DOCSLIB.ORG

CACNA1I (NM 021096) Human Tagged ORF Clone Product Data

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
CACNA1I (NM 021096) Human Tagged ORF Clone Product Data OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for RC219179 CACNA1I (NM_021096) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: CACNA1I (NM_021096) Human Tagged ORF Clone Tag: Myc-DDK Symbol: CACNA1I Synonyms: ca(v)3.3; Cav3.3 Vector: pCMV6-Entry (PS100001) E. coli Selection: Kanamycin (25 ug/mL) Cell Selection: Neomycin ORF Nucleotide >RC219179 representing NM_021096 Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGGCTGAGAGCGCCTCCCCGCCCTCCTCATCTGCAGCAGCCCCAGCCGCTGAGCCAGGAGTCACCACGG AGCAGCCCGGACCCCGGAGCCCCCCATCCTCCCCGCCAGGCCTGGAGGAGCCTCTGGATGGAGCTGATCC TCATGTCCCACACCCAGACCTGGCGCCTATTGCCTTCTTCTGCCTGCGACAGACCACCAGCCCCCGGAAC TGGTGCATCAAGATGGTGTGCAACCCGTGGTTTGAATGTGTCAGCATGCTGGTGATCCTGCTGAACTGCG TGACACTTGGCATGTACCAGCCGTGCGACGACATGGACTGCCTGTCCGACCGCTGCAAGATCCTGCAGGT CTTTGATGACTTCATCTTTATCTTCTTTGCCATGGAGATGGTGCTCAAGATGGTGGCCCTGGGGATTTTT GGCAAGAAGTGCTACCTCGGGGACACATGGAACCGCCTGGATTTCTTCATCGTCATGGCAGGGATGGTCG AGTACTCCCTGGACCTTCAGAACATCAACCTGTCAGCCATCCGCACCGTGCGCGTCCTGAGGCCCCTCAA AGCCATCAACCGCGTGCCCAGTATGCGGATCCTGGTGAACCTGCTCCTGGACACACTGCCCATGCTGGGG AATGTCCTGCTGCTCTGCTTCTTTGTCTTCTTCATCTTTGGCATCATAGGTGTGCAGCTCTGGGCGGGCC TGCTGCGTAACCGCTGCTTCCTGGAGGAGAACTTCACCATACAAGGGGATGTGGCCTTGCCCCCATACTA CCAGCCGGAGGAGGATGATGAGATGCCCTTCATCTGCTCCCTGTCGGGCGACAATGGGATAATGGGCTGC CATGAGATCCCCCCGCTCAAGGAGCAGGGCCGTGAGTGCTGCCTGTCCAAGGACGACGTCTACGACTTTG GGGCGGGGCGCCAGGACCTCAATGCCAGCGGCCTCTGTGTCAACTGGAACCGTTACTACAATGTGTGCCG CACGGGCAGCGCCAACCCCCACAAGGGTGCCATCAACTTTGACAACATCGGTTATGCTTGGATTGTCATC TTCCAGGTGATCACTCTGGAAGGCTGGGTGGAGATCATGTACTACGTGATGGATGCTCACTCCTTCTACA ACTTCATCTACTTCATCCTGCTTATCATAGTGGGCTCCTTCTTCATGATCAACCTGTGCCTCGTTGTCAT AGCGACCCAGTTCTCGGAGACCAAGCAACGGGAGCACCGGCTGATGCTGGAGCAGCGGCAGCGCTACCTG TCCTCCAGCACGGTGGCCAGCTACGCCGAGCCTGGCGACTGCTACGAGGAGATCTTCCAGTATGTCTGCC ACATCCTGCGCAAGGCCAAGCGCCGCGCCCTGGGCCTCTACCAGGCCCTGCAGAGCCGGCGCCAGGCCCT GGGCCCGGAGGCCCCGGCCCCCGCCAAACCTGGGCCCCACGCCAAGGAGCCCCGGCACTACCATGGGAAG ACTAAGGGTCAGGGAGATGAAGGGAGACATCTCGGAAGCCGGCATTGCCAGACTTTGCATGGGCCTGCCT This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 7 CACNA1I (NM_021096) Human Tagged ORF Clone – RC219179 CCCCTGGAAATGATCACTCGGGAAGAGAGCTGTGCCCGCAACATAGCCCCCTGGATGCGACGCCCCACAC CCTGGTGCAGCCCATCCCCGCCACGCTGGCTTCCGATCCCGCCAGCTGCCCTTGCTGCCAGCATGAGGAC GGCCGGCGGCCCTCGGGCCTGGGCAGCACCGACTCGGGCCAGGAGGGCTCGGGCTCCGGGAGCTCCGCTG GTGGCGAGGACGAGGCGGATGGGGACGGGGCCCGGAGCAGCGAGGACGGAGCCTCCTCAGAACTGGGGAA GGAGGAGGAGGAGGAGGAGCAGGCGGATGGGGCGGTCTGGCTGTGCGGGGATGTGTGGCGGGAGACGCGA GCCAAGCTGCGCGGCATCGTGGACAGCAAGTACTTCAACCGGGGCATCATGATGGCCATCCTGGTCAACA CCGTCAGCATGGGCATCGAGCACCACGAGCAGCCGGAGGAGCTGACCAACATCCTGGAGATCTGCAATGT GGTCTTCACCAGCATGTTTGCCCTGGAGATGATCCTGAAGCTGGCTGCATTTGGGCTCTTCGACTACCTG CGTAACCCCTACAACATCTTCGACAGCATCATTGTCATCATCAGCATCTGGGAGATTGTGGGGCAGGCGG ACGGTGGGCTGTCGGTGCTGCGGACCTTCCGGCTGCTGCGCGTGCTGAAACTGGTGCGCTTCATGCCTGC CCTGCGGCGCCAGCTCGTGGTGCTCATGAAGACCATGGACAACGTGGCCACCTTCTGCATGCTGCTCATG CTCTTCATCTTCATCTTCAGCATCCTTGGGATGCATATTTTTGGCTGCAAGTTCAGCCTCCGCACGGACA CTGGAGACACGGTGCCCGACAGGAAGAACTTCGACTCCCTGCTGTGGGCCATCGTCACTGTGTTCCAGAT CCTCACCCAGGAGGACTGGAACGTCGTTCTCTACAATGGCATGGCCTCCACTTCTCCCTGGGCCTCCCTC TACTTTGTCGCCCTCATGACCTTCGGCAACTATGTGCTCTTCAACCTGCTGGTGGCCATCCTGGTGGAGG GCTTCCAGGCGGAGGGTGACGCCAATCGCTCCTACTCGGACGAGGACCAGAGCTCATCCAACATAGAAGA GTTTGATAAGCTCCAGGAAGGCCTGGACAGCAGCGGAGATCCCAAGCTCTGCCCAATCCCCATGACCCCC AATGGGCACCTGGACCCCAGTCTCCCACTGGGTGGGCACCTAGGTCCTGCTGGGGCTGCGGGACCTGCCC CCCGACTCTCACTGCAGCCGGACCCCATGCTGGTGGCCCTGGGCTCCCGAAAGAGCAGTGTCATGTCTCT AGGGAGGATGAGCTATGACCAGCGCTCCCTGTCCAGCTCCCGGAGCTCCTACTACGGGCCATGGGGCCGC AGCGCGGCCTGGGCCAGCCGTCGCTCCAGCTGGAACAGCCTCAAGCACAAGCCGCCGTCGGCGGAGCATG AGTCCCTGCTCTCTGCGGAGCGCGGCGGCGGCGCCCGGGTCTGCGAGGTTGCCGCGGACGAGGGGCCGCC GCGGGCCGCACCCCTGCACACCCCACACGCCCACCACATTCATCACGGGCCCCATCTGGCGCACCGCCAC CGCCACCACCGCCGGACGCTGTCCCTCGACAACAGGGACTCGGTGGACCTGGCCGAGCTGGTGCCCGCGG TGGGCGCCCACCCCCGGGCCGCCTGGAGGGCGGCAGGCCCGGCCCCCGGGCATGAGGACTGCAATGGCAG GATGCCCAGCATCGCCAAAGACGTCTTCACCAAGATGGGCGACCGCGGGGATCGCGGGGAGGATGAGGAG GAAATCGACTACACCCTGTGCTTCCGCGTCCGCAAGATGATCGACGTCTATAAGCCCGACTGGTGCGAGG TCCGCGAAGACTGGTCTGTCTACCTCTTCTCTCCCGAGAACAGGTTCCGGGTCCTGTGTCAGACCATTAT TGCCCACAAACTCTTCGACTACGTCGTCCTGGCCTTCATCTTTCTCAACTGCATCACCATCGCCCTGGAG CGGCCTCAGATCGAGGCCGGCAGCACCGAACGCATCTTTCTCACCGTGTCCAACTACATCTTCACGGCCA TCTTCGTGGGCGAGATGACATTGAAGGTAGTCTCGCTGGGCCTGTACTTCGGCGAGCAGGCGTACCTACG CAGCAGCTGGAACGTGCTGGATGGCTTTCTTGTCTTCGTGTCCATCATCGACATCGTGGTGTCCCTGGCC TCAGCCGGGGGAGCCAAGATCTTGGGGGTCCTCCGAGTCTTGCGGCTCCTGCGCACCCTACGCCCCCTGC GTGTCATCAGCCGGGCGCCGGGCCTGAAGCTGGTGGTGGAGACACTCATCTCCTCCCTCAAGCCCATCGG CAACATCGTGCTCATCTGCTGTGCCTTCTTCATCATCTTTGGCATCCTGGGAGTGCAGCTCTTCAAGGGC AAGTTCTACCACTGTCTGGGCGTGGACACCCGCAACATCACCAACCGCTCGGACTGCATGGCCGCCAACT ACCGCTGGGTCCATCACAAATACAACTTCGACAACCTGGGCCAGGCTCTGATGTCCCTCTTTGTCCTGGC ATCCAAGGATGGTTGGGTGAACATCATGTACAATGGACTGGATGCTGTTGCTGTGGACCAGCAGCCTGTG ACCAACCACAACCCCTGGATGCTGCTGTACTTCATCTCCTTCCTGCTCATCGTCAGCTTCTTTGTGCTCA ACATGTTTGTGGGTGTCGTGGTGGAGAACTTCCACAAGTGCCGGCAGCACCAGGAGGCTGAAGAGGCACG GCGGCGTGAGGAGAAGCGGCTGCGGCGCCTGGAGAAGAAGCGCCGGAAGGCCCAGCGGCTGCCCTACTAT GCCACCTATTGTCACACCCGGCTGCTCATCCACTCCATGTGCACCAGCCACTACCTGGACATCTTCATCA CCTTCATCATCTGCCTCAACGTGGTCACCATGTCCCTGGAGCACTACAATCAGCCCACGTCCCTGGAGAC AGCCCTCAAGTACTGCAACTATATGTTCACCACTGTCTTTGTGCTGGAGGCTGTGCTGAAGCTGGTGGCA TTTGGTCTGAGGCGCTTCTTCAAGGACCGATGGAACCAGCTGGACCTGGCCATTGTGCTACTGTCAGTCA TGGGCATCACCCTGGAGGAGATCGAGATCAATGCGGCCCTGCCCATCAATCCCACCATCATCCGCATCAT GAGGGTTCTGCGCATTGCCCGAGTGCTGAAGCTGTTGAAGATGGCCACAGGAATGCGGGCCCTGCTGGAC ACGGTGGTGCAAGCTTTGCCCCAGGTGGGCAACCTGGGCCTCCTCTTCATGCTGCTCTTCTTCATCTATG CTGCTCTCGGGGTGGAGCTCTTTGGGAAGCTGGTCTGCAACGACGAGAACCCGTGCGAGGGCATGAGCCG GCATGCCACCTTCGAGAACTTCGGCATGGCCTTCCTCACACTCTTCCAGGTCTCCACGGGTGACAACTGG AACGGGATCATGAAGGACACGCTGCGGGACTGCACCCACGACGAGCGCAGCTGCCTGAGCAGCCTGCAGT TTGTGTCGCCGCTGTACTTCGTGAGCTTCGTGCTCACCGCGCAGTTCGTGCTCATCAACGTGGTGGTGGC This product is to be used for laboratory only. Not for diagnostic or therapeutic use. ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 2 / 7 CACNA1I (NM_021096) Human Tagged ORF Clone – RC219179 TGTGCTCATGAAGCACCTGGACGACAGCAACAAGGAGGCGCAGGAGGACGCCGAGATGGATGCCGAGCTC GAGCTGGAGATGGCCCATGGCCTGGGCCCTGGCCCGAGGCTGCCTACCGGCTCCCCGGGCGCCCCTGGCC GAGGGCCGGGAGGGGCGGGCGGCGGGGGCGACACCGAGGGCGGCTTGTGCCGGCGCTGCTACTCGCCTGC CCAGGAGAACCTGTGGCTGGACAGCGTCTCTTTAATCATCAAGGACTCCTTGGAGGGGGAGCTGACCATC ATCGACAACCTGTCGGGCTCCATCTTCCACCACTACTCCTCGCCTGCCGGCTGCAAGAAGTGTCACCACG ACAAGCAAGAGGTGCAGCTGGCTGAGACGGAGGCCTTCTCCCTGAACTCAGACAGGTCCTCGTCCATCCT GCTGGGTGACGACCTGAGTCTCGAGGACCCCACAGCCTGCCCACCTGGCCGCAAAGACAGCAAGGGTGAG CTGGACCCACCTGAGCCCATGCGTGTGGGAGACCTGGGCGAATGCTTCTTCCCCTTGTCCTCTACGGCCG TCTCGCCGGATCCAGAGAACTTCCTGTGTGAGATGGAGGAGATCCCATTCAACCCTGTCCGGTCCTGGCT GAAACATGACAGCAGTCAAGCACCCCCAAGTCCCTTCTCCCCGGATGCCTCCAGCCCTCTCCTGCCCATG CCAGCCGAGTTCTTCCACCCTGCAGTGTCTGCCAGCCAGAAAGGCCCAGAAAAGGGCACTGGCACTGGAA CCCTCCCCAAGATTGCGCTGCAGGGCTCCTGGGCATCTCTGCGGTCACCAAGGGTCAACTGTACCCTCCT CCGGCAGGCCACCGGGAGCGACACGTCGCTGGACGCCAGCCCCAGCAGCTCCGCGGGCAGCCTGCAGACC ACGCTCGAGGACAGCCTGACCCTGAGCGACAGCCCCCGGCGTGCCCTGGGGCCGCCCGCGCCTGCTCCAG GACCCCGGGCCGGCCTGTCCCCCGCCGCTCGCCGCCGCCTGAGCCTGCGCGGCCGGGGCCTCTTCAGCCT GCGGGGGCTGCGGGCGCATCAGCGCAGCCACAGCAGCGGGGGCTCCACCAGCCCGGGCTGCACCCACCAC GACTCCATGGACCCCTCGGACGAGGAGGGCCGCGGTGGCGCGGGCGGCGGGGGCGCGGGCAGCGAGCACT CGGAGACCCTCAGCAGCCTCTCGCTCACCTCCCTCTTCTGCCCGCCGCCCCCGCCGCCAGCCCCCGGCCT CACGCCCGCCAGGAAGTTCAGCAGCACCAGCAGCCTGGCCGCCCCCGGCCGCCCCCACGCCGCCGCCCTG GCCCACGGCCTGGCCCGGAGCCCCTCGTGGGCCGCGGACCGCAGCAAGGACCCCCCCGGCCGGGCACCGC TGCCCATGGGCCTGGGCCCCTTGGCGCCCCCGCCGCAACCGCTCCCCGGAGAGCTGGAGCCGGGAGACGC CGCCAGCAAGAGGAAGAGA ACGCGTACGCGGCCGCTCGAGCAGAAACTCATCTCAGAAGAGGATCTGGCAGCAAATGATATCCTGGATT ACAAGGATGACGACGATAAGGTTTAA This product is to be used for laboratory only. Not for diagnostic or therapeutic use. ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 3 / 7 CACNA1I (NM_021096) Human Tagged ORF Clone – RC219179 Protein Sequence: >RC219179 representing NM_021096 Red=Cloning site Green=Tags(s) MAESASPPSSSAAAPAAEPGVTTEQPGPRSPPSSPPGLEEPLDGADPHVPHPDLAPIAFFCLRQTTSPRN WCIKMVCNPWFECVSMLVILLNCVTLGMYQPCDDMDCLSDRCKILQVFDDFIFIFFAMEMVLKMVALGIF GKKCYLGDTWNRLDFFIVMAGMVEYSLDLQNINLSAIRTVRVLRPLKAINRVPSMRILVNLLLDTLPMLG NVLLLCFFVFFIFGIIGVQLWAGLLRNRCFLEENFTIQGDVALPPYYQPEEDDEMPFICSLSGDNGIMGC HEIPPLKEQGRECCLSKDDVYDFGAGRQDLNASGLCVNWNRYYNVCRTGSANPHKGAINFDNIGYAWIVI FQVITLEGWVEIMYYVMDAHSFYNFIYFILLIIVGSFFMINLCLVVIATQFSETKQREHRLMLEQRQRYL SSSTVASYAEPGDCYEEIFQYVCHILRKAKRRALGLYQALQSRRQALGPEAPAPAKPGPHAKEPRHYHGK TKGQGDEGRHLGSRHCQTLHGPASPGNDHSGRELCPQHSPLDATPHTLVQPIPATLASDPASCPCCQHED GRRPSGLGSTDSGQEGSGSGSSAGGEDEADGDGARSSEDGASSELGKEEEEEEQADGAVWLCGDVWRETR AKLRGIVDSKYFNRGIMMAILVNTVSMGIEHHEQPEELTNILEICNVVFTSMFALEMILKLAAFGLFDYL RNPYNIFDSIIVIISIWEIVGQADGGLSVLRTFRLLRVLKLVRFMPALRRQLVVLMKTMDNVATFCMLLM LFIFIFSILGMHIFGCKFSLRTDTGDTVPDRKNFDSLLWAIVTVFQILTQEDWNVVLYNGMASTSPWASL YFVALMTFGNYVLFNLLVAILVEGFQAEGDANRSYSDEDQSSSNIEEFDKLQEGLDSSGDPKLCPIPMTP NGHLDPSLPLGGHLGPAGAAGPAPRLSLQPDPMLVALGSRKSSVMSLGRMSYDQRSLSSSRSSYYGPWGR SAAWASRRSSWNSLKHKPPSAEHESLLSAERGGGARVCEVAADEGPPRAAPLHTPHAHHIHHGPHLAHRH RHHRRTLSLDNRDSVDLAELVPAVGAHPRAAWRAAGPAPGHEDCNGRMPSIAKDVFTKMGDRGDRGEDEE EIDYTLCFRVRKMIDVYKPDWCEVREDWSVYLFSPENRFRVLCQTIIAHKLFDYVVLAFIFLNCITIALE RPQIEAGSTERIFLTVSNYIFTAIFVGEMTLKVVSLGLYFGEQAYLRSSWNVLDGFLVFVSIIDIVVSLA
Load more

Recommended publications
  • Genetic Associations Between Voltage-Gated Calcium Channels (Vgccs) and Autism Spectrum Disorder (ASD)
    Liao and Li Molecular Brain (2020) 13:96 https://doi.org/10.1186/s13041-020-00634-0 REVIEW Open Access Genetic associations between voltage- gated calcium channels and autism spectrum disorder: a systematic review Xiaoli Liao1,2 and Yamin Li2* Abstract Objectives: The present review systematically summarized existing publications regarding the genetic associations between voltage-gated calcium channels (VGCCs) and autism spectrum disorder (ASD). Methods: A comprehensive literature search was conducted to gather pertinent studies in three online databases. Two authors independently screened the included records based on the selection criteria. Discrepancies in each step were settled through discussions. Results: From 1163 resulting searched articles, 28 were identified for inclusion. The most prominent among the VGCCs variants found in ASD were those falling within loci encoding the α subunits, CACNA1A, CACNA1B, CACN A1C, CACNA1D, CACNA1E, CACNA1F, CACNA1G, CACNA1H, and CACNA1I as well as those of their accessory subunits CACNB2, CACNA2D3, and CACNA2D4. Two signaling pathways, the IP3-Ca2+ pathway and the MAPK pathway, were identified as scaffolds that united genetic lesions into a consensus etiology of ASD. Conclusions: Evidence generated from this review supports the role of VGCC genetic variants in the pathogenesis of ASD, making it a promising therapeutic target. Future research should focus on the specific mechanism that connects VGCC genetic variants to the complex ASD phenotype. Keywords: Autism spectrum disorder, Voltage-gated calcium
    [Show full text]
  • The Mineralocorticoid Receptor Leads to Increased Expression of EGFR
    www.nature.com/scientificreports OPEN The mineralocorticoid receptor leads to increased expression of EGFR and T‑type calcium channels that support HL‑1 cell hypertrophy Katharina Stroedecke1,2, Sandra Meinel1,2, Fritz Markwardt1, Udo Kloeckner1, Nicole Straetz1, Katja Quarch1, Barbara Schreier1, Michael Kopf1, Michael Gekle1 & Claudia Grossmann1* The EGF receptor (EGFR) has been extensively studied in tumor biology and recently a role in cardiovascular pathophysiology was suggested. The mineralocorticoid receptor (MR) is an important efector of the renin–angiotensin–aldosterone‑system and elicits pathophysiological efects in the cardiovascular system; however, the underlying molecular mechanisms are unclear. Our aim was to investigate the importance of EGFR for MR‑mediated cardiovascular pathophysiology because MR is known to induce EGFR expression. We identifed a SNP within the EGFR promoter that modulates MR‑induced EGFR expression. In RNA‑sequencing and qPCR experiments in heart tissue of EGFR KO and WT mice, changes in EGFR abundance led to diferential expression of cardiac ion channels, especially of the T‑type calcium channel CACNA1H. Accordingly, CACNA1H expression was increased in WT mice after in vivo MR activation by aldosterone but not in respective EGFR KO mice. Aldosterone‑ and EGF‑responsiveness of CACNA1H expression was confrmed in HL‑1 cells by Western blot and by measuring peak current density of T‑type calcium channels. Aldosterone‑induced CACNA1H protein expression could be abrogated by the EGFR inhibitor AG1478. Furthermore, inhibition of T‑type calcium channels with mibefradil or ML218 reduced diameter, volume and BNP levels in HL‑1 cells. In conclusion the MR regulates EGFR and CACNA1H expression, which has an efect on HL‑1 cell diameter, and the extent of this regulation seems to depend on the SNP‑216 (G/T) genotype.
    [Show full text]
  • 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.
    [Show full text]
  • SUPPLEMENTARY APPENDIX Inflammation Regulates Long Non-Coding RNA-PTTG1-1:1 in Myeloid Leukemia
    SUPPLEMENTARY APPENDIX Inflammation regulates long non-coding RNA-PTTG1-1:1 in myeloid leukemia Sébastien Chateauvieux, 1,2 Anthoula Gaigneaux, 1° Déborah Gérard, 1 Marion Orsini, 1 Franck Morceau, 1 Barbora Orlikova-Boyer, 1,2 Thomas Farge, 3,4 Christian Récher, 3,4,5 Jean-Emmanuel Sarry, 3,4 Mario Dicato 1 and Marc Diederich 2 °Current address: University of Luxembourg, Faculty of Science, Technology and Communication, Life Science Research Unit, Belvaux, Luxemburg. 1Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Hôpital Kirchberg, Luxembourg, Luxembourg; 2College of Pharmacy, Seoul National University, Gwanak-gu, Seoul, Korea; 3Cancer Research Center of Toulouse, UMR 1037 INSERM/ Université Toulouse III-Paul Sabatier, Toulouse, France; 4Université Toulouse III Paul Sabatier, Toulouse, France and 5Service d’Hématologie, Centre Hospitalier Universitaire de Toulouse, Institut Universitaire du Cancer de Toulouse Oncopôle, Toulouse, France Correspondence: MARC DIEDERICH - [email protected] doi:10.3324/haematol.2019.217281 Supplementary data Inflammation regulates long non-coding RNA-PTTG1-1:1 in myeloid leukemia Sébastien Chateauvieux1,2, Anthoula Gaigneaux1*, Déborah Gérard1, Marion Orsini1, Franck Morceau1, Barbora Orlikova-Boyer1,2, Thomas Farge3,4, Christian Récher3,4,5, Jean-Emmanuel Sarry3,4, Mario Dicato1 and Marc Diederich2 1 Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Hôpital Kirchberg, 9, rue Edward Steichen, 2540 Luxembourg, Luxemburg; 2 College of Pharmacy, Seoul National University, 1 Gwanak-ro,
    [Show full text]
  • Identification of 42 Genes Linked to Stage II Colorectal Cancer Metastatic Relapse
    Int. J. Mol. Sci. 2016, 17, 598; doi:10.3390/ijms17040598 S1 of S16 Supplementary Materials: Identification of 42 Genes Linked to Stage II Colorectal Cancer Metastatic Relapse Rabeah A. Al-Temaimi, Tuan Zea Tan, Makia J. Marafie, Jean Paul Thiery, Philip Quirke and Fahd Al-Mulla Figure S1. Cont. Int. J. Mol. Sci. 2016, 17, 598; doi:10.3390/ijms17040598 S2 of S16 Figure S1. Mean expression levels of fourteen genes of significant association with CRC DFS and OS that are differentially expressed in normal colon compared to CRC tissues. Each dot represents a sample. Table S1. Copy number aberrations associated with poor disease-free survival and metastasis in early stage II CRC as predicted by STAC and SPPS combined methodologies with resident gene symbols. CN stands for copy number, whereas CNV is copy number variation. Region Cytoband % of CNV Count of Region Event Gene Symbols Length Location Overlap Genes chr1:113,025,076–113,199,133 174,057 p13.2 CN Loss 0.0 2 AKR7A2P1, SLC16A1 chr1:141,465,960–141,822,265 356,305 q12–q21.1 CN Gain 95.9 1 SRGAP2B MIR5087, LOC10013000 0, FLJ39739, LOC10028679 3, PPIAL4G, PPIAL4A, NBPF14, chr1:144,911,564–146,242,907 1,331,343 q21.1 CN Gain 99.6 16 NBPF15, NBPF16, PPIAL4E, NBPF16, PPIAL4D, PPIAL4F, LOC645166, LOC388692, FCGR1C chr1:177,209,428–177,226,812 17,384 q25.3 CN Gain 0.0 0 chr1:197,652,888–197,676,831 23,943 q32.1 CN Gain 0.0 1 KIF21B chr1:201,015,278–201,033,308 18,030 q32.1 CN Gain 0.0 1 PLEKHA6 chr1:201,289,154–201,298,247 9093 q32.1 CN Gain 0.0 0 chr1:216,820,186–217,043,421 223,235 q41 CN
    [Show full text]
  • 1 1 2 3 Cell Type-Specific Transcriptomics of Hypothalamic
    1 2 3 4 Cell type-specific transcriptomics of hypothalamic energy-sensing neuron responses to 5 weight-loss 6 7 Fredrick E. Henry1,†, Ken Sugino1,†, Adam Tozer2, Tiago Branco2, Scott M. Sternson1,* 8 9 1Janelia Research Campus, Howard Hughes Medical Institute, 19700 Helix Drive, Ashburn, VA 10 20147, USA. 11 2Division of Neurobiology, Medical Research Council Laboratory of Molecular Biology, 12 Cambridge CB2 0QH, UK 13 14 †Co-first author 15 *Correspondence to: [email protected] 16 Phone: 571-209-4103 17 18 Authors have no competing interests 19 1 20 Abstract 21 Molecular and cellular processes in neurons are critical for sensing and responding to energy 22 deficit states, such as during weight-loss. AGRP neurons are a key hypothalamic population 23 that is activated during energy deficit and increases appetite and weight-gain. Cell type-specific 24 transcriptomics can be used to identify pathways that counteract weight-loss, and here we 25 report high-quality gene expression profiles of AGRP neurons from well-fed and food-deprived 26 young adult mice. For comparison, we also analyzed POMC neurons, an intermingled 27 population that suppresses appetite and body weight. We find that AGRP neurons are 28 considerably more sensitive to energy deficit than POMC neurons. Furthermore, we identify cell 29 type-specific pathways involving endoplasmic reticulum-stress, circadian signaling, ion 30 channels, neuropeptides, and receptors. Combined with methods to validate and manipulate 31 these pathways, this resource greatly expands molecular insight into neuronal regulation of 32 body weight, and may be useful for devising therapeutic strategies for obesity and eating 33 disorders.
    [Show full text]
  • Downregulation of Carnitine Acyl-Carnitine Translocase by Mirnas
    Page 1 of 288 Diabetes 1 Downregulation of Carnitine acyl-carnitine translocase by miRNAs 132 and 212 amplifies glucose-stimulated insulin secretion Mufaddal S. Soni1, Mary E. Rabaglia1, Sushant Bhatnagar1, Jin Shang2, Olga Ilkayeva3, Randall Mynatt4, Yun-Ping Zhou2, Eric E. Schadt6, Nancy A.Thornberry2, Deborah M. Muoio5, Mark P. Keller1 and Alan D. Attie1 From the 1Department of Biochemistry, University of Wisconsin, Madison, Wisconsin; 2Department of Metabolic Disorders-Diabetes, Merck Research Laboratories, Rahway, New Jersey; 3Sarah W. Stedman Nutrition and Metabolism Center, Duke Institute of Molecular Physiology, 5Departments of Medicine and Pharmacology and Cancer Biology, Durham, North Carolina. 4Pennington Biomedical Research Center, Louisiana State University system, Baton Rouge, Louisiana; 6Institute for Genomics and Multiscale Biology, Mount Sinai School of Medicine, New York, New York. Corresponding author Alan D. Attie, 543A Biochemistry Addition, 433 Babcock Drive, Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin, (608) 262-1372 (Ph), (608) 263-9608 (fax), [email protected]. Running Title: Fatty acyl-carnitines enhance insulin secretion Abstract word count: 163 Main text Word count: 3960 Number of tables: 0 Number of figures: 5 Diabetes Publish Ahead of Print, published online June 26, 2014 Diabetes Page 2 of 288 2 ABSTRACT We previously demonstrated that micro-RNAs 132 and 212 are differentially upregulated in response to obesity in two mouse strains that differ in their susceptibility to obesity-induced diabetes. Here we show the overexpression of micro-RNAs 132 and 212 enhances insulin secretion (IS) in response to glucose and other secretagogues including non-fuel stimuli. We determined that carnitine acyl-carnitine translocase (CACT, Slc25a20) is a direct target of these miRNAs.
    [Show full text]
  • Graded Co-Expression of Ion Channel, Neurofilament, and Synaptic Genes in Fast- Spiking Vestibular Nucleus Neurons
    Research Articles: Cellular/Molecular Graded co-expression of ion channel, neurofilament, and synaptic genes in fast- spiking vestibular nucleus neurons https://doi.org/10.1523/JNEUROSCI.1500-19.2019 Cite as: J. Neurosci 2019; 10.1523/JNEUROSCI.1500-19.2019 Received: 26 June 2019 Revised: 11 October 2019 Accepted: 25 October 2019 This Early Release article has been peer-reviewed and accepted, but has not been through the composition and copyediting processes. The final version may differ slightly in style or formatting and will contain links to any extended data. Alerts: Sign up at www.jneurosci.org/alerts to receive customized email alerts when the fully formatted version of this article is published. Copyright © 2019 the authors 1 Graded co-expression of ion channel, neurofilament, and synaptic genes in fast-spiking 2 vestibular nucleus neurons 3 4 Abbreviated title: A fast-spiking gene module 5 6 Takashi Kodama1, 2, 3, Aryn Gittis, 3, 4, 5, Minyoung Shin2, Keith Kelleher2, 3, Kristine Kolkman3, 4, 7 Lauren McElvain3, 4, Minh Lam1, and Sascha du Lac1, 2, 3 8 9 1 Johns Hopkins University School of Medicine, Baltimore MD, 21205 10 2 Howard Hughes Medical Institute, La Jolla, CA, 92037 11 3 Salk Institute for Biological Studies, La Jolla, CA, 92037 12 4 Neurosciences Graduate Program, University of California San Diego, La Jolla, CA, 92037 13 5 Carnegie Mellon University, Pittsburgh, PA, 15213 14 15 Corresponding Authors: 16 Takashi Kodama ([email protected]) 17 Sascha du Lac ([email protected]) 18 Department of Otolaryngology-Head and Neck Surgery 19 The Johns Hopkins University School of Medicine 20 Ross Research Building 420, 720 Rutland Avenue, Baltimore, Maryland, 21205 21 22 23 Conflict of Interest 24 The authors declare no competing financial interests.
    [Show full text]
  • Comprehensive Analysis Reveals Novel Gene Signature in Head and Neck Squamous Cell Carcinoma: Predicting Is Associated with Poor Prognosis in Patients
    5892 Original Article Comprehensive analysis reveals novel gene signature in head and neck squamous cell carcinoma: predicting is associated with poor prognosis in patients Yixin Sun1,2#, Quan Zhang1,2#, Lanlin Yao2#, Shuai Wang3, Zhiming Zhang1,2 1Department of Breast Surgery, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China; 2School of Medicine, Xiamen University, Xiamen, China; 3State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China Contributions: (I) Conception and design: Y Sun, Q Zhang; (II) Administrative support: Z Zhang; (III) Provision of study materials or patients: Y Sun, Q Zhang; (IV) Collection and assembly of data: Y Sun, L Yao; (V) Data analysis and interpretation: Y Sun, S Wang; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. #These authors contributed equally to this work. Correspondence to: Zhiming Zhang. Department of Surgery, The First Affiliated Hospital of Xiamen University, Xiamen, China. Email: [email protected]. Background: Head and neck squamous cell carcinoma (HNSC) remains an important public health problem, with classic risk factors being smoking and excessive alcohol consumption and usually has a poor prognosis. Therefore, it is important to explore the underlying mechanisms of tumorigenesis and screen the genes and pathways identified from such studies and their role in pathogenesis. The purpose of this study was to identify genes or signal pathways associated with the development of HNSC. Methods: In this study, we downloaded gene expression profiles of GSE53819 from the Gene Expression Omnibus (GEO) database, including 18 HNSC tissues and 18 normal tissues.
    [Show full text]
  • RT² Profiler PCR Array (96-Well Format and 384-Well [4 X 96] Format)
    RT² Profiler PCR Array (96-Well Format and 384-Well [4 x 96] Format) Mouse Neuronal Ion Channels Cat. no. 330231 PAMM-036ZA For pathway expression analysis Format For use with the following real-time cyclers RT² Profiler PCR Array, Applied Biosystems® models 5700, 7000, 7300, 7500, Format A 7700, 7900HT, ViiA™ 7 (96-well block); Bio-Rad® models iCycler®, iQ™5, MyiQ™, MyiQ2; Bio-Rad/MJ Research Chromo4™; Eppendorf® Mastercycler® ep realplex models 2, 2s, 4, 4s; Stratagene® models Mx3005P®, Mx3000P®; Takara TP-800 RT² Profiler PCR Array, Applied Biosystems models 7500 (Fast block), 7900HT (Fast Format C block), StepOnePlus™, ViiA 7 (Fast block) RT² Profiler PCR Array, Bio-Rad CFX96™; Bio-Rad/MJ Research models DNA Format D Engine Opticon®, DNA Engine Opticon 2; Stratagene Mx4000® RT² Profiler PCR Array, Applied Biosystems models 7900HT (384-well block), ViiA 7 Format E (384-well block); Bio-Rad CFX384™ RT² Profiler PCR Array, Roche® LightCycler® 480 (96-well block) Format F RT² Profiler PCR Array, Roche LightCycler 480 (384-well block) Format G RT² Profiler PCR Array, Fluidigm® BioMark™ Format H Sample & Assay Technologies Description The Mouse Neuronal Ion Channels RT² Profiler PCR Array was developed to profile expression of a panel of 84 genes encoding neuroscience-related ion channels and transporters. The genes represented on the array are listed below, grouped according to their functional and structural features. Included are calcium channels, potassium channels, sodium channels, chloride channels, and transporters. Using real-time PCR, you can easily and reliably analyze expression of a focused panel of genes related to the neuronal ion channels and transporters with this array.
    [Show full text]
  • The Stepwise Evolution of the Exome During Acquisition of Docetaxel
    Hansen et al. BMC Genomics (2016) 17:442 DOI 10.1186/s12864-016-2749-4 RESEARCH ARTICLE Open Access The stepwise evolution of the exome during acquisition of docetaxel resistance in breast cancer cells Stine Ninel Hansen1,3†, Natasja Spring Ehlers1,2†, Shida Zhu1,4, Mathilde Borg Houlberg Thomsen1,5, Rikke Linnemann Nielsen1,2, Dongbing Liu1,4, Guangbiao Wang1,4, Yong Hou1,4, Xiuqing Zhang1,4, Xun Xu1,4, Lars Bolund1,6, Huanming Yang1,4, Jun Wang1,4,9,10,11,12, Jose Moreira1,3, Henrik J Ditzel1,7,8, Nils Brünner1,3, Anne-Sofie Schrohl1,3†, Jan Stenvang1,3*† and Ramneek Gupta1,2*† Abstract Background: Resistance to taxane-based therapy in breast cancer patients is a major clinical problem that may be addressed through insight of the genomic alterations leading to taxane resistance in breast cancer cells. In the current study we used whole exome sequencing to discover somatic genomic alterations, evolving across evolutionary stages during the acquisition of docetaxel resistance in breast cancer cell lines. Results: Two human breast cancer in vitro models (MCF-7 and MDA-MB-231) of the step-wise acquisition of docetaxel resistance were developed by exposing cells to 18 gradually increasing concentrations of docetaxel. Whole exome sequencing performed at five successive stages during this process was used to identify single point mutational events, insertions/deletions and copy number alterations associated with the acquisition of docetaxel resistance. Acquired coding variation undergoing positive selection and harboring characteristics likely to be functional were further prioritized using network-based approaches. A number of genomic changes were found to be undergoing evolutionary selection, some of which were likely to be functional.
    [Show full text]
  • An Enigmatic Case of Cardiac Death in an 18-Years Old Girl
    European Review for Medical and Pharmacological Sciences 2021; 25: 4999-5005 An enigmatic case of cardiac death in an 18-years old girl G.A. LANZA1, M. COLL2, S. GRASSI3, V. ARENA4, O. CAMPUZANO5, L. CALÒ6, E. DE RUVO6, R. BRUGADA7, A. OLIVA3 1Department of Cardiovascular Sciences, Fondazione Policlinico A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, Roma, Italy 2Cardiovascular Genetics Centre, University of Girona, Girona, Spain 3Department of Health Surveillance and Bioethics, Fondazione Policlinico A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, Roma, Italy 4Department of Woman and Child Health and Public Health, Fondazione Policlinico A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, Roma, Italy 5Centro Investigación Biomédica en Red Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain 6Division of Cardiology, Policlinico Casilino, ASL Rome B, Roma, Italy 7Department of Medical Science, University of Girona, Girona, Spain Abstract. – We report a case of unusual and of death related to severe abnormalities of the unexplained cardiac death in an 18-years old electrical activation of the heart, eventually re- female patient with congenital neurosensori- sulting in hemodynamic compromise and death. al deafness. The fatal event was characterized by an initial syncopal episode, associated with Clinical Case a wide QRS tachycardia (around 110 bpm) but stable hemodynamic conditions. The patient, An 18-years old girl was referred to the Emer- however, subsequently developed severe hypo- gency Department (ED) of a hospital in Rome, tension and progressive bradyarrhythmias until Italy, after a syncopal episode, occurring while asystole and lack of cardiac response to resus- she was at school. Syncope was preceded by sub- citation maneuvers and ventricular pacing.
    [Show full text]