DOCSLIB.ORG

Supplementary Table 2

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Supplementary Table 2 Down-regulated accession # Development AF006467 Mpt1, membrane-associated phosphatidylinositol transfer protein (mpt1), X59382 Parvalbumin (small transcript M31811 Mag, Myelin-associated glycoprotein X78667 Ryr2, Ryanodine receptor 2, cardiac, (BALB/c) Ryr2 D78265 Pancortin-4, Olfm1 Olfactomedin 1 AI848518 Zfp385, Zinc finger protein 385 accession # Cell cycle/maintenance AF033350 Sept5, Septin 5, CDCREL-1 homolog (Cdcrel-1) AB033922 Ndr3, N-myc downstream regulated 3, Ndr1 related protein Ndr3 AJ010108 Ak1, Adenylate kinase 1, cytosolic adenylate kinase accession # Apoptosis AF011908 Aatk, Apoptosis-associated tyrosine kinase , apoptosis associated tyrosine kinase (AATYK) accession # Signal transduction AB020239 Ak4, Adenylate kinase 4 X58287 Ptprm, Protein tyrosine phosphatase, receptor-type, M , mR-PTPu for protein tyrosine phosphatase U76758 Ank1, Ankyrin 1 D21165 Vsnl1, Visinin-like 1, Neural visinin-like Ca2+-binding protein type 1 (NVP-1) U05245 Tiam1, T-cell lymphoma invasion and metastasis 1 X85124 Pacsin, Pacsin1 Protein kinase C and casein kinase substrate in neurons 1 AB018194 BIT, Ptpns1 Protein tyrosine phosphatase, non-receptor type substrate 1 M21532 PCD-5, Pcp2 Purkinje cell protein 2 (L7) NM_009788 Calbindin-28K D86176 Pip5k1a, Phosphatidylinositol-4-phosphate 5-kinase, type 1 alpha X73985 Calb2, Calbindin 2, calretinin AW125016 Prkar1b, Protein kinase, cAMP dependent regulatory, type I beta X63615 Camk-2, Ca2+/calmodulin dependent protein kinase II beta subunit M94632 Prkcz, protein kinase C, zeta X61448 Cbln1, Cerebellin 1 precursor L28035 Prkcg, protein kinase C, gamma L21671 Eps8, epidermal growth factor receptor pathway substrate 8 L02241 Pkib, Protein kinase inhibitor beta M30641 FGFA, acidic fibroblast growth factor, Fgf1 Fibroblast growth factor 1 D50621 PSD-95/SAP90A, Dlgh4 Discs, large homolog 4 (Drosophila X59398 Flt3, tyrosine kinase receptor of the PDGF, FMS-like tyrosine kinase 3 D31898 Ptprr, protein tyrosine phosphatase, receptor type, R U38501 Gnai1, Guanine nucleotide binding protein, alpha inhibiting 1, G protein alpha i1 subunit AI853638 Rap1ga1, Rap1, GTPase-activating protein 1 AB016602 Gpr37l1 G protein-coupled receptor 37-like 1, G-protein coupled receptor AJ250489 Ramp1, receptor activity modifying protein 1 AF071562 Gsbs-pending, G substrate, substrate of cyclic GMP-dependent protein kinase AB000828 TYRO3, protein tyrosine kinase 3 AF093261 Homer3-pending, Homer, neuronal immediate early gene AF011360 RGS7, regulator of G-protein signaling M21530 Itpr1, Inositol 1,4,5-triphosphate receptor 1 U71202 Rin, RAS-like protein AB023027 mCaMK1-beta2, Pnck Pregnancy upregulated non-ubiquitously expressed CaM kinase AV336781 Scn1a, sodium channel, voltage-gated, type I, alpha polypeptide Y13439 MAPK12, mitogen-activated protein kinase 12, stress activated protein kinase-3 accession # DNA/RNA processing AV345565 Adarb1, Adenosine deaminase, RNA-specific, B1 X92352 Nap1l2, Nucleosome assembly protein 1-like 2 AI839697 H1f2, H1 histone family, member 2 accession # Gene expression L10426 ER81, Ets-related protein 81, Etv1, Ets variant gene 1 AA762325 Nkx6-2, NK6 transcription factor related, locus 2 (Drosophila AJ001972 Id4,, Idb4 Inhibitor of DNA binding 4, DNA binding U53228 Nuclear hormone receptor ROR-alpha isoform 1 1 U47543 Nab2, Ngfi-A binding protein 2 U02098 Pur-alpha, Pura Purine rich element binding protein A accession # Protein processing and expression M28489 Rps6ka1, Ribosomal protein S6 kinase polypeptide 1, rsk AJ001700 Serpini1, Serine (or cysteine) proteinase inhibitor, Neuroserpin L26479 Eef1a2, Eukaryotic translation elongation factor 1 alpha 2, Elongation factor-1 alpha (MS1) accession # Metabolism CAA17432 ALDH8A1, Aldehyde dehyrdogenase 8 family, member A1, Aldehyde dehydrogenase II Z13969 Ckmt1, Creatine kinase, mitochondrial 1, mitochondrial creatine kinase U37091 Carbonic anhydrase IV AA590675 Ndufs4, NADH dehydrogenase (ubiquinone) Fe-S protein 4 AAA35653 CA8, Carbonic anhydrase VIII AI852672 Pfkm, Phosphofructokinase J05154 Lcat, Lecithin cholesterol acyltransferase, cholesterol acyltransferase (LCAT) AI850363 Pygm, muscle glycogen phosphorylase X83202 Hsd11b1, Hydroxysteroid 11-beta dehydrogenase 1 accession # Cytoskeleton/tubules Y19186 Aczonin, short spliced variant (acz gene), Pclo Piccolo D29951 Kif1a, Kinesin heavy chain member 1A M13444 Alpha-tubulin isotype M-alpha-6 M35131 Nfh, neurofilament heavy polypeptide U51204 APC-binding protein EB2 M55424 Nfl, neurofilament light polypeptide M28730 Beta-tubulin gene M-beta-4 M18775 Mapt, Microtubule-associated protein Y15197 Mtap7, Microtubule-associated protein 7, E-MAP-115 protein accession # Channel/transport D38614 Cplx1, Complexin 1, 921-S for presynaptic protein AAL85094 Nsf, N-ethylmaleimide sensitive fusion protein X16645 Atp1b2, ATPase, Na+/K+ transporting, beta 2 polypeptide , AMOG (AA 1-290 NP_065598 Osbpl1a, Oxysterol binding protein-like 1A AV348528 Atp1b1, ATPase, Na+/K+ transporting, beta 1 polypeptide X15373 Itpr1, Inositol 1,4,5-triphosphate receptor 1, P400 protein X75927 Abca2, ATP-binding cassette, sub-family A (ABC1), member 2 AF091390 Fxyd1, FXYD domain-containing ion transport regulator 1, phospholemman M63801 Gja1, Gap junction membrane channel protein alpha 1, Connexin 43 M90365 Plakoglobin AI846739 Cox7a2l, cytochrome c oxidase subunit VIIa polypeptide 2-like U28960 Pltp, Phospholipid transfer protein Z79787 Dtna, Dystrobrevin AF107780 Kcnd2, Potassium voltage-gated channel, Shal-related family, member 2, Potassium channel Kv4.2 X14961 Fabp3, Fatty acid binding protein 3, muscle and heart Y00305 Kcna1, Potassium voltage-gated channel, shaker-related subfamily, member 1 M92378 Gabt1 Gamma-aminobutyric acid (GABA-A) transporter 1 AF029982 Serca2, Atp2a2 ATPase, Ca++ transporting, cardiac muscle, slow twitch 2 X61430 Gabra1, Gamma-aminobutyric acid (GABA-A) receptor, subunit alpha 1 D83262 Slc1a6, solute carrier family 1, member 6 AF256198 Gabra6 ,Gamma-aminobutyric acid (GABA-A) receptor, subunit alpha 6 AW121154 Slc3a1, solute carrier family 3, member 1 D13266 Grid2, Glutamate receptor, ionotropic, delta 2 L42339 Scn1a, sodium channel, voltage-gated, type I, alpha polypeptide, sodium channel 3 X57497 Gria1, Glutamate receptor, ionotropic, AMPA1 (alpha 1) CAB62974 Syn3, Synapsin III AI847120 Grin1, Glutamate receptor, ionotropic, NMDA1 (zeta 1) X95818 Synaptophysin D10694 Grin2c, Glutamate receptor, ionotropic, NMDA2C (epsilon 3) M22012 Snap25, Synaptosomal-associated protein, 25 kDa. U65592 Kcnab2, Potassium voltage-gated channel, shaker-related subfamily, beta member 2, NP_033334 Syt4, Synaptotagmin 4 AAL07248 Kcnma1, Potassium large conductance calcium-activated channel, subfamily M, alpha member 1 M12379 Thy1, Thymus cell antigen 1 2 Y07812 Mal, Myelin and lymphocyte protein. U60150 VAMP-2, vesicle-associated membrane protein vamp-2 U73625 Mtrp1, alpha (Mtrp1), Trrp1, Transient receptor protein 1 AJ001598 Viaat, Vesicular inhibitory amino acid transporter, vesicular GABA and glycine transporter U62021 NPTX1, Neuronal pentraxin 1 ( L48687 Scn1b, Sodium channel, voltage-gated, type I, beta polypeptide accession # Immune response/defense AV363696 Ii, Ia-associated invariant chain AB006361 Ptgds, Prostaglandin D2 synthase (21 kDa, brain) AF175292 IL-16 AF071549 Scyd1, small inducible cytokine subfamily D 1, fractalkine accession # Etc X59520 CCK, cholecystokinin M16472 Plp, Proteolipid protein (myelin), Proteolipid protein variant DM-20 CAA37199 Chromogranin B (secretogranin I) M55181 Penk1, Preproenkephalin 1, spermatogenic-specific proenkephalin AI836349 Jph3, Junctophilin 3 X92864 Spock1, Sparc/osteonectin, cwcv and kazal-like domains proteoglycan 1, testican AI834776 Mobp, Myelin-associated oligodendrocytic basic protein X95518 Nttp1 Neuronal tyrosine/threonine phosphatase 1 accession # Unknown AF037312 SUR-1, Sulfonylurea receptor-1 AI844269 EST, possibly microtubule-associated protein, RP/EB family, member 2 (MAPRE2) X95279 Thrsp, Thyroid hormone responsive SPOT14 homolog (Rattus) AI846678 EST AW048113 Snrk, SNF related kinase AI847069 EST AI838513 Ppfia4, Protein tyrosine phosphatase, receptor type, f polypeptide, interacting protein (liprin), AI847230 EST alpha 4 D26483 Tm4sf2, Transmembrane 4 superfamily member 2, PE31/TALLA AI850079 EST, possibly phosphatidylinositol (4,5) bisphosphate 5-phosphatase, A (PIB5PA) X17320 Pcp4, Purkinje cell protein 4, Pep-19 AI852087 EST, possibly SEC14-like 1 (S. cerevisiae) (SEC14L1) AB031291 Tagln3, Transgelin 3, NP25 AI852838 EST AW124144 Evt2, evectin-2 AI853332 EST, possibly growth differentiation factor 10 (GDF10) XP_127141 GT12 AI853573 ESTs, Highly similar to HUNTINGTIN-ASSOCIATED PROTEIN-INTERACTING PROTEIN AW046460 Fnbp1, Formin binding protein 1 AI854265 EST AI843164 Dnajb10, DnaJ (Hsp40) homolog, subfamily B, member 10 AV091649 EST, possibly microtubule-associated protein, RP/EB family, member 3 AI850356 Dp1, Deleted in polyposis 1 AV305843 EST U93309 Dlgh1, homolog (dlg1 AW048549 EST, possibly glutamate receptor, ionotropic, AMPA 1 (GRIA1) AW047343 Dbp, D site albumin promoter binding protein AW120767 EST X61450 Brp14, Brain protein 14 AW121364 EST AB013097 Zfp179 Zinc finger protein 179, AW122114 EST AAF44934 BG:DS07851.3 Drosophila melanogaster (BG:DS07851.3) AW122372 EST AW125480 Als2, amyotrophic lateral sclerosis 2 (juvenile) homolog (human) AW122563 EST AA163268 EST AW122596 EST AA683785 EST AW122995 EST AA690483 EST AW123564 EST AI118078 EST AW123662 EST, possibly secretory carrier membrane protein 1 (SCAMP1) AI503362 EST AW124185 EST AI595313 EST AW124196 EST 3 AI835760 EST AW124433 EST AI837497 EST, possibly DAB2 interacting protein (DAB2IP) AW125299 EST AI837921 EST, Similar to hydroxyacyl glutathione hydrolase AW125453 EST AI839662 EST AW215585 EST AI839839 EST BB246828 EST AI841606 EST CAC05310 EST AI842002 EST NP_039033 EST, possibly ubiquitin-like 1 (sentrin) (UBL1) AI842668 EST XP_132315 EST, possibly paxillin (PXN), cell adhesion, cell motility, focal adhesion, signal transduction, AI843884 EST XP_149128 EST 4.
Load more

Recommended publications
  • 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]
  • Pharmacogenomics of Drug-Induced Conditions
    Pharmacogenomics of Drug-Induced Conditions Dan M. Roden, M.D. Professor of Medicine and Pharmacology Director, Oates Institute for Experimental Therapeutics Assistant Vice-Chancellor for Personalized Medicine Vanderbilt University School of Medicine !1 An “idiosyncratic” drug response AR, 78 year old male • Coronary artery disease; 13 years s/p bypass surgery • 2 days after starting dofetilide (potent IKr blocker)… No personal or family history of syncope, sudden death • KCNQ1 variant leading to R583C identified • In vitro: ↓IKs • Not found in >400 ethnically-matched controls • ∴this is likely subclinical congenital Long QT Syndrome !2 Another face of the congenital long QT syndrome !3 Father’s ECG !4 Mother’s ECG !5 9-year-old sister’s ECG !6 Family tree Aunt, cousin, niece with 402 426 syncope 462 405 439 428 (RBBB) 436 428 492 411 419 404 • One episode of syncope, age 20 • Multiple ER visits for acute allergic reactions à epinephrine without incident !7 Mother’s ECG post-exercise !8 Identifying a mutation in KCNQ1 mothersister …YI G FLGLI… …YI D FLGLI… G269D !9 Family tree Aunt, cousin, niece with 402 426 syncope 462 405 439 428 (RBBB) 436 428 492 411 419 404 Incomplete penetrance !10 Grandfather’s ECG !11 Defining the “drug-induced long QT syndrome” • Marked QT prolongation and typical pause-dependent torsades de pointes with drug challenge, both resolving with drug withdrawal • Variants: • Marked QT prolongation (e.g. >520 or 550 or 600 msec), recognized and drug withdrawn (no torsades) • pause-dependent polymorphic VT after administration
    [Show full text]
  • Human Periprostatic Adipose Tissue: Secretome from Patients With
    CANCER GENOMICS & PROTEOMICS 16 : 29-58 (2019) doi:10.21873/cgp.20110 Human Periprostatic Adipose Tissue: Secretome from Patients With Prostate Cancer or Benign Prostate Hyperplasia PAULA ALEJANDRA SACCA 1, OSVALDO NÉSTOR MAZZA 2, CARLOS SCORTICATI 2, GONZALO VITAGLIANO 3, GABRIEL CASAS 4 and JUAN CARLOS CALVO 1,5 1Institute of Biology and Experimental Medicine (IBYME), CONICET, Buenos Aires, Argentina; 2Department of Urology, School of Medicine, University of Buenos Aires, Clínical Hospital “José de San Martín”, Buenos Aires, Argentina; 3Department of Urology, Deutsches Hospital, Buenos Aires, Argentina; 4Department of Pathology, Deutsches Hospital, Buenos Aires, Argentina; 5Department of Biological Chemistry, School of Exact and Natural Sciences, University of Buenos Aires, Buenos Aires, Argentina Abstract. Background/Aim: Periprostatic adipose tissue Prostate cancer (PCa) is the second most common cancer in (PPAT) directs tumour behaviour. Microenvironment secretome men worldwide. While most men have indolent disease, provides information related to its biology. This study was which can be treated properly, the problem consists in performed to identify secreted proteins by PPAT, from both reliably distinguishing between indolent and aggressive prostate cancer and benign prostate hyperplasia (BPH) disease. Evidence shows that the microenvironment affects patients. Patients and Methods: Liquid chromatography-mass tumour behavior. spectrometry-based proteomic analysis was performed in Adipose tissue microenvironment is now known to direct PPAT-conditioned media (CM) from patients with prostate tumour growth, invasion and metastases (1, 2). Adipose cancer (CMs-T) (stage T3: CM-T3, stage T2: CM-T2) or tissue is adjacent to the prostate gland and the site of benign disease (CM-BPH). Results: The highest number and invasion of PCa.
    [Show full text]
  • Heterotrimeric Go Protein Links Wnt-Frizzled Signaling with Ankyrins to Regulate the Neuronal Microtubule Cytoskeleton Anne-Marie Lüchtenborg1,2, Gonzalo P
    © 2014. Published by The Company of Biologists Ltd | Development (2014) 141, 3399-3409 doi:10.1242/dev.106773 RESEARCH ARTICLE Heterotrimeric Go protein links Wnt-Frizzled signaling with ankyrins to regulate the neuronal microtubule cytoskeleton Anne-Marie Lüchtenborg1,2, Gonzalo P. Solis1, Diane Egger-Adam2, Alexey Koval1, Chen Lin1,2, Maxime G. Blanchard1, Stephan Kellenberger1 and Vladimir L. Katanaev1,2,* ABSTRACT The evolutionarily conserved Wg pathway is important for Drosophila neuromuscular junctions (NMJs) represent a powerful numerous developmental programs and cellular processes (Logan model system with which to study glutamatergic synapse formation and Nusse, 2004). In the nervous system of Drosophila,Wg and remodeling. Several proteins have been implicated in these signaling is involved in the formation of neuromuscular junctions processes, including components of canonical Wingless (Drosophila (NMJs) (Packard et al., 2002; Miech et al., 2008). Being a Wnt1) signaling and the giant isoforms of the membrane-cytoskeleton glutamatergic synapse, the Drosophila NMJ provides a useful linker Ankyrin 2, but possible interconnections and cooperation experimental model with which to study mammalian central between these proteins were unknown. Here, we demonstrate that nervous system synapses, their formation and remodeling (Collins the heterotrimeric G protein Go functions as a transducer of Wingless- and DiAntonio, 2007). The Drosophila NMJ is a beads-on-a-string- Frizzled 2 signaling in the synapse. We identify Ankyrin 2 as a target like structure that is formed at the axon terminus and is composed of – – of Go signaling required for NMJ formation. Moreover, the Go-ankyrin distinct circular structures the synaptic boutons which contain interaction is conserved in the mammalian neurite outgrowth pathway.
    [Show full text]
  • Expression Profiling of Ion Channel Genes Predicts Clinical Outcome in Breast Cancer
    UCSF UC San Francisco Previously Published Works Title Expression profiling of ion channel genes predicts clinical outcome in breast cancer Permalink https://escholarship.org/uc/item/1zq9j4nw Journal Molecular Cancer, 12(1) ISSN 1476-4598 Authors Ko, Jae-Hong Ko, Eun A Gu, Wanjun et al. Publication Date 2013-09-22 DOI http://dx.doi.org/10.1186/1476-4598-12-106 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Ko et al. Molecular Cancer 2013, 12:106 http://www.molecular-cancer.com/content/12/1/106 RESEARCH Open Access Expression profiling of ion channel genes predicts clinical outcome in breast cancer Jae-Hong Ko1, Eun A Ko2, Wanjun Gu3, Inja Lim1, Hyoweon Bang1* and Tong Zhou4,5* Abstract Background: Ion channels play a critical role in a wide variety of biological processes, including the development of human cancer. However, the overall impact of ion channels on tumorigenicity in breast cancer remains controversial. Methods: We conduct microarray meta-analysis on 280 ion channel genes. We identify candidate ion channels that are implicated in breast cancer based on gene expression profiling. We test the relationship between the expression of ion channel genes and p53 mutation status, ER status, and histological tumor grade in the discovery cohort. A molecular signature consisting of ion channel genes (IC30) is identified by Spearman’s rank correlation test conducted between tumor grade and gene expression. A risk scoring system is developed based on IC30. We test the prognostic power of IC30 in the discovery and seven validation cohorts by both Cox proportional hazard regression and log-rank test.
    [Show full text]
  • A De Novo ANK1 Mutation Associated to Hereditary Spherocytosis: a Case Report
    Huang et al. BMC Pediatrics (2019) 19:62 https://doi.org/10.1186/s12887-019-1436-4 CASEREPORT Open Access A de novo ANK1 mutation associated to hereditary spherocytosis: a case report Ti-Long Huang1, Bao-Hua Sang1, Qing-Ling Lei1, Chun-Yan Song1, Yun-Bi Lin1,YuLv1, Chun-Hui Yang1,NaLi1, Yue-Huang Yang1, Xian-Wen Zhang2* and Xin Tian1* Abstract Background: Hereditary spherocytosis (HS) is a type of hemolytic anemia caused by abnormal red cell membrane skeletal proteins with few unique clinical manifestations in the neonate and infant. An ANK1 gene mutation is the most common cause of HS. Case presentation: The patient was a 11-month-old boy who suffered from anemia and needed a regular transfusion therapy at an interval of 2–3 months. Hematological investigations showed moderate anemia (Hb80 g/L). Red cells displayed microcytosis (MCV76.4 fl, MCH25.6 pg, MCHC335 g/L). The reticulocytes were elevated (4.8%) and the spherocytes were increased (10%). Direct antiglobulin test was negative. Biochemical test indicated a slight elevation of bilirubin, mainly indirect reacting (TBIL32.5 μmol/L, IBIL24 μmol/L). The neonatal HS ratio is 4.38, obviously up the threshold. Meanwhile, adenovoANK1 mutation (exon 25:c.2693dupC:p.A899Sfs*11) was identified by next-generation sequencing (NGS). Thus, hereditary spherocytosis was finally diagnosed. Conclusions: Gene detection should be considered in some hemolytic anemia which is difficult to diagnose by routine means. We identified a novel de novo ANK1 heterozygous frameshift mutation in a Yi nationality patient while neither of his parents carried this mutation. Keywords: Hereditary spherocytosis- ANK1- frameshift mutation Background (erythrocyte membrane protein band 4.2) are associated Hereditary spherocytosis (HS) results from defects in with HS [5].
    [Show full text]
  • Investigation of the Underlying Hub Genes and Molexular Pathogensis in Gastric Cancer by Integrated Bioinformatic Analyses
    bioRxiv preprint doi: https://doi.org/10.1101/2020.12.20.423656; this version posted December 22, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Investigation of the underlying hub genes and molexular pathogensis in gastric cancer by integrated bioinformatic analyses Basavaraj Vastrad1, Chanabasayya Vastrad*2 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2020.12.20.423656; this version posted December 22, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Abstract The high mortality rate of gastric cancer (GC) is in part due to the absence of initial disclosure of its biomarkers. The recognition of important genes associated in GC is therefore recommended to advance clinical prognosis, diagnosis and and treatment outcomes. The current investigation used the microarray dataset GSE113255 RNA seq data from the Gene Expression Omnibus database to diagnose differentially expressed genes (DEGs). Pathway and gene ontology enrichment analyses were performed, and a proteinprotein interaction network, modules, target genes - miRNA regulatory network and target genes - TF regulatory network were constructed and analyzed. Finally, validation of hub genes was performed. The 1008 DEGs identified consisted of 505 up regulated genes and 503 down regulated genes.
    [Show full text]
  • An Advance About the Genetic Causes of Epilepsy
    E3S Web of Conferences 271, 03068 (2021) https://doi.org/10.1051/e3sconf/202127103068 ICEPE 2021 An advance about the genetic causes of epilepsy Yu Sun1, a, *, †, Licheng Lu2, b, *, †, Lanxin Li3, c, *, †, Jingbo Wang4, d, *, † 1The School of Molecular and Cellular Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801-3633, US 2High School Affiliated to Shanghai Jiao Tong University, Shanghai, 200441, China 3Applied Biology program, University of British Columbia, Vancouver, V6r3b1, Canada 4School of Chemical Machinery and Safety, Dalian University of Technology, Dalian, 116023, China †These authors contributed equally. Abstract: Human hereditary epilepsy has been found related to ion channel mutations in voltage-gated channels (Na+, K+, Ca2+, Cl-), ligand gated channels (GABA receptors), and G-protein coupled receptors, such as Mass1. In addition, some transmembrane proteins or receptor genes, including PRRT2 and nAChR, and glucose transporter genes, such as GLUT1 and SLC2A1, are also about the onset of epilepsy. The discovery of these genetic defects has contributed greatly to our understanding of the pathology of epilepsy. This review focuses on introducing and summarizing epilepsy-associated genes and related findings in recent decades, pointing out related mutant genes that need to be further studied in the future. 1 Introduction Epilepsy is a neurological disorder characterized by 2 Malfunction of Ion channel epileptic seizures caused by abnormal brain activity. 1 in Functional variation in voltage or ligand-gated ion 100 (50 million people) people are affected by symptoms channel mutations is a major cause of idiopathic epilepsy, of this disorder worldwide, with men, young children, and especially in rare genetic forms.
    [Show full text]
  • Review Article Mouse Homologues of Human Hereditary Disease
    I Med Genet 1994;31:1-19 I Review article J Med Genet: first published as 10.1136/jmg.31.1.1 on 1 January 1994. Downloaded from Mouse homologues of human hereditary disease A G Searle, J H Edwards, J G Hall Abstract involve homologous loci. In this respect our Details are given of 214 loci known to be genetic knowledge of the laboratory mouse associated with human hereditary dis- outstrips that for all other non-human mam- ease, which have been mapped on both mals. The 829 loci recently assigned to both human and mouse chromosomes. Forty human and mouse chromosomes3 has now two of these have pathological variants in risen to 900, well above comparable figures for both species; in general the mouse vari- other laboratory or farm animals. In a previous ants are similar in their effects to the publication,4 102 loci were listed which were corresponding human ones, but excep- associated with specific human disease, had tions include the Dmd/DMD and Hprt/ mouse homologues, and had been located in HPRT mutations which cause little, if both species. The number has now more than any, harm in mice. Possible reasons for doubled (table 1A). Of particular interest are phenotypic differences are discussed. In those which have pathological variants in both most pathological variants the gene pro- the mouse and humans: these are listed in table duct seems to be absent or greatly 2. Many other pathological mutations have reduced in both species. The extensive been detected and located in the mouse; about data on conserved segments between half these appear to lie in conserved chromo- human and mouse chromosomes are somal segments.
    [Show full text]
  • Rabbit Anti-Human KCNAB2 Polyclonal Antibody (DPABH-15471) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use
    Rabbit Anti-Human KCNAB2 Polyclonal antibody (DPABH-15471) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Immunogen KCNAB2 fusion protein, sequence: MYPESTTGSPARLSLRQTGSPGMIYSTRYGSPKRQLQFYRNLGKSGLRVSCLGLGTWVTFGG QITDEMAEQLMTLAYDNGINLFDTAEVYAAGKAEVVLGNIIKKKGWRRSSLVITTKIFWGGKAETE RGLSRKHIIEGLKASLERLQLEYVDVVFANRPDPNTPMEETVRAMTHVINQGMAMYWGTSRWS SMEIMEAYSVARQFNLTPPICEQAEYHMFQREKVEVQLPELFHKIGVGAMTWSPLACGIVSGKY DSGIPPYSRASLKGYQWLKDKILSEEGRRQQAKLKELQAIAERLGCTLPQLAIAWCLRNEGVSSV LLGASNADQLMENIGAIQVRVRGPAGQRAHPSPSPVQCILPGSSCVPGSVLGTQDAPVNHQSC APGELAFQQEQT (1-395 aa encoded by BC110351) Isotype IgG Source/Host Rabbit Species Reactivity Human, Mouse, Rat Purification Antigen affinity purification Conjugate Unconjugated Applications WB, IHC, ELISA Positive Control mouse brain tissue, HepG2 cells Format Liquid Size 50 uL; 100 uL Buffer PBS with 0.02% sodium azide and 50% glycerol pH 7.3. Preservative 0.02% Sodium Azide Storage Store at -20°C. Aliquoting is unnecessary for -20°C storage. BACKGROUND Introduction Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and
    [Show full text]
  • A Knowledge-Guided Mechanistic Model of Synthetic Lethality in The
    bioRxiv preprint doi: https://doi.org/10.1101/2021.06.22.449530; this version posted June 23, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. A Knowledge-guided Mechanistic Model of Synthetic Lethality in the HCT116 Vorinostat-resistant Colon Cancer Xenograft Model Cell-line Paul Aiyetan June 22, 2021 Abstract With an overall lifetime risk of about 4.3% and 4.0%, in men and women respectively, colorectal cancer remains the third leading cause of cancer-related deaths in the United States. In persons aged 55 and below, its rate increased at 1% per year in the years 2008 to 2017 despite the steady decline associated with improved screening, early diagnosis and treatment in the general population. Besides standardized therapeutic regimen, many trials continue to evaluate the potential benefits of vorinostat, mostly in combination with other anti-neoplastic agents for its treatment. Vorinostat, an FDA approved anti-cancer drug known as suberoylanilide hydroxamic acid (SAHA), an histone deacylase (HDAC) inhibitor, through many mechanisms, causes cancer cell arrest and death. However, like many other anti-neoplastic agents, resistance and or failures have been observed. In the HCT116 colon cancer cell line xenograft model, exploiting potential lethal molecular interactions by additional gene knockouts restored vorinotat sensitivity. This phenomenon, known as synthetic lethality, offers a promise to selectively target cancer cells. Although without clearly delineated understanding of underlying molecular processes, it has been demonstrated as an effective cancer-killing mechanism.
    [Show full text]
  • Genomics Analysis of Potassium Channel Genes in Songbirds Reveals
    Lovell et al. BMC Genomics 2013, 14:470 http://www.biomedcentral.com/1471-2164/14/470 RESEARCH ARTICLE Open Access Genomics analysis of potassium channel genes in songbirds reveals molecular specializations of brain circuits for the maintenance and production of learned vocalizations Peter V Lovell, Julia B Carleton and Claudio V Mello* Abstract Background: A fundamental question in molecular neurobiology is how genes that determine basic neuronal properties shape the functional organization of brain circuits underlying complex learned behaviors. Given the growing availability of complete vertebrate genomes, comparative genomics represents a promising approach to address this question. Here we used genomics and molecular approaches to study how ion channel genes influence the properties of the brain circuitry that regulates birdsong, a learned vocal behavior with important similarities to human speech acquisition. We focused on potassium (K-)Channels, which are major determinants of neuronal cell excitability. Starting with the human gene set of K-Channels, we used cross-species mRNA/protein alignments, and syntenic analysis to define the full complement of orthologs, paralogs, allelic variants, as well as novel loci not previously predicted in the genome of zebra finch (Taeniopygia guttata). We also compared protein coding domains in chicken and zebra finch orthologs to identify genes under positive selective pressure, and those that contained lineage-specific insertions/deletions in functional domains. Finally, we conducted comprehensive in situ hybridizations to determine the extent of brain expression, and identify K-Channel gene enrichments in nuclei of the avian song system. Results: We identified 107 K-Channel finch genes, including 6 novel genes common to non-mammalian vertebrate lineages.
    [Show full text]