Table Continues on Reverse Perilipin-1 (PLIN1) O60240 Ras Association Domain-Containing Protein 2 (RASSF2) P50749
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Supplemental Information to Mammadova-Bach Et Al., “Laminin Α1 Orchestrates VEGFA Functions in the Ecosystem of Colorectal Carcinogenesis”
Supplemental information to Mammadova-Bach et al., “Laminin α1 orchestrates VEGFA functions in the ecosystem of colorectal carcinogenesis” Supplemental material and methods Cloning of the villin-LMα1 vector The plasmid pBS-villin-promoter containing the 3.5 Kb of the murine villin promoter, the first non coding exon, 5.5 kb of the first intron and 15 nucleotides of the second villin exon, was generated by S. Robine (Institut Curie, Paris, France). The EcoRI site in the multi cloning site was destroyed by fill in ligation with T4 polymerase according to the manufacturer`s instructions (New England Biolabs, Ozyme, Saint Quentin en Yvelines, France). Site directed mutagenesis (GeneEditor in vitro Site-Directed Mutagenesis system, Promega, Charbonnières-les-Bains, France) was then used to introduce a BsiWI site before the start codon of the villin coding sequence using the 5’ phosphorylated primer: 5’CCTTCTCCTCTAGGCTCGCGTACGATGACGTCGGACTTGCGG3’. A double strand annealed oligonucleotide, 5’GGCCGGACGCGTGAATTCGTCGACGC3’ and 5’GGCCGCGTCGACGAATTCACGC GTCC3’ containing restriction site for MluI, EcoRI and SalI were inserted in the NotI site (present in the multi cloning site), generating the plasmid pBS-villin-promoter-MES. The SV40 polyA region of the pEGFP plasmid (Clontech, Ozyme, Saint Quentin Yvelines, France) was amplified by PCR using primers 5’GGCGCCTCTAGATCATAATCAGCCATA3’ and 5’GGCGCCCTTAAGATACATTGATGAGTT3’ before subcloning into the pGEMTeasy vector (Promega, Charbonnières-les-Bains, France). After EcoRI digestion, the SV40 polyA fragment was purified with the NucleoSpin Extract II kit (Machery-Nagel, Hoerdt, France) and then subcloned into the EcoRI site of the plasmid pBS-villin-promoter-MES. Site directed mutagenesis was used to introduce a BsiWI site (5’ phosphorylated AGCGCAGGGAGCGGCGGCCGTACGATGCGCGGCAGCGGCACG3’) before the initiation codon and a MluI site (5’ phosphorylated 1 CCCGGGCCTGAGCCCTAAACGCGTGCCAGCCTCTGCCCTTGG3’) after the stop codon in the full length cDNA coding for the mouse LMα1 in the pCIS vector (kindly provided by P. -
Table 2. Significant
Table 2. Significant (Q < 0.05 and |d | > 0.5) transcripts from the meta-analysis Gene Chr Mb Gene Name Affy ProbeSet cDNA_IDs d HAP/LAP d HAP/LAP d d IS Average d Ztest P values Q-value Symbol ID (study #5) 1 2 STS B2m 2 122 beta-2 microglobulin 1452428_a_at AI848245 1.75334941 4 3.2 4 3.2316485 1.07398E-09 5.69E-08 Man2b1 8 84.4 mannosidase 2, alpha B1 1416340_a_at H4049B01 3.75722111 3.87309653 2.1 1.6 2.84852656 5.32443E-07 1.58E-05 1110032A03Rik 9 50.9 RIKEN cDNA 1110032A03 gene 1417211_a_at H4035E05 4 1.66015788 4 1.7 2.82772795 2.94266E-05 0.000527 NA 9 48.5 --- 1456111_at 3.43701477 1.85785922 4 2 2.8237185 9.97969E-08 3.48E-06 Scn4b 9 45.3 Sodium channel, type IV, beta 1434008_at AI844796 3.79536664 1.63774235 3.3 2.3 2.75319499 1.48057E-08 6.21E-07 polypeptide Gadd45gip1 8 84.1 RIKEN cDNA 2310040G17 gene 1417619_at 4 3.38875643 1.4 2 2.69163229 8.84279E-06 0.0001904 BC056474 15 12.1 Mus musculus cDNA clone 1424117_at H3030A06 3.95752801 2.42838452 1.9 2.2 2.62132809 1.3344E-08 5.66E-07 MGC:67360 IMAGE:6823629, complete cds NA 4 153 guanine nucleotide binding protein, 1454696_at -3.46081884 -4 -1.3 -1.6 -2.6026947 8.58458E-05 0.0012617 beta 1 Gnb1 4 153 guanine nucleotide binding protein, 1417432_a_at H3094D02 -3.13334396 -4 -1.6 -1.7 -2.5946297 1.04542E-05 0.0002202 beta 1 Gadd45gip1 8 84.1 RAD23a homolog (S. -
Role and Regulation of Pdgfra Signaling in Liver Development and Regeneration
The American Journal of Pathology, Vol. 182, No. 5, May 2013 ajp.amjpathol.org GROWTH FACTORS, CYTOKINES, AND CELL CYCLE MOLECULES Role and Regulation of PDGFRa Signaling in Liver Development and Regeneration Prince K. Awuah,* Kari N. Nejak-Bowen,* and Satdarshan P.S. Monga*y From the Division of Experimental Pathology,* Department of Pathology, and the Department of Medicine,y University of Pittsburgh, Pittsburgh, Pennsylvania Accepted for publication January 22, 2013. Aberrant platelet-derived growth factor receptor-a (PDGFRa) signaling is evident in a subset of hepato- cellular cancers (HCCs). However, its role and regulation in hepatic physiology remains elusive. In the Address correspondence to a fi Satdarshan P.S. Monga, M.D., current study, we examined PDGFR signaling in liver development and regeneration. We identi ed a a Divisions of Experimental notable PDGFR activation in hepatic morphogenesis that, when interrupted by PDGFR -blocking anti- Pathology, Pathology and body, led to decreased hepatoblast proliferation and survival in embryonic liver cultures. We also identified Medicine, University of Pitts- temporal PDGFRa overexpression, which is regulated by epidermal growth factor (EGF) and tumor necrosis burgh School of Medicine, 200 factor a, and its activation at 3 to 24 hours after partial hepatectomy. Through generation of hepatocyte- Lothrop St., S-422 BST, Pitts- specific PDGFRA knockout (KO) mice that lack an overt phenotype, we show that absent PDGFRa burgh, PA 15261. E-mail: compromises extracelluar signal-regulated kinases and AKT activation 3 hours after partial hepatectomy, [email protected]. which, however, is alleviated by temporal compensatory increases in the EGF receptor (EGFR) and the hepatocyte growth factor receptor (Met) expression and activation along with rebound activation of extracellular signal-regulated kinases and AKT at 24 hours. -
P-Glycoprotein-Mediated Chemoresistance Is Reversed by Carbonic Anhydrase XII Inhibitors
www.impactjournals.com/oncotarget/ Oncotarget, Advance Publications 2016 P-glycoprotein-mediated chemoresistance is reversed by carbonic anhydrase XII inhibitors Joanna Kopecka1, Gregory M. Rankin2, Iris C. Salaroglio1, Sally-Ann Poulsen2,*, Chiara Riganti1,* 1Department of Oncology, University of Torino, 10126 Torino, Italy 2Eskitis Institute for Drug Discovery, Griffith University, Brisbane, Nathan, Queensland, 4111, Australia *These authors contributed equally to this work Correspondence to: Sally-Ann Poulsen, email: [email protected] Chiara Riganti, email: [email protected] Keywords: carbonic anhydrase XII, P-glycoprotein, doxorubicin, chemoresistance, intracellular pH Received: August 26, 2016 Accepted: October 28, 2016 Published: November 03, 2016 ABSTRACT Carbonic anhydrase XII (CAXII) is a membrane enzyme that maintains pH homeostasis and sustains optimum P-glycoprotein (Pgp) efflux activity in cancer cells. Here, we investigated a panel of eight CAXII inhibitors (compounds 1–8), for their potential to reverse Pgp mediated tumor cell chemoresistance. Inhibitors (5 nM) were screened in human and murine cancer cells (colon, lung, breast, bone) with different expression levels of CAXII and Pgp. We identified three CAXII inhibitors (compounds 1, 2 and 4) that significantly (≥ 2 fold) increased the intracellular retention of the Pgp-substrate and chemotherapeutic doxorubicin, and restored its cytotoxic activity. The inhibitors lowered intracellular pH to indirectly impair Pgp activity. Ca12-knockout assays confirmed that the chemosensitizing property of the compounds was dependent on active CAXII. Furthermore, in a preclinical model of drug-resistant breast tumors compound 1 (1900 ng/kg) restored the efficacy of doxorubicin to the same extent as the direct Pgp inhibitor tariquidar. The expression of carbonic anhydrase IX had no effect on the intracellular doxorubicin accumulation. -
PDGF-C and PDGF-D Signaling in Vascular Diseases and Animal Models
Molecular Aspects of Medicine 62 (2018) 1e11 Contents lists available at ScienceDirect Molecular Aspects of Medicine journal homepage: www.elsevier.com/locate/mam PDGF-C and PDGF-D signaling in vascular diseases and animal models * Erika Folestad a, Anne Kunath b, Dick Wågsater€ b, a Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden b Division of Drug Research, Department of Medical and Health Sciences, Linkoping€ University, Linkoping,€ Sweden article info abstract Article history: Members of the platelet-derived growth factor (PDGF) family are well known to be involved in different Received 31 August 2017 pathological conditions. The cellular and molecular mechanisms induced by the PDGF signaling have Received in revised form been well studied. Nevertheless, there is much more to discover about their functions and some 14 November 2017 important questions to be answered. This review summarizes the known roles of two of the PDGFs, Accepted 22 January 2018 PDGF-C and PDGF-D, in vascular diseases. There are clear implications for these growth factors in several Available online 14 February 2018 vascular diseases, such as atherosclerosis and stroke. The PDGF receptors are broadly expressed in the cardiovascular system in cells such as fibroblasts, smooth muscle cells and pericytes. Altered expression Keywords: Aneurysm of the receptors and the ligands have been found in various cardiovascular diseases and current studies fi Atherosclerosis have shown important implications of PDGF-C and PDGF-D signaling in brosis, neovascularization, Growth factor atherosclerosis and restenosis. Myocardial infarction © 2018 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND Smooth muscle cells license (http://creativecommons.org/licenses/by-nc-nd/4.0/). -
Ep 3217179 A1
(19) TZZ¥ ___T (11) EP 3 217 179 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 13.09.2017 Bulletin 2017/37 G01N 33/68 (2006.01) (21) Application number: 17167637.2 (22) Date of filing: 02.10.2013 (84) Designated Contracting States: • LIU, Xinjun AL AT BE BG CH CY CZ DE DK EE ES FI FR GB San Diego, CA 92130 (US) GR HR HU IE IS IT LI LT LU LV MC MK MT NL NO • HAUENSTEIN, Scott PL PT RO RS SE SI SK SM TR San Diego, CA 92130 (US) • KIRKLAND, Richard (30) Priority: 05.10.2012 US 201261710491 P San Diego, CA 92111 (US) 17.05.2013 US 201361824959 P (74) Representative: Krishnan, Sri (62) Document number(s) of the earlier application(s) in Nestec S.A. accordance with Art. 76 EPC: Centre de Recherche Nestlé 13779638.9 / 2 904 405 Vers-chez-les-Blanc Case Postale 44 (71) Applicant: Nestec S.A. 1000 Lausanne 26 (CH) 1800 Vevey (CH) Remarks: (72) Inventors: This application was filed on 21-04-2017 as a • SINGH, Sharat divisional application to the application mentioned Rancho Santa Fe, CA 92127 (US) under INID code 62. (54) METHODS FOR PREDICTING AND MONITORING MUCOSAL HEALING (57) The present invention provides methods for pre- an individual with a disease such as IBD. Information on dicting the likelihood of mucosal healing in an individual mucosal healing status derived from the use of the with a disease such as inflammatory bowel disease present invention can also aid in optimizing therapy (IBD). -
The Effects of Betaine Treatment on Rats Fed an Acute Bolus of Ethanol at 3 and 12 H Post Bolus: a Microarray Analysis
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central Genes Nutr (2010) 5:321–329 DOI 10.1007/s12263-010-0173-y RESEARCH PAPER The effects of betaine treatment on rats fed an acute bolus of ethanol at 3 and 12 h post bolus: a microarray analysis J. Li • F. Bardag-Gorce • J. Oliva • B. A. French • J. Dedes • S. W. French Received: 24 November 2009 / Accepted: 19 February 2010 / Published online: 19 March 2010 Ó The Author(s) 2010. This article is published with open access at Springerlink.com Abstract Betaine, a methyl donor active in methionine Introduction metabolism, is effective in preventing and reversing experimental alcohol liver disease. The metabolic and Ethanol, given as a bolus of 6 g/kg body weight, increases molecular biologic mechanisms involved in this prevention the blood and urinary alcohol to a high level at 3 h post are only partially known. To further investigate how betaine bolus. At 12 h, the blood and urinary alcohol levels return modifies the effects of ethanol on the liver, rats were given to low a level [2]. At these 2 time points, there are major an acute ethanol bolus with or without betaine and the changes in gene expression in the liver but only minimal results were compared to isocaloric dextrose-fed controls. evidence of epigenetic changes [2]. Only at 12 h is there a Livers were subjected to microarray analysis, and functional decrease in global DNA methylation [2]. pathways and individual gene expression changes were Previously, in using this model, S-adenosylmethionine analyzed. -
Regulation of PDGFC Signalling and Extracellular Matrix Composition by FREM1 in Mice
RESEARCH ARTICLE Disease Models & Mechanisms 6, 1426-1433 (2013) doi:10.1242/dmm.013748 Regulation of PDGFC signalling and extracellular matrix composition by FREM1 in mice Fenny Wiradjaja1, Denny L. Cottle1, Lynelle Jones1 and Ian Smyth1,2,* SUMMARY Fras1-related extracellular matrix protein 1 (FREM1) is required for epidermal adhesion during embryogenesis, and mice lacking the gene develop fetal skin blisters and a range of other developmental defects. Mutations in members of the FRAS/FREM gene family cause diseases of the Fraser syndrome spectrum. Embryonic epidermal blistering is also observed in mice lacking PdgfC and its receptor, PDGFRα. In this article, we show that FREM1 binds to PDGFC and that this interaction regulates signalling downstream of PDGFRα. Fibroblasts from Frem1-mutant mice respond to PDGFC stimulation, but with a shorter duration and amplitude than do wild-type cells. Significantly, PDGFC-stimulated expression of the metalloproteinase inhibitor Timp1 is reduced in cells with Frem1 mutations, leading to reduced basement membrane collagen I deposition. These results show that the physical interaction of FREM1 with PDGFC can regulate remodelling of the extracellular matrix downstream of PDGFRα. We propose that loss of FREM1 function promotes epidermal blistering in Fraser syndrome as a consequence of reduced PDGFC activity, in addition to its stabilising role in the basement membrane. DMM INTRODUCTION The FRAS/FREM family of proteins share characteristic The FRAS/FREM extracellular matrix (ECM) proteins (FRAS1, chondroitin sulphate proteoglycan (CSPG) core repeats similar FREM1 and FREM2) mediate adhesion between the epidermal to those found in the NG2 proteoglycan (Stallcup, 2002). In this basement membrane and the underlying dermis during embryonic protein, they directly bind platelet-derived growth factor A development (reviewed in Short et al., 2007; Petrou et al., 2008). -
PDGFC (Human) Recombinant Protein
PDGFC (Human) Recombinant pH 3.0. protein Storage Instruction: Store at -20°C. Reconstitute in water to a concentration of 0.1-1.0 Catalog Number: P6130 mg/mL. Do not vortex. Regulation Status: For research use only (RUO) For extended storage, it is recommended to further dilute in a buffer containing a carrier protein (example 0.1% Product Description: Human PDGFC (Q9NRA1) partial BSA) and store in working aliquots at -20°C to -80°C. recombinant protein expressed in Escherichia coli. Entrez GeneID: 56034 Sequence: MVVDLNLLTEEVRLYSCTPRNFSVSIREELKRTDTIFW Gene Symbol: PDGFC PGCLLVKRCGGNCACCLHNCNECQCVPSKVTKKYHE Gene Alias: FALLOTEIN, SCDGF VLQLRPKTGVRGLHKSLTDVALEHHEECDCVCRGSTG G Gene Summary: The protein encoded by this gene is a member of the platelet-derived growth factor family. The Host: Escherichia coli four members of this family are mitogenic factors for Theoretical MW (kDa): 25.0 cells of mesenchymal origin and are characterized by a core motif of eight cysteines. This gene product appears Reactivity: Human to form only homodimers. It differs from the platelet-derived growth factor alpha and beta Applications: Func, SDS-PAGE polypeptides in having an unusual N-terminal domain, (See our web site product page for detailed applications the CUB domain. [provided by RefSeq] information) Protocols: See our web site at http://www.abnova.com/support/protocols.asp or product page for detailed protocols Form: Lyophilized Preparation Method: Escherichia coli expression system Purity: 98% Endotoxin Level: Endotoxin level is <0.1 ng/ug of protein (<1 EU/ug). Activity: Determined by the dose-dependent stimulation of the proliferation of Balb/c 3T3 cells. The expected The ED50 for this effect is 15-20 ng/mL. -
The Role of Asic1a in the Regulation of Synaptic Release Probability
The Role of ASIC1a in the Regulation of Synaptic Release Probability THESIS Presented in Partial Fulfillment of the Requirements for the Degree Master of Science in the Graduate School of The Ohio State University By Soluman Culver Graduate Program in Pathology The Ohio State University 2013 Master's Examination Committee: W. James Waldman, Adviser Candice Askwith John Enyeart Copyright by Soluman Culver 2013 Abstract Extracellular pH plays an important role in neuronal signaling. As primary receptors of pH signals, acid-sensing ion channels (ASICs) are able to translate fluctuations in the extracellular pH into membrane potentials and calcium signals. ASICs and pH signaling are thought to play important roles in anxiety, affect, and pain, although the mechanism by which they are able to influence these processes remains poorly understood. During conditions of dysregulated pH aberrant ASIC activity is known to result in cellular dysfunction and death, making a mechanistic explanation of ASIC function of broad importance to our understanding of downstream consequences during pathophysiological circumstances. One significant role of ASIC is in its ability to modulate synaptic vesicle release, a property which may contribute to neuronal dysfunction secondary to disruptions in pH signaling. This study demonstrates that the mechanism of ASIC-dependent regulation of synaptic vesicle does not rely upon rapid local signaling, but rather requires several hours of ASIC block to be interrupted, suggesting that it may take place through the induction of gene regulation and cause global changes in cellular physiology. Similarly, our results suggest that ASIC1a may be responding to endogenous proton flux to accomplish this regulation, refining our understanding of the cause and context of ASIC1a activation in health and disease. -
Structural Characterization of Beta Carbonic Anhydrases from Higher Plants
Louisiana State University LSU Digital Commons LSU Historical Dissertations and Theses Graduate School 1998 Structural Characterization of Beta Carbonic Anhydrases From Higher Plants. Michael H. Bracey Louisiana State University and Agricultural & Mechanical College Follow this and additional works at: https://digitalcommons.lsu.edu/gradschool_disstheses Recommended Citation Bracey, Michael H., "Structural Characterization of Beta Carbonic Anhydrases From Higher Plants." (1998). LSU Historical Dissertations and Theses. 6655. https://digitalcommons.lsu.edu/gradschool_disstheses/6655 This Dissertation is brought to you for free and open access by the Graduate School at LSU Digital Commons. It has been accepted for inclusion in LSU Historical Dissertations and Theses by an authorized administrator of LSU Digital Commons. For more information, please contact [email protected]. INFORMATION TO USERS This manuscript has been reproduced from the microfilm master. UMI films the text directly from the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter face, while others may be from any type o f computer printer. The quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction. In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will be noted. Also, if unauthorized copyright material had to be removed, a note will indicate the deletion. Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, beginning at the upper left-hand comer and continuing from left to right in equal sections with small overlaps. -
Computational Modeling of Solvent Effects on Protein-Ligand
Commun. Comput. Phys. Vol. 13, No. 1, pp. 31-60 doi: 10.4208/cicp.130911.121011s January 2013 Computational Modeling of Solvent Effects on Protein-Ligand Interactions Using Fully Polarizable Continuum Model and Rational Drug Design Fang Zheng and Chang-Guo Zhan∗ Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, 789 South Limestone Street, Lexington, Kentucky 40536, USA. Received 13 September 2011; Accepted (in revised version) 12 October 2011 Available online 12 June 2012 Abstract. This is a brief review of the computational modeling of protein-ligand in- teractions using a recently developed fully polarizable continuum model (FPCM) and rational drug design. Computational modeling has become a powerful tool in under- standing detailed protein-ligand interactions at molecular level and in rational drug design. To study the binding of a protein with multiple molecular species of a ligand, one must accurately determine both the relative free energies of all of the molecular species in solution and the corresponding microscopic binding free energies for all of the molecular species binding with the protein. In this paper, we aim to provide a brief overview of the recent development in computational modeling of the solvent ef- fects on the detailed protein-ligand interactions involving multiple molecular species of a ligand related to rational drug design. In particular, we first briefly discuss the main challenges in computational modeling of the detailed protein-ligand interactions involving the multiple molecular species and then focus on the FPCM model and its applications. The FPCM method allows accurate determination of the solvent effects in the first-principles quantum mechanism (QM) calculations on molecules in solu- tion.