Appendix C Database Derived Peptides Probed for Riiα Binding
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! " " ZINC%HOMEOSTASIS!IN#HEALTH,!EXERCISE!AND$ CHRONIC'DISEASES! " " " " " " Anna Kit Yung Chu BAppSc (Ex&SpSc) / BSc (Nutr) (Hons I) The University of Sydney, 2012 A thesis submitted in fulfilment of the requirements for the degree of Doctor of Philosophy (PhD) Department of Human Nutrition Division of Sciences University of Otago 2016 i" " """""" """""! " Table&of&Contents& & Abstract&...................................................................................................................................&iv" Acknowledgments&...............................................................................................................&vi" List&of&abbreviations&........................................................................................................&viii" List&of&tables&............................................................................................................................&x" List&of&figures&.......................................................................................................................&xii" Publications&arising&from&this&thesis&............................................................................&xv" List&of&other&publications&arising&from&this&thesis&.................................................&xvi" Chapter&1&&&Introduction&and&Literature&Review&.............................................................&1" Introduction&............................................................................................................................&2" Whole&body&zinc&homeostasis&...........................................................................................&5" -
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. -
Loss of the Dermis Zinc Transporter ZIP13 Promotes the Mildness Of
www.nature.com/scientificreports OPEN Loss of the dermis zinc transporter ZIP13 promotes the mildness of fbrosarcoma by inhibiting autophagy Mi-Gi Lee1,8, Min-Ah Choi2,8, Sehyun Chae3,8, Mi-Ae Kang4, Hantae Jo4, Jin-myoung Baek4, Kyu-Ree In4, Hyein Park4, Hyojin Heo4, Dongmin Jang5, Sofa Brito4, Sung Tae Kim6, Dae-Ok Kim 1,7, Jong-Soo Lee4, Jae-Ryong Kim2* & Bum-Ho Bin 4* Fibrosarcoma is a skin tumor that is frequently observed in humans, dogs, and cats. Despite unsightly appearance, studies on fbrosarcoma have not signifcantly progressed, due to a relatively mild tumor severity and a lower incidence than that of other epithelial tumors. Here, we focused on the role of a recently-found dermis zinc transporter, ZIP13, in fbrosarcoma progression. We generated two transformed cell lines from wild-type and ZIP13-KO mice-derived dermal fbroblasts by stably expressing the Simian Virus (SV) 40-T antigen. The ZIP13−/− cell line exhibited an impairment in autophagy, followed by hypersensitivity to nutrient defciency. The autophagy impairment in the ZIP13−/− cell line was due to the low expression of LC3 gene and protein, and was restored by the DNA demethylating agent, 5-aza-2’-deoxycytidine (5-aza) treatment. Moreover, the DNA methyltransferase activity was signifcantly increased in the ZIP13−/− cell line, indicating the disturbance of epigenetic regulations. Autophagy inhibitors efectively inhibited the growth of fbrosarcoma with relatively minor damages to normal cells in xenograft assay. Our data show that proper control over autophagy and zinc homeostasis could allow for the development of a new therapeutic strategy to treat fbrosarcoma. -
Supplementary Information Material and Methods
MCT-11-0474 BKM120: a potent and specific pan-PI3K inhibitor Supplementary Information Material and methods Chemicals The EGFR inhibitor NVP-AEE788 (Novartis), the Jak inhibitor I (Merck Calbiochem, #420099) and anisomycin (Alomone labs, # A-520) were prepared as 50 mM stock solutions in 100% DMSO. Doxorubicin (Adriablastin, Pfizer), EGF (Sigma Ref: E9644), PDGF (Sigma, Ref: P4306) and IL-4 (Sigma, Ref: I-4269) stock solutions were prepared as recommended by the manufacturer. For in vivo administration: Temodal (20 mg Temozolomide capsules, Essex Chemie AG, Luzern) was dissolved in 4 mL KZI/glucose (20/80, vol/vol); Taxotere was bought as 40 mg/mL solution (Sanofi Aventis, France), and prepared in KZI/glucose. Antibodies The primary antibodies used were as follows: anti-S473P-Akt (#9271), anti-T308P-Akt (#9276,), anti-S9P-GSK3β (#9336), anti-T389P-p70S6K (#9205), anti-YP/TP-Erk1/2 (#9101), anti-YP/TP-p38 (#9215), anti-YP/TP-JNK1/2 (#9101), anti-Y751P-PDGFR (#3161), anti- p21Cip1/Waf1 (#2946), anti-p27Kip1 (#2552) and anti-Ser15-p53 (#9284) antibodies were from Cell Signaling Technologies; anti-Akt (#05-591), anti-T32P-FKHRL1 (#06-952) and anti- PDGFR (#06-495) antibodies were from Upstate; anti-IGF-1R (#SC-713) and anti-EGFR (#SC-03) antibodies were from Santa Cruz; anti-GSK3α/β (#44610), anti-Y641P-Stat6 (#611566), anti-S1981P-ATM (#200-301), anti-T2609 DNA-PKcs (#GTX24194) and anti- 1 MCT-11-0474 BKM120: a potent and specific pan-PI3K inhibitor Y1316P-IGF-1R were from Bio-Source International, Becton-Dickinson, Rockland, GenTex and internal production, respectively. The 4G10 antibody was from Millipore (#05-321MG). -
Multistep Regulation of Autophagy by WNK1
Multistep regulation of autophagy by WNK1 Sachith Gallolu Kankanamalagea, A-Young Leea, Chonlarat Wichaidita, Andres Lorente-Rodrigueza, Akansha M. Shaha, Steve Stippeca, Angelique W. Whitehurstb, and Melanie H. Cobba,b,1 aDepartment of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX 75390; and bHarold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390 Contributed by Melanie H. Cobb, October 27, 2016 (sent for review September 6, 2016; reviewed by Jing Liu and Helen Piwnica-Worms) The with-no-lysine (K) (WNK) kinases are an atypical family of components and to supply cells with nutrients and building blocks protein kinases that regulate ion transport across cell membranes. (30–33). Autophagy is induced by cellular stress and protects Mutations that result in their overexpression cause hypertension- against infections by pathogens (34–40). Critical to maintain in- related disorders in humans. Of the four mammalian WNKs, only tracellular homeostasis, autophagy has roles in diseases, such as WNK1 is expressed throughout the body. We report that WNK1 neurodegeneration (41, 42) and cancer (43, 44). In this study, we inhibits autophagy, an intracellular degradation pathway impli- show that WNK1 is involved in regulating autophagy. cated in several human diseases. Using small-interfering RNA- mediated WNK1 knockdown, we show autophagosome formation Results and autophagic flux are accelerated. In cells with reduced WNK1, WNK1 Depletion Increases Autophagy. To analyze its role in auto- basal and starvation-induced autophagy is increased. We also phagy, WNK1 was knocked down with small interfering RNA show that depletion of WNK1 stimulates focal class III phospha- (siRNA) in U2OS cells stably expressing green fluorescent protein- tidylinositol 3-kinase complex (PI3KC3) activity, which is required tagged light chain 3 (GFP-LC3) (32, 45). -
Supplemental Information
Supplemental information Dissection of the genomic structure of the miR-183/96/182 gene. Previously, we showed that the miR-183/96/182 cluster is an intergenic miRNA cluster, located in a ~60-kb interval between the genes encoding nuclear respiratory factor-1 (Nrf1) and ubiquitin-conjugating enzyme E2H (Ube2h) on mouse chr6qA3.3 (1). To start to uncover the genomic structure of the miR- 183/96/182 gene, we first studied genomic features around miR-183/96/182 in the UCSC genome browser (http://genome.UCSC.edu/), and identified two CpG islands 3.4-6.5 kb 5’ of pre-miR-183, the most 5’ miRNA of the cluster (Fig. 1A; Fig. S1 and Seq. S1). A cDNA clone, AK044220, located at 3.2-4.6 kb 5’ to pre-miR-183, encompasses the second CpG island (Fig. 1A; Fig. S1). We hypothesized that this cDNA clone was derived from 5’ exon(s) of the primary transcript of the miR-183/96/182 gene, as CpG islands are often associated with promoters (2). Supporting this hypothesis, multiple expressed sequences detected by gene-trap clones, including clone D016D06 (3, 4), were co-localized with the cDNA clone AK044220 (Fig. 1A; Fig. S1). Clone D016D06, deposited by the German GeneTrap Consortium (GGTC) (http://tikus.gsf.de) (3, 4), was derived from insertion of a retroviral construct, rFlpROSAβgeo in 129S2 ES cells (Fig. 1A and C). The rFlpROSAβgeo construct carries a promoterless reporter gene, the β−geo cassette - an in-frame fusion of the β-galactosidase and neomycin resistance (Neor) gene (5), with a splicing acceptor (SA) immediately upstream, and a polyA signal downstream of the β−geo cassette (Fig. -
9-Azido Analogs of Three Sialic Acid Forms for Metabolic Remodeling Of
Supporting Information 9-Azido Analogs of Three Sialic Acid Forms for Metabolic Remodeling of Cell-Surface Sialoglycans Bo Cheng,†,‡ Lu Dong,†,§ Yuntao Zhu,†,‡ Rongbing Huang,†,‡ Yuting Sun,†,‖ Qiancheng You,†,‡ Qitao Song,†,§ James C. Paton, ∇ Adrienne W. Paton,∇ and Xing Chen*,†,‡,§,⊥,# †College of Chemistry and Molecular Engineering, ‡Beijing National Laboratory for Molecular Sciences, §Peking−Tsinghua Center for Life Sciences,‖Academy for Advanced Interdisciplinary Studies, ⊥Synthetic and Functional Biomolecules Center, and #Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education, Peking University, Beijing 100871, China ∇Research Centre for Infectious Diseases, Department of Molecular and Biomedical Science, University of Adelaide, Adelaide SA 5005, Australia Page S1 Table of Contents: Scheme S1.……………………………………………………….........……………. S3 Figure S1……………………………………………………..………..……………. S3 Figure S2……………………………………………………..………..…………… S4 Figure S3……………………………………………………..………..…………… S4 Figure S4……………………………………………………..………..…………… S5 Figure S5……………………………………………………..………..…………… S6 Figure S6……………………………………………………..………..…………….S7 Figure S7……………………………………………………..………..…………….S8 Figure S8……………………………………………………..………..…………….S9 Experimental Procedures……………………………….…........…………....S10-S27 Table S1………………………………………………..………..…………….S28-S48 Supporting Reference……………………………………………….......………...S49 Page S2 Scheme S1. Synthesis of 9AzNeu5Gc Figure S1: a, b, c, d) Representative scatter plots (FSC vs. SSC) and histograms of flow cytometry analysis -
The Crossroads Between Zinc and Steroidal Implant-Induced Growth of Beef Cattle
animals Review The Crossroads between Zinc and Steroidal Implant-Induced Growth of Beef Cattle Elizabeth M. Messersmith † , Dathan T. Smerchek † and Stephanie L. Hansen * Department of Animal Science, Iowa State University, Ames, IA 50011, USA; [email protected] (E.M.M.); [email protected] (D.T.S.) * Correspondence: [email protected] † These authors contributed equally to this work. Simple Summary: This review addresses the physiological and biochemical connections between steroidal implants and Zn and their interaction to influence growth in beef cattle. Steroidal implants have been widely accepted as a growth-promoting technology that provides an unmatched economic return to the producer and improves beef production’s environmental sustainability. Likewise, decades of research have indicated Zn is vital for skeletal muscle growth. Considering Zn is an essen- tial trace mineral, strategic Zn supplementation to implanted cattle may optimize beef production. Although many interrelationships between steroidal implants and Zn are new and forthcoming, the literature reviewed hereafter indicates roles for Zn in a multitude of growth processes perti- nent to steroidal implant-induced growth and uncover changes in Zn metabolism due to steroidal implant use. Abstract: Growth-promoting technologies such as steroidal implants have been utilized in the beef industry for over 60 years and remain an indispensable tool for improving economic returns through consistently improved average daily gain via increased skeletal muscle hypertrophy. Zinc has been Citation: Messersmith, E.M.; implicated in skeletal muscle growth through protein synthesis, satellite cell function, and many Smerchek, D.T.; Hansen, S.L. The other growth processes. Therefore, the objective of this review was to present the available literature Crossroads between Zinc and linking Zn to steroidal implant-induced protein synthesis and other metabolic processes. -
Supplementary Table 1. in Vitro Side Effect Profiling Study for LDN/OSU-0212320. Neurotransmitter Related Steroids
Supplementary Table 1. In vitro side effect profiling study for LDN/OSU-0212320. Percent Inhibition Receptor 10 µM Neurotransmitter Related Adenosine, Non-selective 7.29% Adrenergic, Alpha 1, Non-selective 24.98% Adrenergic, Alpha 2, Non-selective 27.18% Adrenergic, Beta, Non-selective -20.94% Dopamine Transporter 8.69% Dopamine, D1 (h) 8.48% Dopamine, D2s (h) 4.06% GABA A, Agonist Site -16.15% GABA A, BDZ, alpha 1 site 12.73% GABA-B 13.60% Glutamate, AMPA Site (Ionotropic) 12.06% Glutamate, Kainate Site (Ionotropic) -1.03% Glutamate, NMDA Agonist Site (Ionotropic) 0.12% Glutamate, NMDA, Glycine (Stry-insens Site) 9.84% (Ionotropic) Glycine, Strychnine-sensitive 0.99% Histamine, H1 -5.54% Histamine, H2 16.54% Histamine, H3 4.80% Melatonin, Non-selective -5.54% Muscarinic, M1 (hr) -1.88% Muscarinic, M2 (h) 0.82% Muscarinic, Non-selective, Central 29.04% Muscarinic, Non-selective, Peripheral 0.29% Nicotinic, Neuronal (-BnTx insensitive) 7.85% Norepinephrine Transporter 2.87% Opioid, Non-selective -0.09% Opioid, Orphanin, ORL1 (h) 11.55% Serotonin Transporter -3.02% Serotonin, Non-selective 26.33% Sigma, Non-Selective 10.19% Steroids Estrogen 11.16% 1 Percent Inhibition Receptor 10 µM Testosterone (cytosolic) (h) 12.50% Ion Channels Calcium Channel, Type L (Dihydropyridine Site) 43.18% Calcium Channel, Type N 4.15% Potassium Channel, ATP-Sensitive -4.05% Potassium Channel, Ca2+ Act., VI 17.80% Potassium Channel, I(Kr) (hERG) (h) -6.44% Sodium, Site 2 -0.39% Second Messengers Nitric Oxide, NOS (Neuronal-Binding) -17.09% Prostaglandins Leukotriene, -
Dataset for the Quantitative Proteomics Analysis of the Primary Hepatocellular Carcinoma with Single and Multiple Lesions
Data in Brief 5 (2015) 226–240 Contents lists available at ScienceDirect Data in Brief journal homepage: www.elsevier.com/locate/dib Data Article Dataset for the quantitative proteomics analysis of the primary hepatocellular carcinoma with single and multiple lesions Xiaohua Xing a,b, Yao Huang c, Sen Wang a,b, Minhui Chi a,b,c, Yongyi Zeng a,b,c, Lihong Chen a,b,c, Ling Li a,b,c, Jinhua Zeng a,b,c, Minjie Lin a,b, Xiao Han d, Jingfeng Liu a,b,c, Xiaolong Liu a,b,n a The Liver Center of Fujian Province, Fujian Medical University, Fuzhou 350025, People’s Republic of China b The United Innovation of Mengchao Hepatobiliary Technology Key Laboratory of Fujian Province, Mengchao Hepatobiliary Hospital of Fujian Medical University, Fuzhou 350025, People’s Republic of China c Liver Disease Center, The First Affiliated Hospital of Fujian Medical University, Fuzhou 350007, People’s Republic of China d Biotechnology Research Institute, Chinese Academy of Agricultural Sciences, Beijing 100081, People’s Republic of China article info abstract Article history: Hepatocellular Carcinoma (HCC) is one of the most common malig- Received 18 August 2015 nant tumor, which is causing the second leading cancer-related death Received in revised form worldwide. The tumor tissues and the adjacent noncancerous tissues 27 August 2015 obtained from HCC patients with single and multiple lesions were Accepted 28 August 2015 quantified using iTRAQ. A total of 5513 proteins (FDR of 1%) were Available online 8 September 2015 identified which correspond to roughly 27% of the total liver proteome. -
Antibodies Products
Chapter 2 : Gentaur Products List • Human Signal peptidase complex catalytic subunit • Human Sjoegren syndrome nuclear autoantigen 1 SSNA1 • Human Small proline rich protein 2A SPRR2A ELISA kit SEC11A SEC11A ELISA kit SpeciesHuman ELISA kit SpeciesHuman SpeciesHuman • Human Signal peptidase complex catalytic subunit • Human Sjoegren syndrome scleroderma autoantigen 1 • Human Small proline rich protein 2B SPRR2B ELISA kit SEC11C SEC11C ELISA kit SpeciesHuman SSSCA1 ELISA kit SpeciesHuman SpeciesHuman • Human Signal peptidase complex subunit 1 SPCS1 ELISA • Human Ski oncogene SKI ELISA kit SpeciesHuman • Human Small proline rich protein 2D SPRR2D ELISA kit kit SpeciesHuman • Human Ski like protein SKIL ELISA kit SpeciesHuman SpeciesHuman • Human Signal peptidase complex subunit 2 SPCS2 ELISA • Human Skin specific protein 32 C1orf68 ELISA kit • Human Small proline rich protein 2E SPRR2E ELISA kit kit SpeciesHuman SpeciesHuman SpeciesHuman • Human Signal peptidase complex subunit 3 SPCS3 ELISA • Human SLAIN motif containing protein 1 SLAIN1 ELISA kit • Human Small proline rich protein 2F SPRR2F ELISA kit kit SpeciesHuman SpeciesHuman SpeciesHuman • Human Signal peptide CUB and EGF like domain • Human SLAIN motif containing protein 2 SLAIN2 ELISA kit • Human Small proline rich protein 2G SPRR2G ELISA kit containing protein 2 SCUBE2 ELISA kit SpeciesHuman SpeciesHuman SpeciesHuman • Human Signal peptide CUB and EGF like domain • Human SLAM family member 5 CD84 ELISA kit • Human Small proline rich protein 3 SPRR3 ELISA kit containing protein -
Transcriptome Profiling Revealed Potentially
Wang et al. BMC Genomics (2020) 21:546 https://doi.org/10.1186/s12864-020-06950-y RESEARCH ARTICLE Open Access Transcriptome profiling revealed potentially important roles of defensive gene expression in the divergence of insect biotypes: a case study with the cereal aphid Sitobion avenae Da Wang1,2, Deguang Liu1,2* , Xiaoqin Shi1,2, Yujing Yang1,2, Na Zhang1,2 and Zheming Shang1,2 Abstract Background: Many insects can develop differential biotypes on variable host plants, but the underlying molecular factors and mechanisms are not well understood. To address this issue, transcriptome profiling analyses were conducted for two biotypes of the cereal aphid, Sitobion avenae (Fabricius), on both original and alternative plants. Results: Comparisons between both biotypes generated 4174 differentially expressed unigenes (DEGs). In their response to host plant shift, 39 DEGs were shared by both biotypes, whereas 126 and 861 DEGs occurred only in biotypes 1 and 3, respectively. MMC (modulated modularity clustering) analyses showed that specific DEGs of biotypes 1 and 3 clustered into five and nine transcriptional modules, respectively. Among these DEGs, defense- related genes underwent intensive expression restructuring in both biotypes. However, biotype 3 was found to have relatively lower gene transcriptional plasticity than biotype 1. Gene enrichment analyses of the abovementioned modules showed functional divergence in defensive DEGs for the two biotypes in response to host transfer. The expression plasticity for some defense related genes was showed to be directly related to fecundity of S. avenae biotypes on both original and alternative plants, suggesting that expression plasticity of key defensive genes could have significant impacts on the adaptive potential and differentiation of S.