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Human Cathepsin A/ Lysosomal Carboxypeptidase a Antibody
Human Cathepsin A/ Lysosomal Carboxypeptidase A Antibody Monoclonal Mouse IgG2A Clone # 179803 Catalog Number: MAB1049 DESCRIPTION Species Reactivity Human Specificity Detects human Cathepsin A/Lysosomal Carboxypeptidase A in direct ELISAs and Western blots. In Western blots, detects the single chain (55 kDa) and heavy chain (32 kDa) forms of recombinant human (rh) Cathepsin A. In Western blots, less than 5% crossreactivity with rhCathepsin B, C, D, E, L, O, S, X and Z is observed and no crossreactivity with the light chain (20 kDa) of rhCathepsin A is observed. Source Monoclonal Mouse IgG2A Clone # 179803 Purification Protein A or G purified from hybridoma culture supernatant Immunogen Mouse myeloma cell line NS0derived recombinant human Cathepsin A/Lysosomal Carboxypeptidase A Ala29Tyr480 (predicted) Accession # P10619 Formulation Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. See Certificate of Analysis for details. *Small pack size (SP) is supplied either lyophilized or as a 0.2 μm filtered solution in PBS. APPLICATIONS Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website. Recommended Sample Concentration Western Blot 1 µg/mL Recombinant Human Cathepsin A/Lysosomal Carboxypeptidase A (Catalog # 1049SE) Immunoprecipitation 25 µg/mL Conditioned cell culture medium spiked with Recombinant Human Cathepsin A/Lysosomal Carboxypeptidase A (Catalog # 1049SE), see our available Western blot detection antibodies PREPARATION AND STORAGE Reconstitution Reconstitute at 0.5 mg/mL in sterile PBS. Shipping The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. -
Cloning and Sequence Analysis of Canine Apoptosis-Associated Molecules
Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2007 Cloning and sequence analysis of canine apoptosis-associated molecules Schade, Benjamin Abstract: The aim of the study was to clone and sequence the coding sequences of a representative set of proteins, primarily from the intrinsic apoptotic pathway in dogs and to assess their conservation with hu- man and murine orthologues. cDNA for these proteins, including Bcl-2 family members (Bcl-XL, Bcl-w, Mcl-1, Bax, Bak, Bad, Noxa), caspases (Caspase-3, Caspase-8, Caspase-9), Inhibitors of Apoptosis Pro- teins (XIAP, cIAP-1, cIAP-2, Survivin), their mitochondrial inhibitors (Smac/ DIABLO, Omi/HtrA2) and p53, were generated by RT-PCR with RNA extracted from two canine non-neoplastic cell lines. Eleven sequences are novel for the dog. Interspecies comparison revealed strongest similarity between the sequences of human and canine intrinsic apoptosis pathway members. Differences with potential func- tional impact, however, were observed in both dogs and mice. In dogs, these changes involve the putative Inhibitor of Apoptosis Protein binding motif of canine Omi/HtrA2, some caspase substrate recognition motifs and some functionally relevant residues of p53. Canine XIAP yields a caspase-cleavage site reported as unique to humans. In conclusion, the generally high degree of similarity of canine apoptosis-associated proteins as compared to human counterparts is supportive of the use of dogs as a model for human dis- eases. Single interspecies sequence variations with potential functional relevance under physiologic and neoplastic conditions do exist, however, and will require further analysis. -
Implications in Parkinson's Disease
Journal of Clinical Medicine Review Lysosomal Ceramide Metabolism Disorders: Implications in Parkinson’s Disease Silvia Paciotti 1,2 , Elisabetta Albi 3 , Lucilla Parnetti 1 and Tommaso Beccari 3,* 1 Laboratory of Clinical Neurochemistry, Department of Medicine, University of Perugia, Sant’Andrea delle Fratte, 06132 Perugia, Italy; [email protected] (S.P.); [email protected] (L.P.) 2 Section of Physiology and Biochemistry, Department of Experimental Medicine, University of Perugia, Sant’Andrea delle Fratte, 06132 Perugia, Italy 3 Department of Pharmaceutical Sciences, University of Perugia, Via Fabretti, 06123 Perugia, Italy; [email protected] * Correspondence: [email protected] Received: 29 January 2020; Accepted: 20 February 2020; Published: 21 February 2020 Abstract: Ceramides are a family of bioactive lipids belonging to the class of sphingolipids. Sphingolipidoses are a group of inherited genetic diseases characterized by the unmetabolized sphingolipids and the consequent reduction of ceramide pool in lysosomes. Sphingolipidoses include several disorders as Sandhoff disease, Fabry disease, Gaucher disease, metachromatic leukodystrophy, Krabbe disease, Niemann Pick disease, Farber disease, and GM2 gangliosidosis. In sphingolipidosis, lysosomal lipid storage occurs in both the central nervous system and visceral tissues, and central nervous system pathology is a common hallmark for all of them. Parkinson’s disease, the most common neurodegenerative movement disorder, is characterized by the accumulation and aggregation of misfolded α-synuclein that seem associated to some lysosomal disorders, in particular Gaucher disease. This review provides evidence into the role of ceramide metabolism in the pathophysiology of lysosomes, highlighting the more recent findings on its involvement in Parkinson’s disease. Keywords: ceramide metabolism; Parkinson’s disease; α-synuclein; GBA; GLA; HEX A-B; GALC; ASAH1; SMPD1; ARSA * Correspondence [email protected] 1. -
Supplementary Materials For
Supplementary Materials for Elucidating cellular population dynamics by molecular density function perturbations 1 2,3, Thanneer Malai Perumal and Rudiyanto Gunawan * 1 Sage Bionetworks, Seattle, Washington, USA; [email protected] 2 Institute for Chemical and Bioengineering, ETH Zurich, Zurich, Switzerland; [email protected] 3 Swiss Institute of Bioinformatics, Lausanne, Switzerland * Correspondence: [email protected]; Tel.: +41-44-633-2134 Supplementary Material S1. Probability Distance Metrics Signed Engineering Metric: ∞ 2 ∆ (f A (t, x )||f B (t, x )) = sign(∆μ ) ∫ (x f A (t, x ) − x f B (t, x )) dx (S. 1) E Xi i Xi i Xi i Xi i i Xi i i −∞ Signed Jeffrey Divergence: ∞ f A (t,x ) A B A B Xi i ∆ (f (t, x )||f (t, x )) = sgn(∆μ ) ∫ (f (t, x ) − f (t, x ))ln ( B ) )dx (S. 2) JD Xi i Xi i Xi Xi i Xi i f (t,x ) i −∞ Xi i Signed Kullback-Leibler Distance: ∞ f B (t,x ) A B B Xi i ∆ (f (t, x )||f (t, x )) = sgn(∆μ ) ∫ f (t, x )ln ( A ) dx (S. 3) KLD Xi i Xi i Xi Xi i f (t,x ) i −∞ Xi i Signed Jensen-Shannon Divergence: f + (t,x )+f − (t,x ) Xi i Xi i ∆ f (t, x ) = sgn(∆μ ) (S. 4) JSD Xi i Xi 2 Signed Kolmogorov-Smirnov Metric: ∆ (f A (t, x )||f B (t, x )) = sgn(∆μ )sup|F A (t, x ) − F B (t, x )| (S. 5) KS Xi i Xi i Xi Xi i Xi i Supplementary Material S2. -
Epithelial Delamination Is Protective During Pharmaceutical-Induced Enteropathy
Epithelial delamination is protective during pharmaceutical-induced enteropathy Scott T. Espenschieda, Mark R. Cronana, Molly A. Mattya, Olaf Muellera, Matthew R. Redinbob,c,d, David M. Tobina,e,f, and John F. Rawlsa,e,1 aDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710; bDepartment of Chemistry, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; cDepartment of Biochemistry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599; dDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599; eDepartment of Medicine, Duke University School of Medicine, Durham, NC 27710; and fDepartment of Immunology, Duke University School of Medicine, Durham, NC 27710 Edited by Dennis L. Kasper, Harvard Medical School, Boston, MA, and approved July 15, 2019 (received for review February 12, 2019) Intestinal epithelial cell (IEC) shedding is a fundamental response to in mediating intestinal responses to injury remains poorly un- intestinal damage, yet underlying mechanisms and functions have derstood for most xenobiotics. been difficult to define. Here we model chronic intestinal damage in Gastrointestinal pathology is common in people using phar- zebrafish larvae using the nonsteroidal antiinflammatory drug maceuticals, including nonsteroidal antiinflammatory drugs (NSAID) Glafenine. Glafenine induced the unfolded protein response (NSAIDs) (11). While gastric ulceration has historically been a (UPR) and inflammatory pathways in IECs, leading to delamination. defining clinical presentation of NSAID-induced enteropathy, Glafenine-induced inflammation was augmented by microbial colo- small intestinal pathology has also been observed, although the nizationandassociatedwithchanges in intestinal and environmental incidence may be underreported due to diagnostic limitations microbiotas. -
Global Analysis of Protein Folding Thermodynamics for Disease State Characterization
Global Analysis of Protein Folding Thermodynamics for Disease State Characterization and Biomarker Discovery by Jagat Adhikari Department of Biochemistry Duke University Date:_______________________ Approved: ___________________________ Michael C. Fitzgerald, Supervisor ___________________________ Kenneth Kreuzer ___________________________ Terrence G. Oas ___________________________ Jiyong Hong ___________________________ Seok-Yong Lee Dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Biochemistry in the Graduate School of Duke University 2015 ABSTRACT Global Analysis of Protein Folding Thermodynamics for Disease State Characterization and Biomarker Discovery by Jagat Adhikari Department of Biochemistry Duke University Date:_______________________ Approved: ___________________________ Michael C. Fitzgerald, Supervisor ___________________________ Kenneth Kreuzer ___________________________ Terrence G. Oas ___________________________ Jiyong Hong ___________________________ Seok-Yong Lee An abstract of a dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Biochemistry in the Graduate School of Duke University 2015 Copyright by Jagat Adhikari 2015 Abstract Protein biomarkers can facilitate the diagnosis of many diseases such as cancer and they can be important for the development of effective therapeutic interventions. Current large-scale biomarker discovery and disease state characterization -
Neurodevelopmental Signatures of Narcotic and Neuropsychiatric Risk Factors in 3D Human-Derived Forebrain Organoids
Molecular Psychiatry www.nature.com/mp ARTICLE OPEN Neurodevelopmental signatures of narcotic and neuropsychiatric risk factors in 3D human-derived forebrain organoids 1 1 1 1 2 2 3 Michael Notaras , Aiman Lodhi , Estibaliz✉ Barrio-Alonso , Careen Foord , Tori Rodrick , Drew Jones , Haoyun Fang , David Greening 3,4 and Dilek Colak 1,5 © The Author(s) 2021 It is widely accepted that narcotic use during pregnancy and specific environmental factors (e.g., maternal immune activation and chronic stress) may increase risk of neuropsychiatric illness in offspring. However, little progress has been made in defining human- specific in utero neurodevelopmental pathology due to ethical and technical challenges associated with accessing human prenatal brain tissue. Here we utilized human induced pluripotent stem cells (hiPSCs) to generate reproducible organoids that recapitulate dorsal forebrain development including early corticogenesis. We systemically exposed organoid samples to chemically defined “enviromimetic” compounds to examine the developmental effects of various narcotic and neuropsychiatric-related risk factors within tissue of human origin. In tandem experiments conducted in parallel, we modeled exposure to opiates (μ-opioid agonist endomorphin), cannabinoids (WIN 55,212-2), alcohol (ethanol), smoking (nicotine), chronic stress (human cortisol), and maternal immune activation (human Interleukin-17a; IL17a). Human-derived dorsal forebrain organoids were consequently analyzed via an array of unbiased and high-throughput analytical approaches, including state-of-the-art TMT-16plex liquid chromatography/mass- spectrometry (LC/MS) proteomics, hybrid MS metabolomics, and flow cytometry panels to determine cell-cycle dynamics and rates of cell death. This pipeline subsequently revealed both common and unique proteome, reactome, and metabolome alterations as a consequence of enviromimetic modeling of narcotic use and neuropsychiatric-related risk factors in tissue of human origin. -
Supplementary Table S1. Upregulated Genes Differentially
Supplementary Table S1. Upregulated genes differentially expressed in athletes (p < 0.05 and 1.3-fold change) Gene Symbol p Value Fold Change 221051_s_at NMRK2 0.01 2.38 236518_at CCDC183 0.00 2.05 218804_at ANO1 0.00 2.05 234675_x_at 0.01 2.02 207076_s_at ASS1 0.00 1.85 209135_at ASPH 0.02 1.81 228434_at BTNL9 0.03 1.81 229985_at BTNL9 0.01 1.79 215795_at MYH7B 0.01 1.78 217979_at TSPAN13 0.01 1.77 230992_at BTNL9 0.01 1.75 226884_at LRRN1 0.03 1.74 220039_s_at CDKAL1 0.01 1.73 236520_at 0.02 1.72 219895_at TMEM255A 0.04 1.72 201030_x_at LDHB 0.00 1.69 233824_at 0.00 1.69 232257_s_at 0.05 1.67 236359_at SCN4B 0.04 1.64 242868_at 0.00 1.63 1557286_at 0.01 1.63 202780_at OXCT1 0.01 1.63 1556542_a_at 0.04 1.63 209992_at PFKFB2 0.04 1.63 205247_at NOTCH4 0.01 1.62 1554182_at TRIM73///TRIM74 0.00 1.61 232892_at MIR1-1HG 0.02 1.61 204726_at CDH13 0.01 1.6 1561167_at 0.01 1.6 1565821_at 0.01 1.6 210169_at SEC14L5 0.01 1.6 236963_at 0.02 1.6 1552880_at SEC16B 0.02 1.6 235228_at CCDC85A 0.02 1.6 1568623_a_at SLC35E4 0.00 1.59 204844_at ENPEP 0.00 1.59 1552256_a_at SCARB1 0.02 1.59 1557283_a_at ZNF519 0.02 1.59 1557293_at LINC00969 0.03 1.59 231644_at 0.01 1.58 228115_at GAREM1 0.01 1.58 223687_s_at LY6K 0.02 1.58 231779_at IRAK2 0.03 1.58 243332_at LOC105379610 0.04 1.58 232118_at 0.01 1.57 203423_at RBP1 0.02 1.57 AMY1A///AMY1B///AMY1C///AMY2A///AMY2B// 208498_s_at 0.03 1.57 /AMYP1 237154_at LOC101930114 0.00 1.56 1559691_at 0.01 1.56 243481_at RHOJ 0.03 1.56 238834_at MYLK3 0.01 1.55 213438_at NFASC 0.02 1.55 242290_at TACC1 0.04 1.55 ANKRD20A1///ANKRD20A12P///ANKRD20A2/// -
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. -
Supplementary Table S1. Prioritization of Candidate FPC Susceptibility Genes by Private Heterozygous Ptvs
Supplementary Table S1. Prioritization of candidate FPC susceptibility genes by private heterozygous PTVs Number of private Number of private Number FPC patient heterozygous PTVs in heterozygous PTVs in tumors with somatic FPC susceptibility Hereditary cancer Hereditary Gene FPC kindred BCCS samples mutation DNA repair gene Cancer driver gene gene gene pancreatitis gene ATM 19 1 - Yes Yes Yes Yes - SSPO 12 8 1 - - - - - DNAH14 10 3 - - - - - - CD36 9 3 - - - - - - TET2 9 1 - - Yes - - - MUC16 8 14 - - - - - - DNHD1 7 4 1 - - - - - DNMT3A 7 1 - - Yes - - - PKHD1L1 7 9 - - - - - - DNAH3 6 5 - - - - - - MYH7B 6 1 - - - - - - PKD1L2 6 6 - - - - - - POLN 6 2 - Yes - - - - POLQ 6 7 - Yes - - - - RP1L1 6 6 - - - - - - TTN 6 5 4 - - - - - WDR87 6 7 - - - - - - ABCA13 5 3 1 - - - - - ASXL1 5 1 - - Yes - - - BBS10 5 0 - - - - - - BRCA2 5 6 1 Yes Yes Yes Yes - CENPJ 5 1 - - - - - - CEP290 5 5 - - - - - - CYP3A5 5 2 - - - - - - DNAH12 5 6 - - - - - - DNAH6 5 1 1 - - - - - EPPK1 5 4 - - - - - - ESYT3 5 1 - - - - - - FRAS1 5 4 - - - - - - HGC6.3 5 0 - - - - - - IGFN1 5 5 - - - - - - KCP 5 4 - - - - - - LRRC43 5 0 - - - - - - MCTP2 5 1 - - - - - - MPO 5 1 - - - - - - MUC4 5 5 - - - - - - OBSCN 5 8 2 - - - - - PALB2 5 0 - Yes - Yes Yes - SLCO1B3 5 2 - - - - - - SYT15 5 3 - - - - - - XIRP2 5 3 1 - - - - - ZNF266 5 2 - - - - - - ZNF530 5 1 - - - - - - ACACB 4 1 1 - - - - - ALS2CL 4 2 - - - - - - AMER3 4 0 2 - - - - - ANKRD35 4 4 - - - - - - ATP10B 4 1 - - - - - - ATP8B3 4 6 - - - - - - C10orf95 4 0 - - - - - - C2orf88 4 0 - - - - - - C5orf42 4 2 - - - - -
Differential Proteomic Analysis of the Pancreas of Diabetic Db/Db Mice Reveals the Proteins Involved in the Development of Complications of Diabetes Mellitus
Int. J. Mol. Sci. 2014, 15, 9579-9593; doi:10.3390/ijms15069579 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 www.mdpi.com/journal/ijms Article Differential Proteomic Analysis of the Pancreas of Diabetic db/db Mice Reveals the Proteins Involved in the Development of Complications of Diabetes Mellitus Victoriano Pérez-Vázquez 1,*, Juan M. Guzmán-Flores 1, Daniela Mares-Álvarez 1, Magdalena Hernández-Ortiz 2, Maciste H. Macías-Cervantes 1, Joel Ramírez-Emiliano 1 and Sergio Encarnación-Guevara 2 1 Depto. de Ciencias Médicas, División de Ciencias de la Salud, Campus León, Universidad de Guanajuato, León, Guanajuato 37320, Mexico; E-Mails: [email protected] (J.M.G.-F.); [email protected] (D.M.-A.); [email protected] (M.H.M.-C.); [email protected] (J.R.-E.) 2 Centro de Ciencias Genómicas, Universidad Nacional Autónoma de México, Cuernavaca, Morelos 62210, Mexico; E-Mails: [email protected] (M.H.-O.); [email protected] (S.E.-G.) * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +52-477-7143-812; Fax: +52-477-7167-623. Received: 4 April 2014; in revised form: 14 May 2014 / Accepted: 19 May 2014 / Published: 30 May 2014 Abstract: Type 2 diabetes mellitus is characterized by hyperglycemia and insulin-resistance. Diabetes results from pancreatic inability to secrete the insulin needed to overcome this resistance. We analyzed the protein profile from the pancreas of ten-week old diabetic db/db and wild type mice through proteomics. Pancreatic proteins were separated in two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and significant changes in db/db mice respect to wild type mice were observed in 27 proteins. -
Investigation of Candidate Genes and Mechanisms Underlying Obesity
Prashanth et al. BMC Endocrine Disorders (2021) 21:80 https://doi.org/10.1186/s12902-021-00718-5 RESEARCH ARTICLE Open Access Investigation of candidate genes and mechanisms underlying obesity associated type 2 diabetes mellitus using bioinformatics analysis and screening of small drug molecules G. Prashanth1 , Basavaraj Vastrad2 , Anandkumar Tengli3 , Chanabasayya Vastrad4* and Iranna Kotturshetti5 Abstract Background: Obesity associated type 2 diabetes mellitus is a metabolic disorder ; however, the etiology of obesity associated type 2 diabetes mellitus remains largely unknown. There is an urgent need to further broaden the understanding of the molecular mechanism associated in obesity associated type 2 diabetes mellitus. Methods: To screen the differentially expressed genes (DEGs) that might play essential roles in obesity associated type 2 diabetes mellitus, the publicly available expression profiling by high throughput sequencing data (GSE143319) was downloaded and screened for DEGs. Then, Gene Ontology (GO) and REACTOME pathway enrichment analysis were performed. The protein - protein interaction network, miRNA - target genes regulatory network and TF-target gene regulatory network were constructed and analyzed for identification of hub and target genes. The hub genes were validated by receiver operating characteristic (ROC) curve analysis and RT- PCR analysis. Finally, a molecular docking study was performed on over expressed proteins to predict the target small drug molecules. Results: A total of 820 DEGs were identified between