ABSTRACT ZHANG, NANSHAN. Design Of

Total Page:16

File Type:pdf, Size:1020Kb

ABSTRACT ZHANG, NANSHAN. Design Of ABSTRACT ZHANG, NANSHAN. Design of Safer Flame Retardant Textiles through Inclusion Complex Formation with Cyclodextrins: A Combined Experimental and Modeling Study. (Under the direction of Dr. Melissa Pasquinelli and Dr. Hinks). Triphenyl phosphate (TPP) is widely used as a phosphorus flame retardant. It is also one component of a commercial flame retardant mixture known as Firemaster 550. TPP is likely to be released into the environment due to its high volatility and has been detected at a concentration as high as 47,000 ng/m3 in air. Recent studies have also indicated that FRs like TPP could contribute to obesity and osteoporosis in humans. Cyclodextrins (CDs) are enzymatic degradation products of starch and consist of several (α-1,4)-linked α-D- glucopyranose units. CDs own a hydrophilic outside and a hydrophobic inner cavity, which enables the formation of non-covalently bonded cyclodextrin inclusion complexes (CD-ICs) with a vast array of molecules. We hypothesize that the formation of inclusion complexes between TPP and cyclodextrins will reduce its exposure yet also retain flame retarding properties of TPP, since the formation of FR-CD-ICs is expected to eliminate unnecessary loss of FRs, especially volatile FR compounds like TPP, and release them only during a fire when they are actually needed. After creating the TPP-β-CD-IC, we applied it to polyethylene terephthalate (PET) films by a hot press technique. Flame tests indicated TPP-β-CD-IC exhibited flame resistant performance matching that of neat TPP, even though much less TPP was contained in its β-CD-IC. Incorporation of FRs and other chemical additives into textile substrates in the form of their crystalline CD-ICs is a promising way to reduce the exposure of hazardous chemicals to humans and to our environment while not impacting their efficacy. Two other parent CDs (α-CD and γ-CD) were applied and their abilities to form ICs with guest TPP were studied. Results from a series of characterization methods, including FTIR, DSC, TGA, XRD and NMR indicated the successful synthesis of TPP-γ-CD-IC via two routes. However, α-CD appears unable to form an IC with TPP, which is likely attributable to a size mismatch between them. A novel analytical chemistry technique -- tandem mass spectrometry (ESI-Q-TOF) was used to study the inclusion complexes of TPP and CDs. Successful formation of TPP-β-/γ-CD-IC was further proved by ESI mass spec in the positive mode. Experimental results demonstrated that 1:1 inclusion complex ions of the guest FR and the host CDs were detected. Experimentally α-CD cannot form an IC with TPP and this was further confirmed by tandem mass spec. Mass spectrometry provides a fast and accurate method to investigate cyclodextrin inclusion complexes and verify the formation of ICs Computational methods were applied to help understand the energetically favorable geometry of TPP and β-/γ-CD in their IC form. Semi-empirical theoretical methods (PM3 and PM6) were used to find the global minima of TPP-CD geometry and density functional theory calculations at a B3LYP/6-31G(d) level were employed for elaborate geometry optimization. Solvent effect was also considered using the polarized continuum model (IEF-PCM). Analysis of the results indicated that after optimization, IC geometries provided by PM6 had stronger interactions and were more energetically favorable than the ones calculated by PM3. DFT calculations are more accurate than PM3/PM6 and enabled more interactions between the host and the guest than two semi-empirical approaches. DFT calculations also proved that initial structures prepared by PM6 were more favorable in H-bonding profiles and key energy parameters. For TPP-β-CD system in vacuum and water, Model A owned a lower total and complexation energy while a stronger interaction between them was present in Model B. In TPP-γ-CD system, Model B was preferred than Model A in both vacuum and water. This was potentially attributed to more H-bonds formed between TPP and γ-CD in Model B and its ability to retain most of the internal linkages among primary hydroxyl groups. © Copyright 2016 by Nanshan Zhang All Rights Reserved Design of Safer Flame Retardant Textiles through Inclusion Complex Formation with Cyclodextrins: A Combined Experimental and Modeling Study by Nanshan Zhang A dissertation submitted to the Graduate Faculty of North Carolina State University in partial fulfillment of the requirements for the degree of Doctor of Philosophy Fiber and Polymer Science Raleigh, North Carolina 2015 APPROVED BY: _______________________________ _______________________________ Dr. Melissa Pasquinelli Dr. David Hinks Co-chair of Advisory Committee Co-chair of Advisory Committee _______________________________ _______________________________ Dr. Alan Tonelli Dr. Ahmed El-Shafei _______________________________ Dr. Heather Patisaul ii DEDICATION This work is dedicated to my family and dear friends for their unselfish love and encouragement in all my endeavors. iii BIOGRAPHY Nanshan was born in Zhengzhou, Henan Province of China. He was majored in Textile Testing and Business and received Bachelor’s degree from Donghua University in 2011. Nanshan attended the ‘3+X’ program and joined North Carolina State University in August, 2010 to pursue a Master’s degree in Textile Engineering. He was then enrolled in Fiber and Polymer Science Program in College of Textiles to pursue his PhD degree. iv ACKNOWLEDGMENTS I would like to express my sincere thanks to Dr. Melissa Pasquinelli and Dr. Alan Tonelli for their great guidance and patience throughout my research and dissertation writing. Without their encouragement and confidence in me, this research and dissertation would not have been possible. I greatly appreciate the financial support from Dr. Hinks and for offering his support in green chemistry. I’m also very thankful to Dr. Ahmed El-Shafei and Dr. Heather Patisaul for serving critical roles as my graduate committee. Besides, I would like thank Yufei Chen, Jing Chen, Jialong Shen, Erol Yildirim, Mr. Jeff Krauss, Ms. Judy Elson, Ms. Xiaoyan Sun and Ms. Birgit Andersen for all their kind help during my PhD work. I’m grateful for all the impressive help from my friends, classmates and colleagues who have assisted me in my research work and made my life colorful. Last but not least, I want to give a special thanks to my girlfriend, Sha, the light of my life. You are too good to be true and I will always love you. v TABLE OF CONTENTS LIST OF TABLES ................................................................................................................. ix LIST OF FIGURES .................................................................................................................x CHAPTER 1 BACKGROUND TO THE PROBLEM .........................................................1 CHAPTER 2 MOTIVATION AND OBJECTIVES .............................................................3 2.1. Motivation .................................................................................................................. 3 2.2. Objectives ................................................................................................................... 5 CHAPTER 3 LITERATURE REVIEW ................................................................................6 3.1. Flame Retardants ........................................................................................................ 6 3.1.1. Background ......................................................................................................... 6 3.1.2. The Flammability of Textiles ............................................................................ 11 3.1.3. Impeding the Combustion Cycle ...................................................................... 13 3.1.3.1. The Condensed Phase Mechanism ............................................................ 15 3.1.3.2. The Gas Phase Mechanism ........................................................................ 17 3.1.3.3. Physical Effects ......................................................................................... 20 3.1.4. Classifications of Flame Retardants .................................................................. 22 3.1.4.1. Halogenated Flame Retardants .................................................................. 22 3.1.4.2. Phosphorus Flame Retardants ................................................................... 24 3.1.4.3. Other Flame Retardants ............................................................................. 29 3.1.5. Health and Environmental Concerns of Flame Retardants ............................... 31 3.1.5.1. Polybrominated Diphenyl Ethers ............................................................... 31 3.1.5.2. Fire Safety and Standards .......................................................................... 34 3.1.5.3. Firemaster 550 and Its Components .......................................................... 36 3.2. Cyclodextrins ........................................................................................................... 65 3.2.1. History ............................................................................................................... 65 3.2.2. Physical and Chemical Properties ..................................................................... 66 3.2.3. Crystallography of Cyclodextrins ..................................................................... 68 3.2.3.1. Cage Type Structures ................................................................................
Recommended publications
  • 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.
    [Show full text]
  • Examination of the Transcription Factors Acting in Bone Marrow
    THESIS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY (PHD) Examination of the transcription factors acting in bone marrow derived macrophages by Gergely Nagy Supervisor: Dr. Endre Barta UNIVERSITY OF DEBRECEN DOCTORAL SCHOOL OF MOLECULAR CELL AND IMMUNE BIOLOGY DEBRECEN, 2016 Table of contents Table of contents ........................................................................................................................ 2 1. Introduction ............................................................................................................................ 5 1.1. Transcriptional regulation ................................................................................................... 5 1.1.1. Transcriptional initiation .................................................................................................. 5 1.1.2. Co-regulators and histone modifications .......................................................................... 8 1.2. Promoter and enhancer sequences guiding transcription factors ...................................... 11 1.2.1. General transcription factors .......................................................................................... 11 1.2.2. The ETS superfamily ..................................................................................................... 17 1.2.3. The AP-1 and CREB proteins ........................................................................................ 20 1.2.4. Other promoter specific transcription factor families ...................................................
    [Show full text]
  • Supplemental Materials ZNF281 Enhances Cardiac Reprogramming
    Supplemental Materials ZNF281 enhances cardiac reprogramming by modulating cardiac and inflammatory gene expression Huanyu Zhou, Maria Gabriela Morales, Hisayuki Hashimoto, Matthew E. Dickson, Kunhua Song, Wenduo Ye, Min S. Kim, Hanspeter Niederstrasser, Zhaoning Wang, Beibei Chen, Bruce A. Posner, Rhonda Bassel-Duby and Eric N. Olson Supplemental Table 1; related to Figure 1. Supplemental Table 2; related to Figure 1. Supplemental Table 3; related to the “quantitative mRNA measurement” in Materials and Methods section. Supplemental Table 4; related to the “ChIP-seq, gene ontology and pathway analysis” and “RNA-seq” and gene ontology analysis” in Materials and Methods section. Supplemental Figure S1; related to Figure 1. Supplemental Figure S2; related to Figure 2. Supplemental Figure S3; related to Figure 3. Supplemental Figure S4; related to Figure 4. Supplemental Figure S5; related to Figure 6. Supplemental Table S1. Genes included in human retroviral ORF cDNA library. Gene Gene Gene Gene Gene Gene Gene Gene Symbol Symbol Symbol Symbol Symbol Symbol Symbol Symbol AATF BMP8A CEBPE CTNNB1 ESR2 GDF3 HOXA5 IL17D ADIPOQ BRPF1 CEBPG CUX1 ESRRA GDF6 HOXA6 IL17F ADNP BRPF3 CERS1 CX3CL1 ETS1 GIN1 HOXA7 IL18 AEBP1 BUD31 CERS2 CXCL10 ETS2 GLIS3 HOXB1 IL19 AFF4 C17ORF77 CERS4 CXCL11 ETV3 GMEB1 HOXB13 IL1A AHR C1QTNF4 CFL2 CXCL12 ETV7 GPBP1 HOXB5 IL1B AIMP1 C21ORF66 CHIA CXCL13 FAM3B GPER HOXB6 IL1F3 ALS2CR8 CBFA2T2 CIR1 CXCL14 FAM3D GPI HOXB7 IL1F5 ALX1 CBFA2T3 CITED1 CXCL16 FASLG GREM1 HOXB9 IL1F6 ARGFX CBFB CITED2 CXCL3 FBLN1 GREM2 HOXC4 IL1F7
    [Show full text]
  • Mouse Population-Guided Resequencing Reveals That Variants in CD44 Contribute to Acetaminophen-Induced Liver Injury in Humans
    Downloaded from genome.cshlp.org on October 2, 2021 - Published by Cold Spring Harbor Laboratory Press Letter Mouse population-guided resequencing reveals that variants in CD44 contribute to acetaminophen-induced liver injury in humans Alison H. Harrill,1,2,12 Paul B. Watkins,3,12 Stephen Su,6 Pamela K. Ross,2 David E. Harbourt,5 Ioannis M. Stylianou,7 Gary A. Boorman,8 Mark W. Russo,3 Richard S. Sackler,9 Stephen C. Harris,11 Philip C. Smith,5 Raymond Tennant,8 Molly Bogue,7 Kenneth Paigen,7 Christopher Harris,9,10 Tanupriya Contractor,9 Timothy Wiltshire,5 Ivan Rusyn,1,2,14 and David W. Threadgill1,4,13,14,15 1Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina 27599, USA; 2Department of Environmental Sciences and Engineering, University of North Carolina, Chapel Hill, North Carolina 27599, USA; 3Division of Gastroenterology and Hepatology, University of North Carolina, Chapel Hill, North Carolina 27599, USA; 4Department of Genetics, University of North Carolina, Chapel Hill, North Carolina 27599, USA; 5School of Pharmacy, University of North Carolina, Chapel Hill, North Carolina 27599, USA; 6Department of Mouse Genetics, Genomics Institute of the Novartis Research Foundation, San Diego, California 92121, USA; 7The Jackson Laboratory, Bar Harbor, Maine 04609, USA; 8National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA; 9Verto Institute Research Laboratories, New Brunswick, New Jersey 08903, USA; 10Cancer Institute of New Jersey, New Brunswick, New Jersey 08903, USA; 11Purdue Pharma L.P., Stamford, Connecticut 06901, USA; 12Hamner-UNC Center for Drug Safety Sciences, The Hamner Institutes for Health Sciences, Research Triangle Park, North Carolina 27709, USA; 13Department of Genetics, North Carolina State University, Raleigh, North Carolina 27695, USA Interindividual variability in response to chemicals and drugs is a common regulatory concern.
    [Show full text]
  • Has Critical Roles in Epithelial Dysfunction in Airway Disease
    JBC Papers in Press. Published on May 1, 2017 as Manuscript M117.775304 The latest version is at http://www.jbc.org/cgi/doi/10.1074/jbc.M117.775304 EHF has critical roles in airway epithelial dysfunction Ets Homologous Factor (EHF) has critical roles in epithelial dysfunction in airway disease Sara L Fossum1,2, Michael J. Mutolo1,2, Antonio Tugores3, Sujana Ghosh1,2, Scott H. Randell4, Lisa C. Jones4, Shih-Hsing Leir1,2,5, Ann Harris1,2,5 1Human Molecular Genetics Program, Lurie Children’s Research Center, Chicago, IL 60614, USA, 2Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA, 3 Unidad de Investigación, Complejo Hospitalario Universitario Insular Materno Infantil, Las Palmas de Gran Canaria, Spain, 4Marsico Lung Institute, University of North Carolina Cystic Fibrosis Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA, 5 Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH 44016, USA Running title: EHF has critical roles in airway epithelial dysfunction Downloaded from To whom correspondence should be addressed: Ann Harris, Department of Genetics and Genome Sciences, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, Ohio, 44106; Email: [email protected] http://www.jbc.org/ Keywords: genomics, gene regulation, epithelium, lung, transcription factor at University of North Carolina Chapel Hill on August 16, 2019 ABSTRACT The airway epithelium forms a barrier between the internal and external environments. The airway epithelium plays a critical role Epithelial dysfunction is critical in the pathology in lung function in both normal and pathological of many respiratory diseases including cystic states.
    [Show full text]
  • Local Genetic and Environmental Factors in Asthma Disease Pathogenesis: Chronicity and Persistence Mechanisms
    Eur Respir J 2007; 29: 793–803 DOI: 10.1183/09031936.00087506 CopyrightßERS Journals Ltd 2007 SERIES ‘‘GENETICS OF ASTHMA AND COPD IN THE POSTGENOME ERA’’ Edited by E. von Mutius, M. Kabesch and F. Kauffmann Number 4 in this Series Local genetic and environmental factors in asthma disease pathogenesis: chronicity and persistence mechanisms S.T. Holgate*, D.E. Davies*, R.M. Powell*, P.H. Howarth*, H.M. Haitchi# and J.W. Holloway" ABSTRACT: While asthma is an inflammatory disorder of the airways usually associated with AFFILIATIONS atopy, an important additional component is involvement of the epithelium and underlying *Allergy and Inflammation Research, Division of Infection, Inflammation mesenchyme acting as a trophic unit (EMTU). and Repair, In addition to allergens, a wide range of environmental factors interact with the EMTU, such as #IIR Division and virus infections, environmental tobacco smoke and pollutants, to initiate tissue damage and "Division of Human Genetics, School aberrant repair responses that are translated into remodelling of the airways. While candidate of Medicine, Southampton General Hospital, Southampton, UK. gene association studies have revealed polymorphic variants that influence asthmatic inflamma- tion, positional cloning of previously unknown genes is identifying a high proportion of novel CORRESPONDENCE genes in the EMTU. S.T. Holgate Dipeptidyl peptidase (DPP) 10 and disintegrin and metalloproteinase (ADAM)33 are newly Allergy and Inflammation Research MP810 identified genes strongly associated with asthma that are preferentially expressed in the airway Level D epithelium and underlying mesenchyme, respectively. Centre Block Also of increasing importance is the recognition that genes associated with asthma and atopy Southampton General Hospital have important interactions with the environment through epigenetic mechanisms that influence Southampton SO16 6YD UK their expression.
    [Show full text]
  • Chloride Channels Regulate Differentiation and Barrier Functions
    RESEARCH ARTICLE Chloride channels regulate differentiation and barrier functions of the mammalian airway Mu He1†*, Bing Wu2†, Wenlei Ye1, Daniel D Le2, Adriane W Sinclair3,4, Valeria Padovano5, Yuzhang Chen6, Ke-Xin Li1, Rene Sit2, Michelle Tan2, Michael J Caplan5, Norma Neff2, Yuh Nung Jan1,7,8, Spyros Darmanis2*, Lily Yeh Jan1,7,8* 1Department of Physiology, University of California, San Francisco, San Francisco, United States; 2Chan Zuckerberg Biohub, San Francisco, United States; 3Department of Urology, University of California, San Francisco, San Francisco, United States; 4Division of Pediatric Urology, University of California, San Francisco, Benioff Children’s Hospital, San Francisco, United States; 5Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Heaven, United States; 6Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, United States; 7Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, United States; 8Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, United States *For correspondence: Abstract The conducting airway forms a protective mucosal barrier and is the primary target of [email protected] (MH); [email protected] airway disorders. The molecular events required for the formation and function of the airway (SD); mucosal barrier, as well as the mechanisms by which barrier dysfunction leads to early onset airway [email protected] (LYJ) diseases,
    [Show full text]
  • Appendix 2. Significantly Differentially Regulated Genes in Term Compared with Second Trimester Amniotic Fluid Supernatant
    Appendix 2. Significantly Differentially Regulated Genes in Term Compared With Second Trimester Amniotic Fluid Supernatant Fold Change in term vs second trimester Amniotic Affymetrix Duplicate Fluid Probe ID probes Symbol Entrez Gene Name 1019.9 217059_at D MUC7 mucin 7, secreted 424.5 211735_x_at D SFTPC surfactant protein C 416.2 206835_at STATH statherin 363.4 214387_x_at D SFTPC surfactant protein C 295.5 205982_x_at D SFTPC surfactant protein C 288.7 1553454_at RPTN repetin solute carrier family 34 (sodium 251.3 204124_at SLC34A2 phosphate), member 2 238.9 206786_at HTN3 histatin 3 161.5 220191_at GKN1 gastrokine 1 152.7 223678_s_at D SFTPA2 surfactant protein A2 130.9 207430_s_at D MSMB microseminoprotein, beta- 99.0 214199_at SFTPD surfactant protein D major histocompatibility complex, class II, 96.5 210982_s_at D HLA-DRA DR alpha 96.5 221133_s_at D CLDN18 claudin 18 94.4 238222_at GKN2 gastrokine 2 93.7 1557961_s_at D LOC100127983 uncharacterized LOC100127983 93.1 229584_at LRRK2 leucine-rich repeat kinase 2 HOXD cluster antisense RNA 1 (non- 88.6 242042_s_at D HOXD-AS1 protein coding) 86.0 205569_at LAMP3 lysosomal-associated membrane protein 3 85.4 232698_at BPIFB2 BPI fold containing family B, member 2 84.4 205979_at SCGB2A1 secretoglobin, family 2A, member 1 84.3 230469_at RTKN2 rhotekin 2 82.2 204130_at HSD11B2 hydroxysteroid (11-beta) dehydrogenase 2 81.9 222242_s_at KLK5 kallikrein-related peptidase 5 77.0 237281_at AKAP14 A kinase (PRKA) anchor protein 14 76.7 1553602_at MUCL1 mucin-like 1 76.3 216359_at D MUC7 mucin 7,
    [Show full text]
  • Downloaded from (2007)
    ARTICLE https://doi.org/10.1038/s41467-020-14796-x OPEN Alterations in promoter interaction landscape and transcriptional network underlying metabolic adaptation to diet ✉ Yufeng Qin1, Sara A. Grimm2, John D. Roberts1, Kaliopi Chrysovergis1 & Paul A. Wade 1 Metabolic adaptation to nutritional state requires alterations in gene expression in key tis- sues. Here, we investigated chromatin interaction dynamics, as well as alterations in cis- 1234567890():,; regulatory loci and transcriptional network in a mouse model system. Chronic consumption of a diet high in saturated fat, when compared to a diet high in carbohydrate, led to dramatic reprogramming of the liver transcriptional network. Long-range interaction of promoters with distal regulatory loci, monitored by promoter capture Hi-C, was regulated by metabolic status in distinct fashion depending on diet. Adaptation to a lipid-rich diet, mediated largely by nuclear receptors including Hnf4α, relied on activation of preformed enhancer/promoter loops. Adaptation to carbohydrate-rich diet led to activation of preformed loops and to de novo formation of new promoter/enhancer interactions. These results suggest that adapta- tion to nutritional changes and metabolic stress occurs through both de novo and pre-existing chromatin interactions which respond differently to metabolic signals. 1 Eukaryotic Transcriptional Regulation Group, Epigenetics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. 2 Integrative Bioinformatics
    [Show full text]
  • Table SII. Significantly Differentially Expressed Mrnas of GSE23558 Data Series with the Criteria of Adjusted P<0.05 And
    Table SII. Significantly differentially expressed mRNAs of GSE23558 data series with the criteria of adjusted P<0.05 and logFC>1.5. Probe ID Adjusted P-value logFC Gene symbol Gene title A_23_P157793 1.52x10-5 6.91 CA9 carbonic anhydrase 9 A_23_P161698 1.14x10-4 5.86 MMP3 matrix metallopeptidase 3 A_23_P25150 1.49x10-9 5.67 HOXC9 homeobox C9 A_23_P13094 3.26x10-4 5.56 MMP10 matrix metallopeptidase 10 A_23_P48570 2.36x10-5 5.48 DHRS2 dehydrogenase A_23_P125278 3.03x10-3 5.40 CXCL11 C-X-C motif chemokine ligand 11 A_23_P321501 1.63x10-5 5.38 DHRS2 dehydrogenase A_23_P431388 2.27x10-6 5.33 SPOCD1 SPOC domain containing 1 A_24_P20607 5.13x10-4 5.32 CXCL11 C-X-C motif chemokine ligand 11 A_24_P11061 3.70x10-3 5.30 CSAG1 chondrosarcoma associated gene 1 A_23_P87700 1.03x10-4 5.25 MFAP5 microfibrillar associated protein 5 A_23_P150979 1.81x10-2 5.25 MUCL1 mucin like 1 A_23_P1691 2.71x10-8 5.12 MMP1 matrix metallopeptidase 1 A_23_P350005 2.53x10-4 5.12 TRIML2 tripartite motif family like 2 A_24_P303091 1.23x10-3 4.99 CXCL10 C-X-C motif chemokine ligand 10 A_24_P923612 1.60x10-5 4.95 PTHLH parathyroid hormone like hormone A_23_P7313 6.03x10-5 4.94 SPP1 secreted phosphoprotein 1 A_23_P122924 2.45x10-8 4.93 INHBA inhibin A subunit A_32_P155460 6.56x10-3 4.91 PICSAR P38 inhibited cutaneous squamous cell carcinoma associated lincRNA A_24_P686965 8.75x10-7 4.82 SH2D5 SH2 domain containing 5 A_23_P105475 7.74x10-3 4.70 SLCO1B3 solute carrier organic anion transporter family member 1B3 A_24_P85099 4.82x10-5 4.67 HMGA2 high mobility group AT-hook 2 A_24_P101651
    [Show full text]
  • Genetic Analysis of FLRT Protein Family During Early Mouse Embryonic Development
    Genetic analysis of the FLRT family of proteins during early mouse embryonic development Dissertation Der Fakultät für Biologie der Ludwig-Maximilians-Universität München Eingereicht am 17. Februar 2009 von Christian Erlacher 1. Gutachter: Prof. Dr. Rüdiger Klein 2. Gutachter: PD Dr. Angelika Böttger Tag der mündlichen Prüfung: 24.04.2009 Work presented in this dissertation was performed in the laboratory of Prof. Dr. Rüdiger Klein, Department of Molecular Neurobiology, Max Planck Institute of Neurobiology, Martinsried, Germany. Work was performed under the supervision of Prof. Dr. Rüdiger Klein and Dr. Joaquim E g e a Ehrenwörtliche Versicherung Ich versichere hiermit ehrenwörtlich, dass die vorgelegte Dissertation von mir selbständig und ohne unerlaubte Beihilfe angefertigt ist. München, den (Unterschrift) Erklärung Hiermit erkläre ich, dass ich mich anderweitig einer Doktorprüfung ohne Erfolg nicht unterzogen habe. München, den (Unterschrift) Publication from the work presented in this dissertation # Joaquim E g e a* , Christian Erlacher*, Eloi Montanez, Ingo Burtscher, Satoru Yamagishi, Martin Heß, Falko Hampel, Rodrigo Sanchez, Maria Teresa Rodriguez-Manzaneque, Michael R. Bösl, Reinhard Fässler, Heiko Lickert, and Rüdiger Klein# „Genetic ablation of FLRT3 reveals a novel morphogenetic function for the anterior visceral endoderm in suppressing mesoderm differentiation.“ Genes & Development 22, Nr. 23 (Dec 2008): 3349-3362. * and #: These authors contributed equally to this work. Für Margareta und Hans Table of contents Abbreviations V List of Figures IX 1. Introduction 1 1.1. Preimplantation development 3 1.2. Postimplantation development 4 1.3. Axis specification 8 1.4. Molecular basis of axis formation 11 1.5. Gastrulation 15 1.6. Molecular mechanisms guiding gastrulation 18 1.7.
    [Show full text]
  • Induction of Α Cell-Restricted Gc in Dedifferentiating Β Cells Contributes to Stress-Induced Β-Cell Dysfunction
    Induction of α cell-restricted Gc in dedifferentiating β cells contributes to stress-induced β-cell dysfunction Taiyi Kuo, … , Mitchell A. Lazar, Domenico Accili JCI Insight. 2019. https://doi.org/10.1172/jci.insight.128351. Research In-Press Preview Endocrinology Metabolism Diabetic β cell failure is associated with β cell dedifferentiation. To identify effector genes of dedifferentiation, we integrated analyses of histone methylation as a surrogate of gene activation status and RNA expression in β cells sorted from mice with multiparity-induced diabetes. Interestingly, only a narrow subset of genes demonstrated concordant changes to histone methylation and RNA levels in dedifferentiating β cells. Notable among them was the α cell signature gene Gc, encoding a vitamin D-binding protein. While diabetes was associated with Gc induction, Gc-deficient islets did not induce β cell dedifferentiation markers and maintained normal ex vivo insulin secretion in the face of metabolic challenge. Moreover, Gc-deficient mice exhibited a more robust insulin secretory response than normal controls during hyperglycemic clamps. The data are consistent with a functional role of Gc activation in β cell dysfunction, and indicate that multiparity-induced diabetes is associated with altered β cell fate. Find the latest version: https://jci.me/128351/pdf Kuo et al, Chromatin in dedifferentiated β-cells Induction of α cell-restricted Gc in dedifferentiating β cells contributes to stress-induced β-cell dysfunction Taiyi Kuo1, Manashree Damle2, Bryan J. González1,3,
    [Show full text]