RT² Profiler PCR Array (96-Well Format and 384-Well [4 X 96] Format)
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Supplementary Data
Supplementary Data for Quantitative Changes in the Mitochondrial Proteome from Subjects with Mild Cognitive Impairment, Early Stage and Late Stage Alzheimer’s disease Table 1 - 112 unique, non-redundant proteins identified and quantified in at least two of the three analytical replicates for all three disease stages. Table 2 - MCI mitochondrial samples, Protein Summary Table 3 - MCI mitochondrial samples, Experiment 1 Table 4 - MCI mitochondrial samples, Experiment 2 Table 5 - MCI mitochondrial samples, Experiment 3 Table 6 - EAD Mitochondrial Study, Protein Summary Table 7 - EAD Mitochondrial Study, Experiment 1 Table 8 - EAD Mitochondrial Study, Experiment 2 Table 9 - EAD Mitochondrial Study, Experiment 3 Table 10 - LAD Mitochondrial Study, Protein Summary Table 11 - LAD Mitochondrial Study, Experiment 1 Table 12 - LAD Mitochondrial Study, Experiment 2 Table 13 - LAD Mitochondrial Study, Experiment 3 Supplemental Table 1. 112 unique, non-redundant proteins identified and quantified in at least two of the three analytical replicates for all three disease stages. Description Data MCI EAD LAD AATM_HUMAN (P00505) Aspartate aminotransferase, mitochondrial precursor (EC Mean 1.43 1.70 1.31 2.6.1.1) (Transaminase A) (Glutamate oxaloacetate transaminase 2) [MASS=47475] SEM 0.07 0.09 0.09 Count 3.00 3.00 3.00 ACON_HUMAN (Q99798) Aconitate hydratase, mitochondrial precursor (EC 4.2.1.3) Mean 1.24 1.61 1.19 (Citrate hydro-lyase) (Aconitase) [MASS=85425] SEM 0.05 0.17 0.18 Count 3.00 2.00 3.00 ACPM_HUMAN (O14561) Acyl carrier protein, mitochondrial -
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Item Occurences Present In Fever, Pneumonia, Heart Disease, Kidney Disease, Lung Disease, Diabetes, Hypertension, Cancer, Sepsis, Acute Kidney Injury, Neutrophilia, Lymphophenia, Thrombocytopenia, Multiple Organ TNF 16 Failure, SARS-CoV, Viral Life Cycle Cough, Fever, Dyspnea, Pneumonia, Kidney Disease, Lung Disease, Diabetes, Hypertension, Cancer, Sepsis, Neutrophilia, CXCL8 15 Leukocytosis, Thrombocytopenia, SARS-CoV, Viral Life Cycle Cough, Fever, Pneumonia, Heart Disease, Kidney Disease, Lung Disease, Diabetes, Hypertension, Cancer, Sepsis, Neutrophilia, IL1B 13 Leukocytosis, Lymphophenia Fever, Pneumonia, Heart Disease, Kidney Disease, Lung Disease, Diabetes, Hypertension, Cancer, Sepsis, Acute Kidney Injury, IL6 13 Neutrophilia, Thrombocytopenia, SARS-CoV Cough, Fever, Pneumonia, Heart Disease, Kidney Disease, Lung Disease, Diabetes, Hypertension, Cancer, Sepsis, Neutrophilia, MMP9 13 Leukocytosis, Multiple Organ Failure Cough, Fever, Dyspnea, Pneumonia, Heart Disease, Kidney Disease, Lung Disease, Diabetes, Hypertension, Cancer, Sepsis, TGFB1 13 Acute Kidney Injury, Thrombocytopenia Cough, Fever, Pneumonia, Heart Disease, Kidney Disease, Lung Disease, Diabetes, Hypertension, Sepsis, SARS-CoV, Viral Entry, ACE2 12 Viral Life Cycle Fever, Pneumonia, Lung Disease, Diabetes, Hypertension, Cancer, Sepsis, Neutrophilia, Lymphophenia, Thrombocytopenia, CXCR4 12 Viral Entry, Viral Life Cycle Cough, Fever, Dyspnea, Heart Disease, Kidney Disease, Lung Disease, Diabetes, Hypertension, Cancer, Acute Kidney Injury, EGFR 12 Viral Entry, Viral -
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. -
Impact of SGLT-2 Inhibition on Cardiometabolic Abnormalities in a Rat Model of Polycystic Ovary Syndrome
International Journal of Molecular Sciences Article Impact of SGLT-2 Inhibition on Cardiometabolic Abnormalities in a Rat Model of Polycystic Ovary Syndrome Jacob E. Pruett 1 , Edgar D. Torres Fernandez 1, Steven J. Everman 1 , Ruth M. Vinson 1, Kacey Davenport 1 , Madelyn K. Logan 1, Stephanie A. Ye 1, Damian G. Romero 1,2,3,4 and Licy L. Yanes Cardozo 1,2,3,4,5,* 1 Department of Cell and Molecular Biology, University of Mississippi Medical Center, Jackson, MS 39216, USA; [email protected] (J.E.P.); [email protected] (E.D.T.F.); [email protected] (S.J.E.); [email protected] (R.M.V.); [email protected] (K.D.); [email protected] (M.K.L.); [email protected] (S.A.Y.); [email protected] (D.G.R.) 2 Mississippi Center of Excellence in Perinatal Research, University of Mississippi Medical Center, Jackson, MS 39216, USA 3 Women’s Health Research Center, University of Mississippi Medical Center, Jackson, MS 39216, USA 4 Cardio Renal Research Center, University of Mississippi Medical Center, Jackson, MS 39216, USA 5 Division of Endocrinology, Department of Medicine, University of Mississippi Medical Center, Jackson, MS 39216, USA * Correspondence: [email protected] Abstract: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in reproductive- age women. PCOS is characterized by hyperandrogenism and ovulatory dysfunction. Women with PCOS have a high prevalence of obesity, insulin resistance (IR), increased blood pressure (BP), and activation of the renin angiotensin system (RAS). Effective evidence-based therapeutics to Citation: Pruett, J.E.; Torres ameliorate the cardiometabolic complications in PCOS are lacking. -
Transport of Sugars
BI84CH32-Frommer ARI 29 April 2015 12:34 Transport of Sugars Li-Qing Chen,1,∗ Lily S. Cheung,1,∗ Liang Feng,3 Widmar Tanner,2 and Wolf B. Frommer1 1Department of Plant Biology, Carnegie Institution for Science, Stanford, California 94305; email: [email protected] 2Zellbiologie und Pflanzenbiochemie, Universitat¨ Regensburg, 93040 Regensburg, Germany 3Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, California 94305 Annu. Rev. Biochem. 2015. 84:865–94 Keywords First published online as a Review in Advance on glucose, sucrose, carrier, GLUT, SGLT, SWEET March 5, 2015 The Annual Review of Biochemistry is online at Abstract biochem.annualreviews.org Soluble sugars serve five main purposes in multicellular organisms: as sources This article’s doi: of carbon skeletons, osmolytes, signals, and transient energy storage and as 10.1146/annurev-biochem-060614-033904 transport molecules. Most sugars are derived from photosynthetic organ- Copyright c 2015 by Annual Reviews. isms, particularly plants. In multicellular organisms, some cells specialize All rights reserved in providing sugars to other cells (e.g., intestinal and liver cells in animals, ∗ These authors contributed equally to this review. photosynthetic cells in plants), whereas others depend completely on an ex- Annu. Rev. Biochem. 2015.84:865-894. Downloaded from www.annualreviews.org ternal supply (e.g., brain cells, roots and seeds). This cellular exchange of Access provided by b-on: Universidade de Lisboa (UL) on 09/05/16. For personal use only. sugars requires transport proteins to mediate uptake or release from cells or subcellular compartments. Thus, not surprisingly, sugar transport is criti- cal for plants, animals, and humans. -
Distribution of Glucose Transporters in Renal Diseases Leszek Szablewski
Szablewski Journal of Biomedical Science (2017) 24:64 DOI 10.1186/s12929-017-0371-7 REVIEW Open Access Distribution of glucose transporters in renal diseases Leszek Szablewski Abstract Kidneys play an important role in glucose homeostasis. Renal gluconeogenesis prevents hypoglycemia by releasing glucose into the blood stream. Glucose homeostasis is also due, in part, to reabsorption and excretion of hexose in the kidney. Lipid bilayer of plasma membrane is impermeable for glucose, which is hydrophilic and soluble in water. Therefore, transport of glucose across the plasma membrane depends on carrier proteins expressed in the plasma membrane. In humans, there are three families of glucose transporters: GLUT proteins, sodium-dependent glucose transporters (SGLTs) and SWEET. In kidney, only GLUTs and SGLTs protein are expressed. Mutations within genes that code these proteins lead to different renal disorders and diseases. However, diseases, not only renal, such as diabetes, may damage expression and function of renal glucose transporters. Keywords: Kidney, GLUT proteins, SGLT proteins, Diabetes, Familial renal glucosuria, Fanconi-Bickel syndrome, Renal cancers Background Because glucose is hydrophilic and soluble in water, lipid Maintenance of glucose homeostasis prevents pathological bilayer of plasma membrane is impermeable for it. There- consequences due to prolonged hyperglycemia or fore, transport of glucose into cells depends on carrier pro- hypoglycemia. Hyperglycemia leads to a high risk of vascu- teins that are present in the plasma membrane. In humans, lar complications, nephropathy, neuropathy and retinop- there are three families of glucose transporters: GLUT pro- athy. Hypoglycemia may damage the central nervous teins, encoded by SLC2 genes; sodium-dependent glucose system and lead to a higher risk of death. -
Epistasis-Driven Identification of SLC25A51 As a Regulator of Human
ARTICLE https://doi.org/10.1038/s41467-020-19871-x OPEN Epistasis-driven identification of SLC25A51 as a regulator of human mitochondrial NAD import Enrico Girardi 1, Gennaro Agrimi 2, Ulrich Goldmann 1, Giuseppe Fiume1, Sabrina Lindinger1, Vitaly Sedlyarov1, Ismet Srndic1, Bettina Gürtl1, Benedikt Agerer 1, Felix Kartnig1, Pasquale Scarcia 2, Maria Antonietta Di Noia2, Eva Liñeiro1, Manuele Rebsamen1, Tabea Wiedmer 1, Andreas Bergthaler1, ✉ Luigi Palmieri2,3 & Giulio Superti-Furga 1,4 1234567890():,; About a thousand genes in the human genome encode for membrane transporters. Among these, several solute carrier proteins (SLCs), representing the largest group of transporters, are still orphan and lack functional characterization. We reasoned that assessing genetic interactions among SLCs may be an efficient way to obtain functional information allowing their deorphanization. Here we describe a network of strong genetic interactions indicating a contribution to mitochondrial respiration and redox metabolism for SLC25A51/MCART1, an uncharacterized member of the SLC25 family of transporters. Through a combination of metabolomics, genomics and genetics approaches, we demonstrate a role for SLC25A51 as enabler of mitochondrial import of NAD, showcasing the potential of genetic interaction- driven functional gene deorphanization. 1 CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria. 2 Laboratory of Biochemistry and Molecular Biology, Department of Biosciences, Biotechnologies and Biopharmaceutics, -
Datasheet: AHP1152
Datasheet: AHP1152 Description: RABBIT ANTI HUMAN SLC5A4 (C-TERMINAL) Specificity: SLC5A4 (C-TERMINAL) Other names: SGLT2 Format: Purified Product Type: Polyclonal Antibody Isotype: Polyclonal IgG Quantity: 50 µg Product Details Applications This product has been reported to work in the following applications. This information is derived from testing within our laboratories, peer-reviewed publications or personal communications from the originators. Please refer to references indicated for further information. For general protocol recommendations, please visit www.bio-rad-antibodies.com/protocols. Yes No Not Determined Suggested Dilution Flow Cytometry Immunohistology - Frozen Immunohistology - Paraffin 10 - 30ug/ml ELISA Immunoprecipitation Western Blotting Functional Assays Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Target Species Human Product Form Purified IgG - liquid Antiserum Preparation Antisera to SLC5A4 were raised by repeated immunisations of rabbit with highly purified antigen. Purified IgG prepared by affinity chromatography. Buffer Solution Phosphate buffered saline Preservative 0.09% Sodium Azide (NaN ) Stabilisers 3 Approx. Protein IgG concentration 1.0mg/ml Concentrations Immunogen Synthetic peptide corresponding to the C-terminal domain of human SLC5A4, conjugated to KLH. External Database UniProt: Links Page 1 of 3 Q9NY91 Related reagents Entrez Gene: 6527 SLC5A4 Related reagents Synonyms SAAT1, SGLT2 Specificity Rabbit anti Human SGLT2 antibody detects an epitope within the C-terminal (CT) region of Na+-coupled glucose transporter 3 (SGLT2), also known as SLC5A4. -
Glucose Transporters As a Target for Anticancer Therapy
cancers Review Glucose Transporters as a Target for Anticancer Therapy Monika Pliszka and Leszek Szablewski * Chair and Department of General Biology and Parasitology, Medical University of Warsaw, 5 Chalubinskiego Str., 02-004 Warsaw, Poland; [email protected] * Correspondence: [email protected]; Tel.: +48-22-621-26-07 Simple Summary: For mammalian cells, glucose is a major source of energy. In the presence of oxygen, a complete breakdown of glucose generates 36 molecules of ATP from one molecule of glucose. Hypoxia is a hallmark of cancer; therefore, cancer cells prefer the process of glycolysis, which generates only two molecules of ATP from one molecule of glucose, and cancer cells need more molecules of glucose in comparison with normal cells. Increased uptake of glucose by cancer cells is due to increased expression of glucose transporters. However, overexpression of glucose transporters, promoting the process of carcinogenesis, and increasing aggressiveness and invasiveness of tumors, may have also a beneficial effect. For example, upregulation of glucose transporters is used in diagnostic techniques such as FDG-PET. Therapeutic inhibition of glucose transporters may be a method of treatment of cancer patients. On the other hand, upregulation of glucose transporters, which are used in radioiodine therapy, can help patients with cancers. Abstract: Tumor growth causes cancer cells to become hypoxic. A hypoxic condition is a hallmark of cancer. Metabolism of cancer cells differs from metabolism of normal cells. Cancer cells prefer the process of glycolysis as a source of ATP. Process of glycolysis generates only two molecules of ATP per one molecule of glucose, whereas the complete oxidative breakdown of one molecule of glucose yields 36 molecules of ATP. -
Inaugural-Dissertation Zur Erlangung Des Doktorgrades Der
Role of TNFα and hepatic glutamine synthetase in pathogenesis of hepatic encephalopathy. Inaugural-Dissertation zur Erlangung des Doktorgrades der Mathematisch-Naturwissenschaftlichen Fakultät der Heinrich-Heine-Universität Düsseldorf vorgelegt von Vitaly Pozdeev aus Pavlograd, USSR Düsseldorf, October 2018 aus dem Institut für Molekulare Medizin II der Heinrich-Heine-Universität Düsseldorf Gedruckt mit der Genehmigung der Mathematisch-Naturwissenschaftlichen Fakultät der Heinrich-Heine-Universität Düsseldorf Berichterstatter: 1.Prof. Dr. Philipp Lang 2. Prof. Dr. Eckhard Lammert Tag der mündlichen Prüfung: 11.10.2018 (bitte bei der Abgabe Ihrer Dissertation noch offen lassen) (bitte bei der Abgabe Ihrer Dissertation noch offen lassen) ii Table of content Table of figures ........................................................................................................... vi List of tables .............................................................................................................. vii Abstract .................................................................................................................... viii Zusammenfassung ...................................................................................................... x Acknowledgment ....................................................................................................... xii List of abbreviations .................................................................................................. xiii 1. Introduction ............................................................................................................ -
Analysis of the Impact of Pufas on Placental Gene Expression V2.28 Uploadx
TECHNISCHE UNIVERSITÄT MÜNCHEN Lehrstuhl für Ernährungsmedizin Analysis of the Impact of Polyunsaturated Fatty Acids (PUFAs) on Placental Gene Expression Eva-Maria Sedlmeier Vollständiger Abdruck der von der Fakultät Wissenschaftszentrum Weihenstephan für Ernährung, Landnutzung und Umwelt der Technischen Universität München zur Erlangung des akademischen Grades eines Doktors der Naturwissenschaften genehmigten Dissertation. Vorsitzender: Univ.-Prof. Dr. M. Klingenspor Prüfer der Dissertation: 1. Univ.-Prof. Dr. J. J. Hauner 2. Univ.-Prof. Dr. H. Daniel Die Dissertation wurde am 17.10.2013 bei der Technischen Universität München eingereicht und durch die Fakultät Wissenschaftszentrum Weihenstephan für Ernährung, Landnutzung und Umwelt am 12.12.2013 angenommen. Table of contents Table of contents Table of contents ....................................................................................................... I Summary .................................................................................................................. VI Zusammenfassung ................................................................................................ VIII 1. Introduction ........................................................................................................ 1 1.1. Fetal programming - a strategy to prevent the obesity epidemic? ...........................................1 1.1.1. The obesity epidemic ........................................................................................................1 1.1.2. Fetal programming -
Chr CNV Start CNV Stop Gene Gene Feature 1 37261312 37269719
chr CNV start CNV stop Gene Gene feature 1 37261312 37269719 Tmem131 closest upstream gene 1 37261312 37269719 Cnga3 closest downstream gene 1 41160869 41180390 Tmem182 closest upstream gene 1 41160869 41180390 2610017I09Rik closest downstream gene 1 66835123 66839616 1110028C15Rik in region 2 88714200 88719211 Olfr1206 closest upstream gene 2 88714200 88719211 Olfr1208 closest downstream gene 2 154840037 154846228 a in region 3 30065831 30417157 Mecom closest upstream gene 3 30065831 30417157 Arpm1 closest downstream gene 3 35476875 35495913 Sox2ot closest upstream gene 3 35476875 35495913 Atp11b closest downstream gene 3 39563408 39598697 Fat4 closest upstream gene 3 39563408 39598697 Intu closest downstream gene 3 94246481 94410611 Celf3 in region 3 94246481 94410611 Mrpl9 in region 3 94246481 94410611 Riiad1 in region 3 94246481 94410611 Snx27 in region 3 104311901 104319916 Lrig2 in region 3 144613709 144619149 Clca6 in region 3 144613709 144619149 Clca6 in region 4 108673 137301 Vmn1r2 closest downstream gene 4 3353037 5882883 6330407A03Rik in region 4 3353037 5882883 Chchd7 in region 4 3353037 5882883 Fam110b in region 4 3353037 5882883 Impad1 in region 4 3353037 5882883 Lyn in region 4 3353037 5882883 Mos in region 4 3353037 5882883 Penk in region 4 3353037 5882883 Plag1 in region 4 3353037 5882883 Rps20 in region 4 3353037 5882883 Sdr16c5 in region 4 3353037 5882883 Sdr16c6 in region 4 3353037 5882883 Tgs1 in region 4 3353037 5882883 Tmem68 in region 4 5919294 6304249 Cyp7a1 in region 4 5919294 6304249 Sdcbp in region 4 5919294