Table SI. Phosphorylated Proteins Identified in Rats with Cancer-Induced Bone Pain
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ABSTRACT ANGSTADT, ANDREA Y. Evaluation of the Genomic
ABSTRACT ANGSTADT, ANDREA Y. Evaluation of the Genomic Aberrations in Canine Osteosarcoma and Their Resemblance to the Human Counterpart. (Under the direction of Dr. Matthew Breen). In the last decade the domestic dog has emerged as an ideal biomedical model of complex genetic diseases such as cancers. Cancer in the dog occurs spontaneously and several studies have concluded that human and canine cancers have similar characteristics such as presentation of disease, rate of metastases, genetic dysregulation, and survival rates. Furthermore, in the genomic era the dog genome was found more homologous in sequence conservation to humans than mice, making it a valuable model organism for genetic study in addition to pathophysiological analysis. Osteosarcoma (OS), the most commonly diagnosed malignant bone tumor in humans and dogs, is one such cancer that would benefit from comparative genomic analysis. In humans, OS is a rare cancer diagnosed in fewer than 1,000 people per year in the USA, while in the domestic dog population the annual number of new cases is estimated to far exceed 10,000. This high rate of disease occurrence in dogs provides a unique opportunity to study the genomic imbalances in canine OS and their translational value to human OS as a means to identify important alterations involved in disease etiology. OS in humans is characterized by extremely complex karyotypes which contain both structural changes (translocations and/or rearrangements) and DNA copy number changes. Metaphase and array comparative genomic hybridization (aCGH) has assisted in uncovering the genetic imbalances that are associated with human OS phenotype. In dog OS, previous low-resolution (10-20Mb) aCGH analysis identified a wide range of recurrent copy number aberrations (CNAs), indicative of a similar level of genomic instability to human OS. -
1 1 Alpha-Smooth Muscle Actin (ACTA2) Is Required for Metastatic Potential of Human 1 Lung Adenocarcinoma 2 3 Hye Won Lee*1,2,3
Author Manuscript Published OnlineFirst on August 30, 2013; DOI: 10.1158/1078-0432.CCR-13-1181 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. 1 1 Alpha-smooth muscle actin (ACTA2) is required for metastatic potential of human 2 lung adenocarcinoma 3 4 Hye Won Lee*1,2,3, Young Mi Park*3,4, Se Jeong Lee1,4,5, Hyun Jung Cho1,2, Duk-Hwan Kim6,7, 5 Jung-Il Lee2, Myung-Soo Kang3, Ho Jun Seol2, Young Mog Shim8, Do-Hyun Nam1,2,3, Hyeon 6 Ho Kim3,4, Kyeung Min Joo1,3,4,5 7 8 Authors’ Affiliations: 9 1Cancer Stem Cell Research Center, 2Department of Neurosurgery, 3Department of Health 10 Sciences and Technology, Samsung Advanced Institute for Health Sciences and 11 Technology (SAIHST), 4Samsung Biomedical Research Institute, 5Department of Anatomy 12 and Cell Biology, 6Department of Molecular Cell Biology, 7Center for Genome Research, 13 8Department of Thoracic Surgery, Samsung Medical Center, Sungkyunkwan University 14 School of Medicine, Seoul, Korea 15 16 *These authors contributed equally to this work. 17 18 Running title: ACTA2 confers metastatic potential on lung adenocarcinoma 19 Keywords: Non-small cell lung adenocarcinoma, alpha-smooth muscle actin, migration, 20 invasion, metastasis 1 Downloaded from clincancerres.aacrjournals.org on September 26, 2021. © 2013 American Association for Cancer Research. Author Manuscript Published OnlineFirst on August 30, 2013; DOI: 10.1158/1078-0432.CCR-13-1181 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. 2 1 Financial support: This study was supported by a grant from the Korea Healthcare 2 Technology R&D Project, Ministry for Health & Welfare Affairs, Republic of Korea (A092255), 3 and the Basic Science Research Program, National Research Foundation of Korea by the 4 Ministry of Education, Science, and Technology (2011-009329 to H. -
Small Cell Ovarian Carcinoma: Genomic Stability and Responsiveness to Therapeutics
Gamwell et al. Orphanet Journal of Rare Diseases 2013, 8:33 http://www.ojrd.com/content/8/1/33 RESEARCH Open Access Small cell ovarian carcinoma: genomic stability and responsiveness to therapeutics Lisa F Gamwell1,2, Karen Gambaro3, Maria Merziotis2, Colleen Crane2, Suzanna L Arcand4, Valerie Bourada1,2, Christopher Davis2, Jeremy A Squire6, David G Huntsman7,8, Patricia N Tonin3,4,5 and Barbara C Vanderhyden1,2* Abstract Background: The biology of small cell ovarian carcinoma of the hypercalcemic type (SCCOHT), which is a rare and aggressive form of ovarian cancer, is poorly understood. Tumourigenicity, in vitro growth characteristics, genetic and genomic anomalies, and sensitivity to standard and novel chemotherapeutic treatments were investigated in the unique SCCOHT cell line, BIN-67, to provide further insight in the biology of this rare type of ovarian cancer. Method: The tumourigenic potential of BIN-67 cells was determined and the tumours formed in a xenograft model was compared to human SCCOHT. DNA sequencing, spectral karyotyping and high density SNP array analysis was performed. The sensitivity of the BIN-67 cells to standard chemotherapeutic agents and to vesicular stomatitis virus (VSV) and the JX-594 vaccinia virus was tested. Results: BIN-67 cells were capable of forming spheroids in hanging drop cultures. When xenografted into immunodeficient mice, BIN-67 cells developed into tumours that reflected the hypercalcemia and histology of human SCCOHT, notably intense expression of WT-1 and vimentin, and lack of expression of inhibin. Somatic mutations in TP53 and the most common activating mutations in KRAS and BRAF were not found in BIN-67 cells by DNA sequencing. -
PRODUCT SPECIFICATION Anti-C12orf43
Anti-C12orf43 Product Datasheet Polyclonal Antibody PRODUCT SPECIFICATION Product Name Anti-C12orf43 Product Number HPA046148 Gene Description chromosome 12 open reading frame 43 Clonality Polyclonal Isotype IgG Host Rabbit Antigen Sequence Recombinant Protein Epitope Signature Tag (PrEST) antigen sequence: AWGLEQRPHVAGKPRAGAANSQLSTSQPSLRHKVNEHEQDGNELQTTPEF RAHVAKKLGALLDSFITISEAAKEPAKAKVQKVALEDDGFRLFFTSVPGG REKEESPQPR Purification Method Affinity purified using the PrEST antigen as affinity ligand Verified Species Human Reactivity Recommended IHC (Immunohistochemistry) Applications - Antibody dilution: 1:50 - 1:200 - Retrieval method: HIER pH6 WB (Western Blot) - Working concentration: 0.04-0.4 µg/ml ICC-IF (Immunofluorescence) - Fixation/Permeabilization: PFA/Triton X-100 - Working concentration: 0.25-2 µg/ml Characterization Data Available at atlasantibodies.com/products/HPA046148 Buffer 40% glycerol and PBS (pH 7.2). 0.02% sodium azide is added as preservative. Concentration Lot dependent Storage Store at +4°C for short term storage. Long time storage is recommended at -20°C. Notes Gently mix before use. Optimal concentrations and conditions for each application should be determined by the user. For protocols, additional product information, such as images and references, see atlasantibodies.com. Product of Sweden. For research use only. Not intended for pharmaceutical development, diagnostic, therapeutic or any in vivo use. No products from Atlas Antibodies may be resold, modified for resale or used to manufacture commercial products without prior written approval from Atlas Antibodies AB. Warranty: The products supplied by Atlas Antibodies are warranted to meet stated product specifications and to conform to label descriptions when used and stored properly. Unless otherwise stated, this warranty is limited to one year from date of sales for products used, handled and stored according to Atlas Antibodies AB's instructions. -
Identification of the Binding Partners for Hspb2 and Cryab Reveals
Brigham Young University BYU ScholarsArchive Theses and Dissertations 2013-12-12 Identification of the Binding arP tners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactions and Non- Redundant Roles for Small Heat Shock Proteins Kelsey Murphey Langston Brigham Young University - Provo Follow this and additional works at: https://scholarsarchive.byu.edu/etd Part of the Microbiology Commons BYU ScholarsArchive Citation Langston, Kelsey Murphey, "Identification of the Binding Partners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactions and Non-Redundant Roles for Small Heat Shock Proteins" (2013). Theses and Dissertations. 3822. https://scholarsarchive.byu.edu/etd/3822 This Thesis is brought to you for free and open access by BYU ScholarsArchive. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of BYU ScholarsArchive. For more information, please contact [email protected], [email protected]. Identification of the Binding Partners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactions and Non-Redundant Roles for Small Heat Shock Proteins Kelsey Langston A thesis submitted to the faculty of Brigham Young University in partial fulfillment of the requirements for the degree of Master of Science Julianne H. Grose, Chair William R. McCleary Brian Poole Department of Microbiology and Molecular Biology Brigham Young University December 2013 Copyright © 2013 Kelsey Langston All Rights Reserved ABSTRACT Identification of the Binding Partners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactors and Non-Redundant Roles for Small Heat Shock Proteins Kelsey Langston Department of Microbiology and Molecular Biology, BYU Master of Science Small Heat Shock Proteins (sHSP) are molecular chaperones that play protective roles in cell survival and have been shown to possess chaperone activity. -
Table 1 Gene Name Increased Or Decreased in LTD
Table_1 gene_name increased or decreased in LTD protein_id description keep_supernatant keep_pellet comparison sample hit_annotation_methodpvalue fdr hit hit_annotation 2010300C02RIK increased E9Q3M9 Protein 2010300C02Rik OS=Mus musculus GN=2010300C02Rik PE=1 SV=1 TRUE TRUE NMDA - control pellet fdrtool 0,074667 0,584087 FALSE trend 2310035C23RIK|KIAA1468increased A0A087WSS1|E9QM90|Q148V7|Q148V7-2 Protein 2310035C23Rik OS=Mus musculus GN=2310035C23Rik PE=1 SV=1|Protein 2310035C23Rik OS=Mus musculusTRUE GN=2310035C23Rik PE=1 SV=2|LisH FALSE domain NMDAand HEAT - control repeat-containing protein KIAA1468 supernatant OS=Mus musculus GN=Kiaa1468 fdrtoolPE=1 SV=1|Isoform 0,080056 2 of 0,589077LisH domain FALSEand HEAT trend repeat-containing protein KIAA1468 OS=Mus musculus GN=Kiaa1468 ABR increased E9PUE7|Q5SSL4|Q5SSL4-2|Q5SSL4-3|Q5SSL4-4 Active breakpoint cluster region-related protein OS=Mus musculus GN=Abr PE=1 SV=1|Isoform 2 of Active breakpointTRUE cluster region-related protein TRUE OS=Mus musculus NMDA GN=Abr|Isoform - control 3 of Active breakpoint supernatant cluster region-related protein OS=Mus fdrtool musculus 0,08128 GN=Abr|Isoform 0,592743 4 of Active FALSE breakpoint trend cluster region-related protein OS=Mus musculus GN=Abr ADAM22 increased D3YUP9|Q9R1V6|Q9R1V6-10|Q9R1V6-11|Q9R1V6-12|Q9R1V6-13|Q9R1V6-14|Q9R1V6-15|Q9R1V6-17|Q9R1V6-4|Q9R1V6-5|Q9R1V6-6|Q9R1V6-7|Q9R1V6-8Disintegrin and metalloproteinase domain-containing protein 22 OS=Mus musculus GN=Adam22 PE=1 SV=1|DisintegrinFALSE and metalloproteinase domain-containing TRUE -
Differential Physiological Role of BIN1 Isoforms in Skeletal Muscle Development, Function and Regeneration
bioRxiv preprint doi: https://doi.org/10.1101/477950; this version posted December 11, 2018. 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. Differential physiological role of BIN1 isoforms in skeletal muscle development, function and regeneration Ivana Prokic1,2,3,4, Belinda Cowling1,2,3,4, Candice Kutchukian5, Christine Kretz1,2,3,4, Hichem Tasfaout1,2,3,4, Josiane Hergueux1,2,3,4, Olivia Wendling1,2,3,4, Arnaud Ferry10, Anne Toussaint1,2,3,4, Christos Gavriilidis1,2,3,4, Vasugi Nattarayan1,2,3,4, Catherine Koch1,2,3,4, Jeanne Lainné6,7, Roy Combe2,3,4,8, Laurent Tiret9, Vincent Jacquemond5, Fanny Pilot-Storck9, Jocelyn Laporte1,2,3,4 1Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France 2Centre National de la Recherche Scientifique (CNRS), UMR7104, Illkirch, France 3Institut National de la Santé et de la Recherche Médicale (INSERM), U1258, Illkirch, France 4Université de Strasbourg, Illkirch, France 5Univ Lyon, Université Claude Bernard Lyon 1, CNRS UMR-5310, INSERM U-1217, Institut NeuroMyoGène, 8 avenue Rockefeller, 69373 Lyon, France 6Sorbonne Université, INSERM, Institute of Myology, Centre of Research in Myology, UMRS 974, F- 75013, Paris, France 7Sorbonne Université, Department of Physiology, UPMC Univ Paris 06, Pitié-Salpêtrière Hospital, F- 75013, Paris, France 8CELPHEDIA-PHENOMIN, Institut Clinique de la Souris (ICS), Illkirch, France 9U955 – IMRB, Team 10 - Biology of the neuromuscular system, Inserm, UPEC, Ecole nationale vétérinaire d’Alfort, Maisons-Alfort, 94700, France 10Sorbonne Université, INSERM, Institute of Myology, Centre of Research in Myology, UMRS 794, F- 75013, Paris, France Correspondence to: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/477950; this version posted December 11, 2018. -
Structural Characterization of Polysaccharides from Cordyceps Militaris and Their Hypolipidemic Effects Cite This: RSC Adv.,2018,8,41012 in High Fat Diet Fed Mice†
RSC Advances View Article Online PAPER View Journal | View Issue Structural characterization of polysaccharides from Cordyceps militaris and their hypolipidemic effects Cite this: RSC Adv.,2018,8,41012 in high fat diet fed mice† Zhen-feng Huang, ‡ Ming-long Zhang,‡ Song Zhang,* Ya-hui Wang and Xue-wen Jiang Cordyceps militaris is a crude dietary therapeutic mushroom with high nutritional and medicinal values. Mushroom-derived polysaccharides have been found to possess antihyperglycemic and antihyperlipidemic activities. This study aimed to partially clarify the structural characterization and comparatively evaluate hypolipidemic potentials of intracellular- (IPCM) and extracellular polysaccharides of C. militaris (EPCM) in high fat diet fed mice. Results indicated that IPCM-2 is a-pyran polysaccharide with an average molecular weight of 32.5 kDa, was mainly composed of mannose, glucose and galactose with mass percentages of 51.94%, 10.54%, and 37.25%, respectively. EPCM-2 is an a-pyran Creative Commons Attribution 3.0 Unported Licence. polysaccharide with an average molecular weight of 20 kDa that is mainly composed of mannose, glucose and galactose with mass percentages of 44.51%, 18.33%, and 35.38%, respectively. In in vivo study, EPCM-1 treatment (100 mg kgÀ1 dÀ1) showed potential effects on improving serum lipid profiles of hyperlipidemic mice, reflected by decreasing serum total cholesterol (TC), triglyceride (TG) and low density lipoprotein-cholesterol (LDL-C) levels by 20.05%, 45.45% and 52.63%, respectively, while IPCM-1 treatment -
Table S1 the Four Gene Sets Derived from Gene Expression Profiles of Escs and Differentiated Cells
Table S1 The four gene sets derived from gene expression profiles of ESCs and differentiated cells Uniform High Uniform Low ES Up ES Down EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol 269261 Rpl12 11354 Abpa 68239 Krt42 15132 Hbb-bh1 67891 Rpl4 11537 Cfd 26380 Esrrb 15126 Hba-x 55949 Eef1b2 11698 Ambn 73703 Dppa2 15111 Hand2 18148 Npm1 11730 Ang3 67374 Jam2 65255 Asb4 67427 Rps20 11731 Ang2 22702 Zfp42 17292 Mesp1 15481 Hspa8 11807 Apoa2 58865 Tdh 19737 Rgs5 100041686 LOC100041686 11814 Apoc3 26388 Ifi202b 225518 Prdm6 11983 Atpif1 11945 Atp4b 11614 Nr0b1 20378 Frzb 19241 Tmsb4x 12007 Azgp1 76815 Calcoco2 12767 Cxcr4 20116 Rps8 12044 Bcl2a1a 219132 D14Ertd668e 103889 Hoxb2 20103 Rps5 12047 Bcl2a1d 381411 Gm1967 17701 Msx1 14694 Gnb2l1 12049 Bcl2l10 20899 Stra8 23796 Aplnr 19941 Rpl26 12096 Bglap1 78625 1700061G19Rik 12627 Cfc1 12070 Ngfrap1 12097 Bglap2 21816 Tgm1 12622 Cer1 19989 Rpl7 12267 C3ar1 67405 Nts 21385 Tbx2 19896 Rpl10a 12279 C9 435337 EG435337 56720 Tdo2 20044 Rps14 12391 Cav3 545913 Zscan4d 16869 Lhx1 19175 Psmb6 12409 Cbr2 244448 Triml1 22253 Unc5c 22627 Ywhae 12477 Ctla4 69134 2200001I15Rik 14174 Fgf3 19951 Rpl32 12523 Cd84 66065 Hsd17b14 16542 Kdr 66152 1110020P15Rik 12524 Cd86 81879 Tcfcp2l1 15122 Hba-a1 66489 Rpl35 12640 Cga 17907 Mylpf 15414 Hoxb6 15519 Hsp90aa1 12642 Ch25h 26424 Nr5a2 210530 Leprel1 66483 Rpl36al 12655 Chi3l3 83560 Tex14 12338 Capn6 27370 Rps26 12796 Camp 17450 Morc1 20671 Sox17 66576 Uqcrh 12869 Cox8b 79455 Pdcl2 20613 Snai1 22154 Tubb5 12959 Cryba4 231821 Centa1 17897 -
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. -
An Animal Model with a Cardiomyocyte-Specific Deletion of Estrogen Receptor Alpha: Functional, Metabolic, and Differential Netwo
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2014 An animal model with a cardiomyocyte-specific deletion of estrogen receptor alpha: Functional, metabolic, and differential network analysis Sriram Devanathan Washington University School of Medicine in St. Louis Timothy Whitehead Washington University School of Medicine in St. Louis George G. Schweitzer Washington University School of Medicine in St. Louis Nicole Fettig Washington University School of Medicine in St. Louis Attila Kovacs Washington University School of Medicine in St. Louis See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Devanathan, Sriram; Whitehead, Timothy; Schweitzer, George G.; Fettig, Nicole; Kovacs, Attila; Korach, Kenneth S.; Finck, Brian N.; and Shoghi, Kooresh I., ,"An animal model with a cardiomyocyte-specific deletion of estrogen receptor alpha: Functional, metabolic, and differential network analysis." PLoS One.9,7. e101900. (2014). https://digitalcommons.wustl.edu/open_access_pubs/3326 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. Authors Sriram Devanathan, Timothy Whitehead, George G. Schweitzer, Nicole Fettig, Attila Kovacs, Kenneth S. Korach, Brian N. Finck, and Kooresh I. Shoghi This open access publication is available at Digital Commons@Becker: https://digitalcommons.wustl.edu/open_access_pubs/3326 An Animal Model with a Cardiomyocyte-Specific Deletion of Estrogen Receptor Alpha: Functional, Metabolic, and Differential Network Analysis Sriram Devanathan1, Timothy Whitehead1, George G. Schweitzer2, Nicole Fettig1, Attila Kovacs3, Kenneth S. -
Dual Proteome-Scale Networks Reveal Cell-Specific Remodeling of the Human Interactome
bioRxiv preprint doi: https://doi.org/10.1101/2020.01.19.905109; this version posted January 19, 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. Dual Proteome-scale Networks Reveal Cell-specific Remodeling of the Human Interactome Edward L. Huttlin1*, Raphael J. Bruckner1,3, Jose Navarrete-Perea1, Joe R. Cannon1,4, Kurt Baltier1,5, Fana Gebreab1, Melanie P. Gygi1, Alexandra Thornock1, Gabriela Zarraga1,6, Stanley Tam1,7, John Szpyt1, Alexandra Panov1, Hannah Parzen1,8, Sipei Fu1, Arvene Golbazi1, Eila Maenpaa1, Keegan Stricker1, Sanjukta Guha Thakurta1, Ramin Rad1, Joshua Pan2, David P. Nusinow1, Joao A. Paulo1, Devin K. Schweppe1, Laura Pontano Vaites1, J. Wade Harper1*, Steven P. Gygi1*# 1Department of Cell Biology, Harvard Medical School, Boston, MA, 02115, USA. 2Broad Institute, Cambridge, MA, 02142, USA. 3Present address: ICCB-Longwood Screening Facility, Harvard Medical School, Boston, MA, 02115, USA. 4Present address: Merck, West Point, PA, 19486, USA. 5Present address: IQ Proteomics, Cambridge, MA, 02139, USA. 6Present address: Vor Biopharma, Cambridge, MA, 02142, USA. 7Present address: Rubius Therapeutics, Cambridge, MA, 02139, USA. 8Present address: RPS North America, South Kingstown, RI, 02879, USA. *Correspondence: [email protected] (E.L.H.), [email protected] (J.W.H.), [email protected] (S.P.G.) #Lead Contact: [email protected] bioRxiv preprint doi: https://doi.org/10.1101/2020.01.19.905109; this version posted January 19, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder.