PP1RA Polyclonal Antibody Product Information

Total Page：16

File Type：pdf, Size：1020Kb

PP1RA Polyclonal Antibody Product Information

PP1RA Polyclonal Antibody Cat #: ABP59975 Size: 30μl /100μl /200μl Product Information Product Name: PP1RA Polyclonal Antibody Applications: WB, ELISA Isotype: Rabbit IgG Reactivity: Human, Mouse, Rat Catalog Number: ABP59975 Lot Number: Refer to product label Formulation: Liquid Concentration: 1 mg/ml Storage: Store at -20°C. Avoid repeated Note: Contain sodium azide. freeze / thaw cycles. Background: PPP1R10 (Protein Phosphatase 1 Regulatory Subunit 10) is a Protein Coding gene. Diseases associated with PPP1R10 include Malignant Melanoma, Somatic. Among its related pathways are Beta-Adrenergic Signaling and Activation of cAMP-Dependent PKA. PPP1R10 encodes a protein phosphatase 1 binding protein. The encoded protein plays a role in many cellular processes including cell cycle progression, DNA repair and apoptosis by regulating the activity of protein phosphatase 1. PPP1R10 lies within the major histocompatibility complex class I region on chromosome 6 and alternatively spliced transcript variants have been observed for PPP1R10. Application Notes: Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB (1:500-1:2000), ELISA (1:5000-1:20000). Storage Buffer: PBS, pH 7.4, containing 0.02% Sodium Azide as preservative and 50% Glycerol. Storage Instructions: Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing. Note: The product listed herein is for research use only and is not intended for use in human or clinical diagnosis. Suggested applications of our products are not recommendations to use our products in violation of any patent or as a license. We cannot be responsible for patent infringements or other violations that may occur with the use of this product. Version 201805 Abbkine, Inc • China • www.abbkine.com Not for further distribution without written consent.Copyright © Abbkine, Inc..

Copy Link

Recommended publications

Evidence for Differential Alternative Splicing in Blood of Young Boys With
Stamova et al. Molecular Autism 2013, 4:30 http://www.molecularautism.com/content/4/1/30 RESEARCH Open Access Evidence for differential alternative splicing in blood of young boys with autism spectrum disorders Boryana S Stamova1,2,5*, Yingfang Tian1,2,4, Christine W Nordahl1,3, Mark D Shen1,3, Sally Rogers1,3, David G Amaral1,3 and Frank R Sharp1,2 Abstract Background: Since RNA expression differences have been reported in autism spectrum disorder (ASD) for blood and brain, and differential alternative splicing (DAS) has been reported in ASD brains, we determined if there was DAS in blood mRNA of ASD subjects compared to typically developing (TD) controls, as well as in ASD subgroups related to cerebral volume. Methods: RNA from blood was processed on whole genome exon arrays for 2-4–year-old ASD and TD boys. An ANCOVA with age and batch as covariates was used to predict DAS for ALL ASD (n=30), ASD with normal total cerebral volumes (NTCV), and ASD with large total cerebral volumes (LTCV) compared to TD controls (n=20). Results: A total of 53 genes were predicted to have DAS for ALL ASD versus TD, 169 genes for ASD_NTCV versus TD, 1 gene for ASD_LTCV versus TD, and 27 genes for ASD_LTCV versus ASD_NTCV. These differences were significant at P <0.05 after false discovery rate corrections for multiple comparisons (FDR <5% false positives). A number of the genes predicted to have DAS in ASD are known to regulate DAS (SFPQ, SRPK1, SRSF11, SRSF2IP, FUS, LSM14A). In addition, a number of genes with predicted DAS are involved in pathways implicated in previous ASD studies, such as ROS monocyte/macrophage, Natural Killer Cell, mTOR, and NGF signaling.
[Show full text]
Pharmacodynamic Effects of Seliciclib, an Orally Administered
Cancer Therapy: Clinical Pharmacodynamic Effects of Seliciclib, an Orally Administered Cell Cycle Modulator, in Undifferentiated Nasopharyngeal Cancer Wen-Son Hsieh,4 Ross Soo,1Bee-Keow Peh,2 Thomas Loh,4 Difeng Dong,3 Donny Soh,5 Lim-SoonWong,3,5 Simon Green,6 Judy Chiao,6 Chun-Ying Cui,1Yo k e -F o n g L a i , 4 Soo-Chin Lee,1Benjamin Mow,1 Richie Soong,2 Manuel Salto-Tellez,2 and Boon-Cher Goh1, 2 Abstract Purpose: Cell cycle dysregulation resulting in expression of antiapoptotic genes and uncontrolled proliferation is a feature of undifferentiated nasopharyngeal carcinoma. The pharmacodynamic effects of seliciclib, a cyclin-dependent kinase (CDK) inhibitor, were studied in patients with nasopharyngeal carcinoma. Experimental Design: Patients with treatment-naI«ve locally advanced nasopharyngeal carci- noma received seliciclib at 800 mg or 400 mg twice daily on days1 to 3 and 8 to12.Paired tumor samples obtained at baseline and on day 13 were assessed by light microscopy, immunohisto- chemistry, and transcriptionalprofiling using real-time PCR low-density array consisting of apanel of 380 genes related to cell cycle inhibition, apoptosis, signal transduction, and cell proliferation. Results: At 800 mg bd, one patient experienced grade 3 liver toxicity and another had grade 2 vomiting; no significant toxicities were experienced in 13 patients treated at 400 mg bd. Seven of fourteen evaluable patients had clinical evidence of tumor reduction. Some of these responses were associated with increased tumor apoptosis, necrosis, and decreases in plasma EBV DNA posttreatment. Reduced protein expression of Mcl-1, cyclin D1, phosphorylated retinoblastoma protein pRB (T821), and significant transcriptional down-regulation of genes related to cellular proliferation and survival were shown in some patients posttreatment, indicative of cell cycle modulation by seliciclib, more specifically inhibition of cdk2/cyclin E, cdk7/cyclin H, and cdk9/cyclinT.
[Show full text]
Transcriptional Recapitulation and Subversion Of
Open Access Research2007KaiseretVolume al. 8, Issue 7, Article R131 Transcriptional recapitulation and subversion of embryonic colon comment development by mouse colon tumor models and human colon cancer Sergio Kaiser¤*, Young-Kyu Park¤†, Jeffrey L Franklin†, Richard B Halberg‡, Ming Yu§, Walter J Jessen*, Johannes Freudenberg*, Xiaodi Chen‡, Kevin Haigis¶, Anil G Jegga*, Sue Kong*, Bhuvaneswari Sakthivel*, Huan Xu*, Timothy Reichling¥, Mohammad Azhar#, Gregory P Boivin**, reviews Reade B Roberts§, Anika C Bissahoyo§, Fausto Gonzales††, Greg C Bloom††, Steven Eschrich††, Scott L Carter‡‡, Jeremy E Aronow*, John Kleimeyer*, Michael Kleimeyer*, Vivek Ramaswamy*, Stephen H Settle†, Braden Boone†, Shawn Levy†, Jonathan M Graff§§, Thomas Doetschman#, Joanna Groden¥, William F Dove‡, David W Threadgill§, Timothy J Yeatman††, reports Robert J Coffey Jr† and Bruce J Aronow* Addresses: *Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA. †Departments of Medicine, and Cell and Developmental Biology, Vanderbilt University and Department of Veterans Affairs Medical Center, Nashville, TN 37232, USA. ‡McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI 53706, USA. §Department of Genetics and Lineberger Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA. ¶Molecular Pathology Unit and Center for Cancer Research, Massachusetts deposited research General Hospital, Charlestown, MA 02129, USA. ¥Division of Human Cancer Genetics, The Ohio State University College of Medicine, Columbus, Ohio 43210-2207, USA. #Institute for Collaborative BioResearch, University of Arizona, Tucson, AZ 85721-0036, USA. **University of Cincinnati, Department of Pathology and Laboratory Medicine, Cincinnati, OH 45267, USA. ††H Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA. ‡‡Children's Hospital Informatics Program at the Harvard-MIT Division of Health Sciences and Technology (CHIP@HST), Harvard Medical School, Boston, Massachusetts 02115, USA.
[Show full text]
Multiomic Analysis of the UV-Induced DNA Damage Response
Multiomic Analysis of the UV-Induced DNA Damage Response The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Boeing, Stefan, Laura Williamson, Vesela Encheva, Ilaria Gori, Rebecca E. Saunders, Rachael Instrell, Ozan Aygün, et al. “Multiomic Analysis of the UV-Induced DNA Damage Response.” Cell Reports 15, no. 7 (May 2016): 1597–1610. As Published http://dx.doi.org/10.1016/j.celrep.2016.04.047 Publisher Elsevier Version Final published version Citable link http://hdl.handle.net/1721.1/105271 Terms of Use Creative Commons Attribution 4.0 International License Detailed Terms http://creativecommons.org/licenses/by/4.0/ Resource Multiomic Analysis of the UV-Induced DNA Damage Response Graphical Abstract Authors Stefan Boeing, Laura Williamson, Vesela Encheva, ..., Michael Howell, Ambrosius P. Snijders, Jesper Q. Svejstrup Correspondence [email protected] In Brief Boeing et al. investigate the UV-induced DNA damage response by combining a range of proteomic and genomic screens. A function in this response for the melanoma driver STK19 as well as a number of other factors are uncovered. Highlights d A multiomic screening approach examines the UV-induced DNA damage response d Multiple factors are connected to the transcription-related DNA damage response d Melanoma gene STK19 is required for a normal DNA damage response Boeing et al., 2016, Cell Reports 15, 1597–1610 May 17, 2016 ª 2016 The Author(s) http://dx.doi.org/10.1016/j.celrep.2016.04.047 Cell Reports Resource Multiomic Analysis of the UV-Induced DNA Damage Response Stefan Boeing,1,5 Laura Williamson,1 Vesela Encheva,2 Ilaria Gori,3 Rebecca E.
[Show full text]
Lecture 15. Chromhmm & ENCODE
Lecture 15. ChromHMM & ENCODE Michael Schatz March 23, 2020 JHU 601.749: Applied Comparative Genomics Assignment 5: Due Mon Mar 23 Project Proposal: Due Mon Mar 23 *-seq in 4 short vignettes RNA-seq Methyl-seq ChIP-seq Hi-C Human Evolution ~5 Mya ~75 Mya ~100 Mya ~160 and 210 Mya As expected, the majority of platypus genes (82%; 15,312 out of 18,596) have orthologues in these five other amniotes (Supplementary Table 5). The remaining 'orphan' genes are expected to primarily reflect rapidly evolving genes, for which no other homologues are discernible, erroneous predictions, and true lineage-specific genes that have been lost in each of the other five species under consideration. Genome analysis of the platypus reveals unique signatures of evolution (2008) Nature. 453, 175-183 doi:10.1038/nature06936 Methyl-seq Finding the fifth base: Genome-wide sequencing of cytosine methylation Lister and Ecker (2009) Genome Research. 19: 959-966 Bisulfite Conversion Treating DNA with sodium bisulfite will convert unmethylated C to T • 5-MethyC will be protected and not change, so can look for differences when mapping • Requires great care when analyzing reads, since the complementary strand will also be converted (G to A) • Typically analyzed by mapping to a “reduced alphabet” where we assume all Cs are converted to Ts once on the forward strand and once on the reverse Bismark: a flexible aligner and methylation caller for Bisulfite-Seq applications Krueger and Andrews (2010) Bioinformatics. 27 (11): 1571-1572. ChIP-seq Genome-wide mapping of in vivo protein-DNA interactions. Johnson et al (2007) Science.
[Show full text]
Learning Chroma\N States from Chip-‐Seq Data
Learning Chroman States from ChIP-seq data Luca Pinello GC Yuan Lab Outline • Chroman structure, histone modificaons and combinatorial paerns • How to segment the genome in chroman states • How to use ChromHMM step by step • Further references 2 Epigene-cs and chroman structure • All (almost) the cells of our body share the same genome but have very different gene expression programs…. 3 h?p://jpkc.scu.edu.cn/ywwy/zbsw(E)/edetail12.htm The code over the code • The chroman structure and the accessibility are mainly controlled by: 1. Nucleosome posioning, 2. DNA methylaon, 3. Histone modificaons. 4 Histone Modificaons Specific histone modificaons or combinaons of modificaons confer unique biological func-ons to the region of the genome associated with them: • H3K4me3: promoters, gene acva.on • H3K27me3: promoters, poised enhancers, gene silencing • H2AZ: promoters • H3K4me1: enhancers • H3K36me3: transcribed regions • H3K9me3: gene silencing • H3k27ac: acve enhancers 5 Examples of *-Seq Measuring the genome genome fragmentation assembler DNA DNA reads “genome” ChIP-seq to measure histone data fragments Measuring the regulome (e.g., protein-binding of the genome) Chromatin Immunopreciptation genomic (ChIP) + intervals fragmentation Protein - peak caller bound by DNA bound DNA reads proteins REVIEWS fragments a also informative, as this ratio corresponds to the fraction ChIP–chip of nucleosomes with the particular modification at that location, averaged over all the cells assayed. One of the difficulties in conducting a ChIP–seq con- trol experiment is the large amount of sequencing that ChIP–seq may be necessary. For input DNA and bulk nucleosomes, many of the sequenced tags are spread evenly across the genome.
[Show full text]
Protein Phosphatase Regulatory Protein 10 Cooperates with Neurofibromin Inactivation in Myeloid Leukemogenesis
PROTEIN PHOSPHATASE REGULATORY PROTEIN 10 COOPERATES WITH NEUROFIBROMIN INACTIVATION IN MYELOID LEUKEMOGENESIS By ANGELA HADJIPANAYIS A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA 2008 1 © 2008 Angela Hadjipanayis 2 This work is dedicated to my extended family who never had the opportunity to obtain higher education. To my parents and husband for their loving support and belief in my abilities. To Camilynn I. Brannan whose research expertise led to the discovery of this locus. 3 ACKNOWLEDGMENTS First, I would like to thank my mentor Peggy Wallace for her indispensable support over the years, her encouragement, and her advice on how to become a better scientist. Second, I would like to thank my husband for taking a leap of faith in life and moving to Florida with me when he didn’t have a job at the time. Third, I would like to thank my parents for their love, support, and advice over the years. Fourth, I would like to thank my other committee members, Dr. Jim Resnick, Dr. Paul Oh, Dr. Stephen Hunger and Dr. Dan Driscoll for their valuable advice on the project. I also would like to thank Dr. Jennifer Embury for the tremendous effort on all the pathology of the mice. In addition, I would like to thank Dr. Kevin Shannon and Dr. Scott Kogan for their leukemia expertise and strategies in modeling leukemia. Lastly, I would like to thank the lab for their help on this project, their jokes, and all their personalities that made the days seem not as long.
[Show full text]
Live-Cell Imaging Rnai Screen Identifies PP2A–B55α and Importin-Β1 As Key Mitotic Exit Regulators in Human Cells
LETTERS Live-cell imaging RNAi screen identifies PP2A–B55α and importin-β1 as key mitotic exit regulators in human cells Michael H. A. Schmitz1,2,3, Michael Held1,2, Veerle Janssens4, James R. A. Hutchins5, Otto Hudecz6, Elitsa Ivanova4, Jozef Goris4, Laura Trinkle-Mulcahy7, Angus I. Lamond8, Ina Poser9, Anthony A. Hyman9, Karl Mechtler5,6, Jan-Michael Peters5 and Daniel W. Gerlich1,2,10 When vertebrate cells exit mitosis various cellular structures can contribute to Cdk1 substrate dephosphorylation during vertebrate are re-organized to build functional interphase cells1. This mitotic exit, whereas Ca2+-triggered mitotic exit in cytostatic-factor- depends on Cdk1 (cyclin dependent kinase 1) inactivation arrested egg extracts depends on calcineurin12,13. Early genetic studies in and subsequent dephosphorylation of its substrates2–4. Drosophila melanogaster 14,15 and Aspergillus nidulans16 reported defects Members of the protein phosphatase 1 and 2A (PP1 and in late mitosis of PP1 and PP2A mutants. However, the assays used in PP2A) families can dephosphorylate Cdk1 substrates in these studies were not specific for mitotic exit because they scored pro- biochemical extracts during mitotic exit5,6, but how this relates metaphase arrest or anaphase chromosome bridges, which can result to postmitotic reassembly of interphase structures in intact from defects in early mitosis. cells is not known. Here, we use a live-cell imaging assay and Intracellular targeting of Ser/Thr phosphatase complexes to specific RNAi knockdown to screen a genome-wide library of protein substrates is mediated by a diverse range of regulatory and targeting phosphatases for mitotic exit functions in human cells. We subunits that associate with a small group of catalytic subunits3,4,17.
[Show full text]
PPP1R10 (NM 002714) Human Tagged ORF Clone Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for RG221507 PPP1R10 (NM_002714) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: PPP1R10 (NM_002714) Human Tagged ORF Clone Tag: TurboGFP Symbol: PPP1R10 Synonyms: CAT53; FB19; p99; PNUTS; PP1R10; R111 Vector: pCMV6-AC-GFP (PS100010) E. coli Selection: Ampicillin (100 ug/mL) Cell Selection: Neomycin 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 / 4 PPP1R10 (NM_002714) Human Tagged ORF Clone – RG221507 ORF Nucleotide >RG221507 representing NM_002714 Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGGGTTCGGGTCCCATAGACCCCAAAGAACTTCTCAAGGGCCTGGACAGCTTCCTTAACCGAGATGGGG AAGTCAAAAGTGTGGATGGGATTTCCAAGATCTTCAGTTTGATGAAGGAAGCACGAAAGATGGTGAGTCG ATGCACTTACTTGAACATTCTCCTGCAGACCCGTTCACCAGAAATATTGGTCAAATTTATTGACGTTGGC GGCTACAAACTTCTTAACAATTGGCTGACGTATTCAAAGACAACCAACAACATTCCCCTCCTCCAGCAAA TTCTACTGACCCTGCAGCATCTACCGCTCACTGTAGACCATCTCAAGCAGAACAACACAGCTAAACTGGT GAAGCAGCTGAGCAAGTCAAGTGAGGATGAAGAGCTCCGGAAATTGGCCTCAGTCCTTGTCAGCGACTGG ATGGCTGTCATCCGCTCTCAGAGCAGTACCCAGCCTGCTGAGAAAGATAAGAAGAAACGTAAAGATGAAG GAAAAAGTCGAACTACCCTTCCTGAGCGACCTTTGACAGAGGTGAAGGCTGAGACCCGGGCTGAGGAGGC CCCAGAGAAGAAGAGGGAGAAGCCCAAGTCTCTTCGCACCACAGCACCCAGTCATGCCAAGTTCCGTTCC
[Show full text]
Organization of the Class I Region of the Bovine Major
ORGANIZATION OF THE CLASS I REGION OF THE BOVINE MAJOR HISTOCOMPATIBILITY COMPLEX (BOLA) AND THE CHARACTERIZATION OF A CLASS I FRAMESHIFT DELETION (BOLA-Adel) PREVALENT IN FERAL BOVIDS A Dissertation by NICOLE RAMLACHAN Submitted to the Office of Graduate Studies of Texas A&M University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY December 2004 Major Subject: Genetics ORGANIZATION OF THE CLASS I REGION OF THE BOVINE MAJOR HISTOCOMPATIBILITY COMPLEX (BOLA) AND THE CHARACTERIZATION OF A CLASS I FRAMESHIFT DELETION (BOLA-Adel) PREVALENT IN FERAL BOVIDS A Dissertation by NICOLE RAMLACHAN Submitted to Texas A&M University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY Approved as to style and content by: _________________________ _________________________ Loren C. Skow Bhanu P. Chowdhary (Chair of Committee) (Member) _________________________ _________________________ James E. Womack Rajesh C. Miranda (Member) (Member) _________________________ _________________________ Geoffrey M. Kapler Evelyn Tiffany-Castiglioni (Chair of Genetics Faculty) (Head of Department) December 2004 Major Subject: Genetics iii ABSTRACT Organization of the Class I Region of the Bovine Major Histocompatibility Complex (BoLA) and the Characterization of a Class I Frameshift Deletion (BoLA-Adel) Prevalent in Feral Bovids. (December 2004) Nicole Ramlachan, B.Sc., University of Guelph, Ontario, Canada; M.Sc., University of Guelph, Ontario, Canada Chair of Advisory Committee: Dr. Loren Skow The major histocompatibility complex (MHC) is a genomic region containing genes of immunomodulatory importance. MHC class I genes encode cell-surface glycoproteins that present peptides to circulating T cells, playing a key role in recognition of self and non-self. Studies of MHC loci in vertebrates have examined levels of polymorphism and molecular evolutionary processes generating diversity.
[Show full text]
Novel DNA Damage Checkpoints Mediating Cell Death Induced by the NEDD8-Activating Enzyme Inhibitor MLN4924
Published OnlineFirst October 24, 2012; DOI: 10.1158/0008-5472.CAN-12-1729 Cancer Molecular and Cellular Pathobiology Research Novel DNA Damage Checkpoints Mediating Cell Death Induced by the NEDD8-Activating Enzyme Inhibitor MLN4924 Jonathan L. Blank1, Xiaozhen J. Liu1, Katherine Cosmopoulos1, David C. Bouck1, Khristofer Garcia1, Hugues Bernard1, Olga Tayber1, Greg Hather2, Ray Liu2, Usha Narayanan1, Michael A. Milhollen1, and Eric S. Lightcap1 Abstract MLN4924 is an investigational small-molecule inhibitor of the NEDD8-activating enzyme (NAE) in phase I clinical trials. NAE inhibition prevents the ubiquitination and proteasomal degradation of substrates for cullin-RING ubiquitin E3 ligases that support cancer pathophysiology, but the genetic determinants conferring sensitivity to NAE inhibition are unknown. To address this gap in knowledge, we conducted a genome-wide siRNA screen to identify genes and pathways that affect the lethality of MLN4924 in melanoma cells. Of the 154 genes identiﬁed, approximately one-half interfered with components of the cell cycle, apoptotic machinery, ubiquitin system, and DNA damage response pathways. In particular, genes involved in DNA replication, p53, BRCA1/BRCA2, transcrip- tion-coupled repair, andbaseexcisionrepair seemedtobeimportantforMLN4924lethality. Incontrast, geneswithin the G2–M checkpoint affected sensitivity to MLN4924 in colon cancer cells. Cell-cycle analysis in melanoma cells by ﬂow cytometry following RNAi-mediated silencing showed that MLN4924 prevented the transition of cells from S– G2 phase after induction of rereplication stress. Our analysis suggested an important role for the p21-dependent intra-S-phase checkpoint and extensive rereplication, whereas the ATR-dependent intra-S-phase checkpoint seemed to play a less dominant role. Unexpectedly, induction of the p21-dependent intra-S-phase checkpoint seemed to be independent of both Cdt1 stabilization and ATR signaling.
[Show full text]
SUPPORTING INFORMATION for Regulation of Gene Expression By
SUPPORTING INFORMATION for Regulation of gene expression by the BLM helicase correlates with the presence of G4 motifs Giang Huong Nguyen1,2, Weiliang Tang3, Ana I. Robles1, Richard P. Beyer4, Lucas T. Gray5, Judith A. Welsh1, Aaron J. Schetter1, Kensuke Kumamoto1,6, Xin Wei Wang1, Ian D. Hickson2,7, Nancy Maizels5, 3,8 1 Raymond J. Monnat, Jr. and Curtis C. Harris 1Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, U.S.A; 2Department of Medical Oncology, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, U.K.; 3Department of Pathology, University of Washington, Seattle, WA U.S.A.; 4 Center for Ecogenetics and Environmental Health, University of Washington, Seattle, WA U.S.A.; 5Department of Immunology and Department of Biochemistry, University of Washington, Seattle, WA U.S.A.; 6Department of Organ Regulatory Surgery, Fukushima Medical University, Fukushima, Japan; 7Cellular and Molecular Medicine, Nordea Center for Healthy Aging, University of Copenhagen, Denmark; 8Department of Genome Sciences, University of WA, Seattle, WA U.S.A. SI Index: Supporting Information for this manuscript includes the following 19 items. A more detailed Materials and Methods section is followed by 18 Tables and Figures in order of their appearance in the manuscript text: 1) SI Materials and Methods 2) Figure S1. Study design and experimental workflow. 3) Figure S2. Immunoblot verification of BLM depletion from human fibroblasts. 4) Figure S3. PCA of mRNA and miRNA expression in BLM-depleted human fibroblasts. 5) Figure S4. qPCR confirmation of mRNA array data. 6) Table S1. BS patient and control detail.
[Show full text]