receptor function of CD44 for receptor tyrosine kinases Zur Erlangung des akademischen Grades eines DOKTORS DER NATURWISSENSCHAFTEN (Dr. rer. nat.) Fakultät für Chemie und Biowissenschaften Karlsruher Institut für Technologie (KIT) - Universitätsbereich genehmigte DISSERTATION von Christian Jung aus Karlsruhe Dekan: Prof. Dr. Martin Bastmeyer Referent: PD Dr. Véronique Orian-Rousseau Korreferent: Prof. Dr. Doris Wedlich Tag der mündlichen Prüfung: 18.4.2012 I Ich versichere, dass ich meine Arbeit selbständig angefertigt und keine anderen als die angegebenen Quellen und Hilfsmittel benutzt, sowie die wörtlich oder inhaltlich übernommenen Stellen als solche kenntlich gemacht und die Satzung der Universität Karlsruhe (TH) zur Sicherung guter wissenschaftlicher Praxis in der jeweils gültigen Fassung beachtet habe. Christian Jung, März 2012 II Zusammenfassung Listeria monocytogenes, ein gram-positives Bakterium, verursacht die Krankheit Listeriose. Eine Möglichkeit, wie L.monocytogenes Wirbeltierzellen infizieren kann, ist das Binden des Bakteriums an die Rezeportyrosinkinase (RTK) Met auf der Wirtszelle durch das bakterielle Protein InlB. Dieses Binden führt zur Aktivierung von Met und schließlich zur Aufnahme in die Zelle. Der erste Teil meine Doktorarbeit zeigt, dass die Infektion von nicht-phagozytotischen Zellen mittels InlB zusätzlich vom Ko-Rezeptor CD44v6 abhängig ist. Desweiteren kann diese bakterielle Infektion mit einem CD44v6-Peptid blockiert werden. Zusätzlich zu der Ko-Rezeptorfunktion von CD44v6 für InlB und Met, die ich gezeigt habe, wurde CD44v6 bereits als Ko-Rezeptor für die Induktion von Met und VEGFR- 2 durch ihre authentischen Liganden HGF and VEGF-A identifiziert. Im zweiten und Hauptteil meiner Doktorarbeit habe ich untersucht, ob diese Ko-Rezeptorfunktion von CD44v6 spezifisch von den Liganden, den Rezeptoren oder beiden bestimmt wird. -
In Vivo Dual RNA-Seq Analysis Reveals the Basis for Differential Tissue Tropism of Clinical Isolates of Streptococcus Pneumoniae
In Vivo Dual RNA-Seq Analysis Reveals the Basis for Differential Tissue Tropism of Clinical Isolates of Streptococcus pneumoniae Vikrant Minhas,1,4 Rieza Aprianto,2,4 Lauren J. McAllister,1 Hui Wang,1 Shannon C. David,1 Kimberley T. McLean,1 Iain Comerford,3 Shaun R. McColl,3 James C. Paton,1,5,6,* Jan-Willem Veening,2,5 and Claudia Trappetti,1,5 Supplementary Information Supplementary Table 1. Pneumococcal differential gene expression in the lungs 6 h post-infection, 9-47-Ear vs 9-47M. Genes with fold change (FC) greater than 2 and p < 0.05 are shown. FC values highlighted in blue = upregulated in 9-47-Ear, while values highlighted in red = upregulated in 9- 47M. Locus tag in 9-47- Product padj FC Ear Sp947_chr_00844 Sialidase B 3.08E-10 313.9807 Sp947_chr_02077 hypothetical protein 4.46E-10 306.9412 Sp947_chr_00842 Sodium/glucose cotransporter 2.22E-09 243.4822 Sp947_chr_00841 N-acetylneuraminate lyase 4.53E-09 227.7963 scyllo-inositol 2-dehydrogenase Sp947_chr_00845 (NAD(+)) 4.36E-09 221.051 Sp947_chr_00848 hypothetical protein 1.19E-08 202.7867 V-type sodium ATPase catalytic subunit Sp947_chr_00853 A 1.29E-06 100.5411 Sp947_chr_00846 Beta-glucoside kinase 3.42E-06 98.18951 Sp947_chr_00855 V-type sodium ATPase subunit D 8.34E-06 85.94879 Sp947_chr_00851 V-type sodium ATPase subunit C 2.50E-05 72.46612 Sp947_chr_00843 hypothetical protein 2.17E-05 65.97758 Sp947_chr_00839 HTH-type transcriptional regulator RpiR 3.09E-05 61.28171 Sp947_chr_00854 V-type sodium ATPase subunit B 1.32E-06 50.86992 Sp947_chr_00120 hypothetical protein 3.00E-04 -
Preclinical Evaluation of Protein Disulfide Isomerase Inhibitors for the Treatment of Glioblastoma by Andrea Shergalis
Preclinical Evaluation of Protein Disulfide Isomerase Inhibitors for the Treatment of Glioblastoma By Andrea Shergalis A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Medicinal Chemistry) in the University of Michigan 2020 Doctoral Committee: Professor Nouri Neamati, Chair Professor George A. Garcia Professor Peter J. H. Scott Professor Shaomeng Wang Andrea G. Shergalis [email protected] ORCID 0000-0002-1155-1583 © Andrea Shergalis 2020 All Rights Reserved ACKNOWLEDGEMENTS So many people have been involved in bringing this project to life and making this dissertation possible. First, I want to thank my advisor, Prof. Nouri Neamati, for his guidance, encouragement, and patience. Prof. Neamati instilled an enthusiasm in me for science and drug discovery, while allowing me the space to independently explore complex biochemical problems, and I am grateful for his kind and patient mentorship. I also thank my committee members, Profs. George Garcia, Peter Scott, and Shaomeng Wang, for their patience, guidance, and support throughout my graduate career. I am thankful to them for taking time to meet with me and have thoughtful conversations about medicinal chemistry and science in general. From the Neamati lab, I would like to thank so many. First and foremost, I have to thank Shuzo Tamara for being an incredible, kind, and patient teacher and mentor. Shuzo is one of the hardest workers I know. In addition to a strong work ethic, he taught me pretty much everything I know and laid the foundation for the article published as Chapter 3 of this dissertation. The work published in this dissertation really began with the initial identification of PDI as a target by Shili Xu, and I am grateful for his advice and guidance (from afar!). -
Novel Therapeutic Interventions Towards Improved Management of Septic Arthritis Jian Wang1* and Liucai Wang2
Wang and Wang BMC Musculoskeletal Disorders (2021) 22:530 https://doi.org/10.1186/s12891-021-04383-6 REVIEW Open Access Novel therapeutic interventions towards improved management of septic arthritis Jian Wang1* and Liucai Wang2 Abstract Septic arthritis (SA) represents a medical emergency that needs immediate diagnosis and urgent treatment. Despite aggressive treatment and rapid diagnosis of the causative agent, the mortality and lifelong disability, associated with septic arthritis remain high as close to 11%. Moreover, with the rise in drug resistance, the rates of failure of conventional antibiotic therapy have also increased. Among the etiological agents frequently isolated from cases of septic arthritis, Staphylococcus aureus emerges as a dominating pathogen, and to worsen, the rise in methicillin- resistant S. aureus (MRSA) isolates in bone and joint infections is worrisome. MRSA associated cases of septic arthritis exhibit higher mortality, longer hospital stay, and higher treatment failure with poorer clinical outcomes as compared to cases caused by the sensitive strain i.e methicillin-sensitive S. aureus (MSSA). In addition to this, equal or even greater damage is imposed by the exacerbated immune response mounted by the patient’s body in a futile attempt to eradicate the bacteria. The antibiotic therapy may not be sufficient enough to control the progression of damage to the joint involved thus, adding to higher mortality and disability rates despite the prompt and timely start of treatment. This situation implies that efforts and focus towards studying/ understanding new strategies for improved management of sepsis arthritis is prudent and worth exploring. The review article aims to give a complete insight into the new therapeutic approaches studied by workers lately in this field. -
2011/109440 Al
(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 _ . 9 September 2011 (09.09.2011) 2011/109440 Al (51) International Patent Classification: [CH/CH]; Chemin Des Chevreuils 1, 1188 Gimel (CH). C12Q 1/68 (2006.01) G01N 33/53 (2006.01) HOLTERMAN, Daniel [US/US]; 14465 North 14th St., Phoenix, AZ 85022 (US). (21) International Application Number: PCT/US201 1/026750 (74) Agent: AKHAVAN, Ramin; Caris Life Sciences, Inc., 6655 N. MacArthur Blvd., Irving, TX 75039 (US). (22) International Filing Date: 1 March 201 1 (01 .03.201 1) (81) Designated States (unless otherwise indicated, for every kind of national protection available): AE, AG, AL, AM, English (25) Filing Language: AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, (26) Publication Language: English CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (30) Priority Data: HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, 61/274,124 1 March 2010 (01 .03.2010) US KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, 61/357,5 17 22 June 2010 (22.06.2010) US ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, 61/364,785 15 July 2010 (15.07.2010) us NO, NZ, OM, PE, PG, PH, PL, PT, RO, RS, RU, SC, SD, (71) Applicant (for all designated States except US): CARIS SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, LIFE SCIENCES LUXEMBOURG HOLDINGS [LU/ TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. -
Signal Transduction, Quorum-Sensing, and Extracellular Protease Activity in Enterococcus Faecalis Biofilm Formation
Signal Transduction, Quorum-Sensing, and Extracellular Protease Activity in Enterococcus faecalis Biofilm Formation The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Carniol, K., and M. S. Gilmore. 2004. Signal Transduction, Quorum- Sensing, and Extracellular Protease Activity in Enterococcus Faecalis Biofilm Formation. Journal of Bacteriology 186, no. 24: 8161–8163. doi:10.1128/jb.186.24.8161-8163.2004. Published Version doi:10.1128/JB.186.24.8161-8163.2004 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:33867369 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA JOURNAL OF BACTERIOLOGY, Dec. 2004, p. 8161–8163 Vol. 186, No. 24 0021-9193/04/$08.00ϩ0 DOI: 10.1128/JB.186.24.8161–8163.2004 Copyright © 2004, American Society for Microbiology. All Rights Reserved. GUEST COMMENTARY Signal Transduction, Quorum-Sensing, and Extracellular Protease Activity in Enterococcus faecalis Biofilm Formation Karen Carniol1,2 and Michael S. Gilmore1,2* Department of Ophthalmology, Harvard Medical School,1 and The Schepens Eye Research Institute,2 Boston, Massachusetts Biofilms are surface-attached communities of bacteria, en- sponse regulator proteins (10). Only one of the mutants gen- cased in an extracellular matrix of secreted proteins, carbohy- erated, fsrA, impaired the ability of E. faecalis strain V583A to drates, and/or DNA, that assume phenotypes distinct from form biofilms in vitro. -
Host and Bacterial Determinants of Staphylococcus Aureus Nasal Colonization in Humans
University of Central Florida STARS Electronic Theses and Dissertations, 2004-2019 2014 Host and Bacterial Determinants of Staphylococcus aureus Nasal Colonization in Humans Gowrishankar Muthukrishnan University of Central Florida Part of the Medical Sciences Commons Find similar works at: https://stars.library.ucf.edu/etd University of Central Florida Libraries http://library.ucf.edu This Doctoral Dissertation (Open Access) is brought to you for free and open access by STARS. It has been accepted for inclusion in Electronic Theses and Dissertations, 2004-2019 by an authorized administrator of STARS. For more information, please contact [email protected]. STARS Citation Muthukrishnan, Gowrishankar, "Host and Bacterial Determinants of Staphylococcus aureus Nasal Colonization in Humans" (2014). Electronic Theses and Dissertations, 2004-2019. 1289. https://stars.library.ucf.edu/etd/1289 HOST AND BACTERIAL DETERMINANTS OF STAPHYLOCOCCUS AUREUS NASAL COLONIZATION IN HUMANS by GOWRISHANKAR MUTHUKRISHNAN M.E. Birla Institute of Technology and Science, Pilani, India, 2007 M.S. University of Central Florida, United States of America, 2010 A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Burnett School of Biomedical Sciences in the College of Medicine at the University of Central Florida Orlando, Florida Summer Term 2014 Major Professor: Alexander M. Cole © 2014 Gowrishankar Muthukrishnan ii ABSTRACT Staphylococcus aureus (SA), an opportunistic pathogen colonizing the anterior nares in approximately 30% of the human population, causes severe hospital-associated and community-acquired infections. SA nasal carriage plays a critical role in the pathogenesis of staphylococcal infections and SA eradication from the nares has proven to be effective in reducing endogenous infections. -
(12) Patent Application Publication (10) Pub. No.: US 2006/0110747 A1 Ramseier Et Al
US 200601 10747A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2006/0110747 A1 Ramseier et al. (43) Pub. Date: May 25, 2006 (54) PROCESS FOR IMPROVED PROTEIN (60) Provisional application No. 60/591489, filed on Jul. EXPRESSION BY STRAIN ENGINEERING 26, 2004. (75) Inventors: Thomas M. Ramseier, Poway, CA Publication Classification (US); Hongfan Jin, San Diego, CA (51) Int. Cl. (US); Charles H. Squires, Poway, CA CI2O I/68 (2006.01) (US) GOIN 33/53 (2006.01) CI2N 15/74 (2006.01) Correspondence Address: (52) U.S. Cl. ................................ 435/6: 435/7.1; 435/471 KING & SPALDING LLP 118O PEACHTREE STREET (57) ABSTRACT ATLANTA, GA 30309 (US) This invention is a process for improving the production levels of recombinant proteins or peptides or improving the (73) Assignee: Dow Global Technologies Inc., Midland, level of active recombinant proteins or peptides expressed in MI (US) host cells. The invention is a process of comparing two genetic profiles of a cell that expresses a recombinant (21) Appl. No.: 11/189,375 protein and modifying the cell to change the expression of a gene product that is upregulated in response to the recom (22) Filed: Jul. 26, 2005 binant protein expression. The process can improve protein production or can improve protein quality, for example, by Related U.S. Application Data increasing solubility of a recombinant protein. Patent Application Publication May 25, 2006 Sheet 1 of 15 US 2006/0110747 A1 Figure 1 09 010909070£020\,0 10°0 Patent Application Publication May 25, 2006 Sheet 2 of 15 US 2006/0110747 A1 Figure 2 Ester sers Custer || || || || || HH-I-H 1 H4 s a cisiers TT closers | | | | | | Ya S T RXFO 1961. -
A Bacterial Goldilocks Mechanism
INSIGHT TWO-COMPONENT SIGNALING PATHWAYS A bacterial Goldilocks mechanism Bacillus subtilis can measure the activity of the enzymes that remodel the cell wall to ensure that the levels of activity are ‘just right’. IRENE M KIM AND HENDRIK SZURMANT detector and a transcription factor that commu- Related research article Dobihal GS, Bru- nicate with one another through the transfer of a net YR, Flores-Kim J, Rudner DZ. 2019. phosphoryl group. Homeostatic control of cell wall hydrolysis An important TCS in the soil bacterium Bacil- by the WalRK two-component signaling lus subtilis and other related bacteria is the pathway in Bacillus subtilis. eLife 8:e52088. WalRK system, which is essential for viability DOI: 10.7554/eLife.52088 (Szurmant, 2012). The system, which is com- prised of the signal-detecting protein WalK and the transcription factor WalR, gets its name from its role in maintaining the cell wall (Dubrac et al., 2007). Together these two com- hen mollusks get bigger, their shells ponents regulate the expression of several auto- grow with them to accommodate lysin genes, including those for the enzymes W the changing shape and size of the LytE and CwlO, which are required for cell elon- organism being housed. Something similar also gation (Salzberg et al., 2013). Now, in eLife, happens in bacteria. The cell wall of most bacte- David Rudner and colleagues at Harvard Medical ria consists of a single macromolecule called School – including Genevieve Dobihal and Yan- peptidoglycan that surrounds the cell and is nick Brunet as joint first authors, along with made up of modified sugars that are crosslinked Josue´ Flores-Kim – report on how the WalRK through peptide side chains. -
The Characterization of a Putative Protease Expressed by Sneathia Amnii
Virginia Commonwealth University VCU Scholars Compass Theses and Dissertations Graduate School 2015 The Characterization of a Putative Protease Expressed by Sneathia amnii Rana Mehr Virginia Commonwealth University Follow this and additional works at: https://scholarscompass.vcu.edu/etd Part of the Medicine and Health Sciences Commons © The Author Downloaded from https://scholarscompass.vcu.edu/etd/3931 This Thesis is brought to you for free and open access by the Graduate School at VCU Scholars Compass. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of VCU Scholars Compass. For more information, please contact [email protected]. CHARACTERIZATION OF A PUTATIVE PROTEASE EXPRESSED BY SNEATHIA AMNII A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science at Virginia Commonwealth University by RANA MEHR B.S., Virginia Commonwealth University 2011 Director: Kimberly Jefferson, Ph.D. Associate Professor, Department of Microbiology and Immunology Virginia Commonwealth University Richmond, Virginia Virginia Commonwealth University Richmond, Virginia July, 2015 Acknowledgements I would first like to express my deepest gratitude to my mentor Dr. Kimberly Jefferson. Her continuous mentorship, trust, and support in academic, scientific, and personal experiences have empowered me to successfully complete my graduate career both academically and scientifically. She has aided my development as an independent scientist which would have not been possible without guidance. I would also like to thank the members of my graduate advisory committee: Dr. Dennis Ohman and Dr. Darrell Peterson. Their advice and direction have allowed me to better understand my project and their invaluable knowledge has made me a better scientist. -
Revealing Bacterial Targets of Growth Inhibitors Encoded by Bacteriophage T7
Revealing bacterial targets of growth inhibitors encoded by bacteriophage T7 Shahar Molshanski-Mora, Ido Yosefa, Ruth Kiroa, Rotem Edgara, Miriam Manora, Michael Gershovitsb, Mia Lasersonb, Tal Pupkob, and Udi Qimrona,1 aDepartment of Clinical Microbiology and Immunology, Sackler School of Medicine, and bDepartment of Cell Research and Immunology, George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel Edited* by Sankar Adhya, National Institutes of Health, National Cancer Institute, Bethesda, MD, and approved November 24, 2014 (received for reviewJuly 13, 2014) Today’s arsenal of antibiotics is ineffective against some emerging suggest that there are other phage products that may inhibit strains of antibiotic-resistant pathogens. Novel inhibitors of bacte- other bacterial targets. rial growth therefore need to be found. The target of such bacterial- A model for the systematic study of host–virus interactions growth inhibitors must be identified, and one way to achieve this and for elucidating phage antibacterial strategies is provided by is by locating mutations that suppress their inhibitory effect. Here, bacteriophage T7 and its host, Escherichia coli. The laboratory we identified five growth inhibitors encoded by T7 bacteriophage. strain E. coli K-12 shares many essential genes with pathogenic High-throughput sequencing of genomic DNA of resistant bacterial species, such as E. coli O157:H7 and O104:H4, and therefore, mutants evolving against three of these inhibitors revealed unique growth inhibitors against it should prove effective against these mutations in three specific genes. We found that a nonessential host pathogens as well. E. coli has been studied extensively, and the gene, ppiB, is required for growth inhibition by one bacteriophage putative functions or tentative physiological roles of over half of pcnB inhibitor and another nonessential gene, , is required for its 4,453 genes have been identified. -
A Spaetzle-Like Role for Nerve Growth Factor Beta in Vertebrate Immunity to Staphylococcus Aureus
This is a repository copy of A Spaetzle-like role for nerve growth factor beta in vertebrate immunity to Staphylococcus aureus. White Rose Research Online URL for this paper: http://eprints.whiterose.ac.uk/110810/ Version: Accepted Version Article: Hepburn, L., Prajsnar, T.K., Klapholz, C. et al. (29 more authors) (2014) A Spaetzle-like role for nerve growth factor beta in vertebrate immunity to Staphylococcus aureus. SCIENCE, 346 (6209). pp. 641-646. ISSN 0036-8075 https://doi.org/10.1126/science.1258705 This is the author’s version of the work. It is posted here by permission of the AAAS for personal use, not for redistribution. The definitive version was published in Science on Volume 346, 31 Oct 2014, DOI: 10.1126/science.1258705. Reuse Unless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version - refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher’s website. Takedown If you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing [email protected] including the URL of the record and the reason for the withdrawal request.