Impact of Non-Thermal Plasma on Cell Signaling in Keratinocytes
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Methods for Identifying Circadian Rhythm
(19) *EP003302716B1* (11) EP 3 302 716 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: A61Q 17/04 (2006.01) G01N 33/50 (2006.01) (2006.01) (2006.01) 14.10.2020 Bulletin 2020/42 A61Q 19/08 A61Q 19/00 C12Q 1/68 (2018.01) (21) Application number: 16729482.6 (86) International application number: (22) Date of filing: 08.06.2016 PCT/US2016/036401 (87) International publication number: WO 2016/200905 (15.12.2016 Gazette 2016/50) (54) METHODS FOR IDENTIFYING CIRCADIAN RHYTHM-DEPENDENT COSMETIC AGENTS FOR SKIN CARE COMPOSITIONS VERFAHREN ZUR IDENTIFIZIERUNG VON BIORHYTHMUSABHÄNGIGEN KOSMETISCHEN MITTELN FÜR HAUTPFLEGEZUSAMMENSETZUNGEN PROCÉDÉS D’IDENTIFICATION D’AGENTS COSMÉTIQUES DÉPENDANT DU RYTHME CIRCADIEN POUR DES COMPOSITIONS DE SOIN DE LA PEAU (84) Designated Contracting States: • OSBORNE, Rosemarie AL AT BE BG CH CY CZ DE DK EE ES FI FR GB Cincinnati, Ohio 45202 (US) GR HR HU IE IS IT LI LT LU LV MC MK MT NL NO PL PT RO RS SE SI SK SM TR (74) Representative: P&G Patent Belgium UK N.V. Procter & Gamble Services Company S.A. (30) Priority: 08.06.2015 US 201562172498 P Temselaan 100 1853 Strombeek-Bever (BE) (43) Date of publication of application: 11.04.2018 Bulletin 2018/15 (56) References cited: WO-A1-2010/079285 JP-A- 2010 098 965 (73) Proprietor: The Procter & Gamble Company US-A1- 2009 220 481 US-A1- 2010 028 317 Cincinnati, OH 45202 (US) US-A1- 2015 071 895 (72) Inventors: • GEYFMAN MIKHAIL ET AL: "Clock genes, hair • MULLINS, Lisa, Ann growth and aging", AGING, NEW YORK, NY, US, Cincinnati, Ohio 45202 (US) vol. -
Genetic Variation Across the Human Olfactory Receptor Repertoire Alters Odor Perception
bioRxiv preprint doi: https://doi.org/10.1101/212431; this version posted November 1, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.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 4.0 International license. Genetic variation across the human olfactory receptor repertoire alters odor perception Casey Trimmer1,*, Andreas Keller2, Nicolle R. Murphy1, Lindsey L. Snyder1, Jason R. Willer3, Maira Nagai4,5, Nicholas Katsanis3, Leslie B. Vosshall2,6,7, Hiroaki Matsunami4,8, and Joel D. Mainland1,9 1Monell Chemical Senses Center, Philadelphia, Pennsylvania, USA 2Laboratory of Neurogenetics and Behavior, The Rockefeller University, New York, New York, USA 3Center for Human Disease Modeling, Duke University Medical Center, Durham, North Carolina, USA 4Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina, USA 5Department of Biochemistry, University of Sao Paulo, Sao Paulo, Brazil 6Howard Hughes Medical Institute, New York, New York, USA 7Kavli Neural Systems Institute, New York, New York, USA 8Department of Neurobiology and Duke Institute for Brain Sciences, Duke University Medical Center, Durham, North Carolina, USA 9Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA *[email protected] ABSTRACT The human olfactory receptor repertoire is characterized by an abundance of genetic variation that affects receptor response, but the perceptual effects of this variation are unclear. To address this issue, we sequenced the OR repertoire in 332 individuals and examined the relationship between genetic variation and 276 olfactory phenotypes, including the perceived intensity and pleasantness of 68 odorants at two concentrations, detection thresholds of three odorants, and general olfactory acuity. -
KIAA0101/P15paf) Over Expression and Gene Copy Number Alterations in Hepatocellular Carcinoma Tissues
PCNA-associated Factor (KIAA0101/p15PAF) over expression and Gene Copy Number Alterations in Hepatocellular Carcinoma Tissues Anchalee Tantiwetrueangdet Research Center, Faculty of Medicine, Ramathibodi Hospital Ravat Panvichian ( [email protected] ) Mahidol University Faculty of Medicine Ramathibodi Hospital https://orcid.org/0000-0001-5282-8166 Pattana Sornmayura Department of Pathology, Faculty of Medicine, Ramathibodi Hospital Surasak Leelaudomlipi Department of Surgery, Faculty of Medicine, Ramathibodi Hospital Research article Keywords: PCNA-associated factor (KIAA0101/p15PAF), droplet digital PCR, real-time PCR, p53 tumor suppressor protein, Ki-67 proliferation marker protein, HCC DOI: https://doi.org/10.21203/rs.3.rs-39782/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/18 Abstract Background PCNA-associated factor (KIAA0101/p15PAF) is a cell-cycle regulated oncoprotein that regulates DNA synthesis, maintenance of DNA methylation, and DNA-damage bypass, through the interaction with the human sliding clamp PCNA. KIAA0101 is overexpressed in various cancers, including hepatocellular carcinoma (HCC). However, it remains unknown whether KIAA0101 gene ampliƒcation occurs and causally correlates with the KIAA0101 overexpression in HCC. This question is relevant to the development of the optimal test(s) for KIAA0101 and the strategies to target KIAA0101 in HCC. Methods In this study, we validated KIAA0101 mRNA expression levels by quantitative real-time PCR in 40 pairs of snap-frozen HCC and matched-non-cancerous tissues; we then evaluated KIAA0101 gene copy numbers by droplet digital PCR (ddPCR) in 36 pairs of the tissues. Besides, KIAA0101 protein expression was detected by immunohistochemistry (IHC) in 81 pairs of formalin-ƒxed para∆n-embedded (FFPE) tissues. -
ARTICLES Fibroblast Growth Factors 1, 2, 17, and 19 Are The
0031-3998/07/6103-0267 PEDIATRIC RESEARCH Vol. 61, No. 3, 2007 Copyright © 2007 International Pediatric Research Foundation, Inc. Printed in U.S.A. ARTICLES Fibroblast Growth Factors 1, 2, 17, and 19 Are the Predominant FGF Ligands Expressed in Human Fetal Growth Plate Cartilage PAVEL KREJCI, DEBORAH KRAKOW, PERTCHOUI B. MEKIKIAN, AND WILLIAM R. WILCOX Medical Genetics Institute [P.K., D.K., P.B.M., W.R.W.], Cedars-Sinai Medical Center, Los Angeles, California 90048; Department of Obstetrics and Gynecology [D.K.] and Department of Pediatrics [W.R.W.], UCLA School of Medicine, Los Angeles, California 90095 ABSTRACT: Fibroblast growth factors (FGF) regulate bone growth, (G380R) or TD (K650E) mutations (4–6). When expressed at but their expression in human cartilage is unclear. Here, we deter- physiologic levels, FGFR3-G380R required, like its wild-type mined the expression of entire FGF family in human fetal growth counterpart, ligand for activation (7). Similarly, in vitro cul- plate cartilage. Using reverse transcriptase PCR, the transcripts for tivated human TD chondrocytes as well as chondrocytes FGF1, 2, 5, 8–14, 16–19, and 21 were found. However, only FGF1, isolated from Fgfr3-K644M mice had an identical time course 2, 17, and 19 were detectable at the protein level. By immunohisto- of Fgfr3 activation compared with wild-type chondrocytes and chemistry, FGF17 and 19 were uniformly expressed within the showed no receptor activation in the absence of ligand (8,9). growth plate. In contrast, FGF1 was found only in proliferating and hypertrophic chondrocytes whereas FGF2 localized predominantly to Despite the importance of the FGF ligand for activation of the resting and proliferating cartilage. -
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. -
) (51) International Patent Classification: Columbia V5G 1G3
) ( (51) International Patent Classification: Columbia V5G 1G3 (CA). PANDEY, Nihar R.; 10209 A 61K 31/4525 (2006.01) C07C 39/23 (2006.01) 128A St, Surrey, British Columbia V3T 3E7 (CA). A61K 31/05 (2006.01) C07D 405/06 (2006.01) (74) Agent: ZIESCHE, Sonia et al.; Gowling WLG (Canada) A61P25/22 (2006.01) LLP, 2300 - 550 Burrard Street, Vancouver, British Colum¬ (21) International Application Number: bia V6C 2B5 (CA). PCT/CA2020/050165 (81) Designated States (unless otherwise indicated, for every (22) International Filing Date: kind of national protection av ailable) . AE, AG, AL, AM, 07 February 2020 (07.02.2020) AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DJ, DK, DM, DO, (25) Filing Language: English DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, (26) Publication Language: English HR, HU, ID, IL, IN, IR, IS, JO, JP, KE, KG, KH, KN, KP, KR, KW, KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, (30) Priority Data: MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, 16/270,389 07 February 2019 (07.02.2019) US OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, (63) Related by continuation (CON) or continuation-in-part SC, SD, SE, SG, SK, SL, ST, SV, SY, TH, TJ, TM, TN, TR, (CIP) to earlier application: TT, TZ, UA, UG, US, UZ, VC, VN, WS, ZA, ZM, ZW. US 16/270,389 (CON) (84) Designated States (unless otherwise indicated, for every Filed on 07 Februaiy 2019 (07.02.2019) kind of regional protection available) . -
The Act of Controlling Adult Stem Cell Dynamics: Insights from Animal Models
biomolecules Review The Act of Controlling Adult Stem Cell Dynamics: Insights from Animal Models Meera Krishnan 1, Sahil Kumar 1, Luis Johnson Kangale 2,3 , Eric Ghigo 3,4 and Prasad Abnave 1,* 1 Regional Centre for Biotechnology, NCR Biotech Science Cluster, 3rd Milestone, Gurgaon-Faridabad Ex-pressway, Faridabad 121001, India; [email protected] (M.K.); [email protected] (S.K.) 2 IRD, AP-HM, SSA, VITROME, Aix-Marseille University, 13385 Marseille, France; [email protected] 3 Institut Hospitalo Universitaire Méditerranée Infection, 13385 Marseille, France; [email protected] 4 TechnoJouvence, 13385 Marseille, France * Correspondence: [email protected] Abstract: Adult stem cells (ASCs) are the undifferentiated cells that possess self-renewal and differ- entiation abilities. They are present in all major organ systems of the body and are uniquely reserved there during development for tissue maintenance during homeostasis, injury, and infection. They do so by promptly modulating the dynamics of proliferation, differentiation, survival, and migration. Any imbalance in these processes may result in regeneration failure or developing cancer. Hence, the dynamics of these various behaviors of ASCs need to always be precisely controlled. Several genetic and epigenetic factors have been demonstrated to be involved in tightly regulating the proliferation, differentiation, and self-renewal of ASCs. Understanding these mechanisms is of great importance, given the role of stem cells in regenerative medicine. Investigations on various animal models have played a significant part in enriching our knowledge and giving In Vivo in-sight into such ASCs regulatory mechanisms. In this review, we have discussed the recent In Vivo studies demonstrating the role of various genetic factors in regulating dynamics of different ASCs viz. -
Transcriptional Repression of IFN Regulatory Factor 7 by MYC Is Critical for Type I IFN Production in Human Plasmacytoid Dendrit
Transcriptional Repression of IFN Regulatory Factor 7 by MYC Is Critical for Type I IFN Production in Human Plasmacytoid Dendritic Cells This information is current as of September 28, 2021. Tae Whan Kim, Seunghee Hong, Yin Lin, Elise Murat, HyeMee Joo, Taeil Kim, Virginia Pascual and Yong-Jun Liu J Immunol 2016; 197:3348-3359; Prepublished online 14 September 2016; doi: 10.4049/jimmunol.1502385 Downloaded from http://www.jimmunol.org/content/197/8/3348 Supplementary http://www.jimmunol.org/content/suppl/2016/09/14/jimmunol.150238 http://www.jimmunol.org/ Material 5.DCSupplemental References This article cites 74 articles, 25 of which you can access for free at: http://www.jimmunol.org/content/197/8/3348.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 28, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Transcriptional Repression of IFN Regulatory Factor 7 by MYC Is Critical for Type I IFN Production in Human Plasmacytoid Dendritic Cells Tae Whan Kim,*,1 Seunghee Hong,*,1 Yin Lin,* Elise Murat,* HyeMee Joo,* Taeil Kim,†,2 Virginia Pascual,* and Yong-Jun Liu*,† Type I IFNs are crucial mediators of human innate and adaptive immunity and are massively produced from plasmacytoid dendritic cells (pDCs). -
OR10G4 (NM 001004462) Human Tagged ORF Clone Lentiviral Particle 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 RC222878L3V OR10G4 (NM_001004462) Human Tagged ORF Clone Lentiviral Particle Product data: Product Type: Lentiviral Particles Product Name: OR10G4 (NM_001004462) Human Tagged ORF Clone Lentiviral Particle Symbol: OR10G4 Synonyms: OR11-278 Vector: pLenti-C-Myc-DDK-P2A-Puro (PS100092) ACCN: NM_001004462 ORF Size: 933 bp ORF Nucleotide The ORF insert of this clone is exactly the same as(RC222878). Sequence: OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. RefSeq: NM_001004462.1, NP_001004462.1 RefSeq Size: 936 bp RefSeq ORF: 936 bp Locus ID: 390264 UniProt ID: Q8NGN3, A0A126GWS5 Protein Families: Transmembrane Protein Pathways: Olfactory transduction MW: 34.4 kDa 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 / 2 OR10G4 (NM_001004462) Human Tagged ORF Clone Lentiviral Particle – RC222878L3V Gene Summary: Olfactory receptors interact with odorant molecules in the nose, to initiate a neuronal response that triggers the perception of a smell. -
(12) Patent Application Publication (10) Pub. No.: US 2015/0023954 A1 Wu Et Al
US 2015 0023954A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2015/0023954 A1 Wu et al. (43) Pub. Date: Jan. 22, 2015 (54) POTENTIATING ANTIBODY-INDUCED GOIN33/574 (2006.01) COMPLEMENT-MEDIATED CYTOTOXCITY A613 L/4745 (2006.01) VAPI3K INHIBITION A613 L/4375 (2006.01) (52) U.S. Cl. (71) Applicant: MEMORIAL SLOAN-KETTERING CPC ....... A6IK39/39558 (2013.01); A61 K3I/4745 CANCER CENTER, New York, NY (2013.01); A61 K39/00II (2013.01); A61 K (US) 39/385 (2013.01); A61K31/4375 (2013.01); A6IK3I/5377 (2013.01); A61K.39/39 (72) Inventors: Xiaohong Wu, Forest Hills, NY (US); (2013.01); GOIN33/57484 (2013.01); CI2O Wolfgang W. Scholz, San Diego, CA I/6886 (2013.01); A61 K 2039/505 (2013.01); (US); Govind Ragupathi, New York, C12O 2600/16 (2013.01); C12O 2600/106 NY (US); Philip O. Livingston, (2013.01); A61K 2039/545 (2013.01) Bluffton, SC (US) USPC .................. 424/133.1; 424/277.1; 424/193.1; 424f1 74.1436/5O1435/7.1 : 506/9:435/7.92: (21) Appl. No.: 14/387,153 s s 435/6.12. 436/94 (22) PCT Filed: Mar. 14, 2013 (57) ABSTRACT (86). PCT No.: PCT/US 13/31278 Methodologies and technologies for potentiating antibody S371 (c)(1), based cancer treatments by increasing complement-mediated (2) Date: Sep. 22, 2014 cell cytotoxicity are disclosed. Further provided are method O O ologies and technologies for overcoming ineffective treat Related U.S. Application Data ments correlated with and/or caused by sub-lytic levels of (60) Provisional application No. -
Cellular and Molecular Signatures in the Disease Tissue of Early
Cellular and Molecular Signatures in the Disease Tissue of Early Rheumatoid Arthritis Stratify Clinical Response to csDMARD-Therapy and Predict Radiographic Progression Frances Humby1,* Myles Lewis1,* Nandhini Ramamoorthi2, Jason Hackney3, Michael Barnes1, Michele Bombardieri1, Francesca Setiadi2, Stephen Kelly1, Fabiola Bene1, Maria di Cicco1, Sudeh Riahi1, Vidalba Rocher-Ros1, Nora Ng1, Ilias Lazorou1, Rebecca E. Hands1, Desiree van der Heijde4, Robert Landewé5, Annette van der Helm-van Mil4, Alberto Cauli6, Iain B. McInnes7, Christopher D. Buckley8, Ernest Choy9, Peter Taylor10, Michael J. Townsend2 & Costantino Pitzalis1 1Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Departments of 2Biomarker Discovery OMNI, 3Bioinformatics and Computational Biology, Genentech Research and Early Development, South San Francisco, California 94080 USA 4Department of Rheumatology, Leiden University Medical Center, The Netherlands 5Department of Clinical Immunology & Rheumatology, Amsterdam Rheumatology & Immunology Center, Amsterdam, The Netherlands 6Rheumatology Unit, Department of Medical Sciences, Policlinico of the University of Cagliari, Cagliari, Italy 7Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK 8Rheumatology Research Group, Institute of Inflammation and Ageing (IIA), University of Birmingham, Birmingham B15 2WB, UK 9Institute of -
FGF Signaling Network in the Gastrointestinal Tract (Review)
163-168 1/6/06 16:12 Page 163 INTERNATIONAL JOURNAL OF ONCOLOGY 29: 163-168, 2006 163 FGF signaling network in the gastrointestinal tract (Review) MASUKO KATOH1 and MASARU KATOH2 1M&M Medical BioInformatics, Hongo 113-0033; 2Genetics and Cell Biology Section, National Cancer Center Research Institute, Tokyo 104-0045, Japan Received March 29, 2006; Accepted May 2, 2006 Abstract. Fibroblast growth factor (FGF) signals are trans- Contents duced through FGF receptors (FGFRs) and FRS2/FRS3- SHP2 (PTPN11)-GRB2 docking protein complex to SOS- 1. Introduction RAS-RAF-MAPKK-MAPK signaling cascade and GAB1/ 2. FGF family GAB2-PI3K-PDK-AKT/aPKC signaling cascade. The RAS~ 3. Regulation of FGF signaling by WNT MAPK signaling cascade is implicated in cell growth and 4. FGF signaling network in the stomach differentiation, the PI3K~AKT signaling cascade in cell 5. FGF signaling network in the colon survival and cell fate determination, and the PI3K~aPKC 6. Clinical application of FGF signaling cascade in cell polarity control. FGF18, FGF20 and 7. Clinical application of FGF signaling inhibitors SPRY4 are potent targets of the canonical WNT signaling 8. Perspectives pathway in the gastrointestinal tract. SPRY4 is the FGF signaling inhibitor functioning as negative feedback apparatus for the WNT/FGF-dependent epithelial proliferation. 1. Introduction Recombinant FGF7 and FGF20 proteins are applicable for treatment of chemotherapy/radiation-induced mucosal injury, Fibroblast growth factor (FGF) family proteins play key roles while recombinant FGF2 protein and FGF4 expression vector in growth and survival of stem cells during embryogenesis, are applicable for therapeutic angiogenesis. Helicobacter tissues regeneration, and carcinogenesis (1-4).