Human CILP Blocking Peptide (CDBP0807) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

Total Page：16

File Type：pdf, Size：1020Kb

Human CILP blocking peptide (CDBP0807) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Product Overview Blocking/Immunizing peptide for anti-CILP antibody Antigen Description Major alterations in the composition of the cartilage extracellular matrix occur in joint disease, such as osteoarthrosis. This gene encodes the cartilage intermediate layer protein (CILP), which increases in early osteoarthrosis cartilage. The encoded protein was thought to encode a protein precursor for two different proteins; an N-terminal CILP and a C-terminal homolog of NTPPHase, however, later studies identified no nucleotide pyrophosphatase phosphodiesterase (NPP) activity. The full-length and the N-terminal domain of this protein was shown to function as an IGF-1 antagonist. An allelic variant of this gene has been associated with lumbar disc disease. Nature Synthetic Expression System N/A Species Human Species Reactivity Human, Mouse, Dog, Rat Conjugate Unconjugated Applications Apuri, BL, ELISA Procedure None Format Lyophilized powder Size 100 μg Preservative None Storage Shipped at ambient temperature, store at -20°C. ANTIGEN GENE INFORMATION Gene Name CILP cartilage intermediate layer protein, nucleotide pyrophosphohydrolase [ Homo sapiens ] Official Symbol CILP Synonyms CILP; cartilage intermediate layer protein, nucleotide pyrophosphohydrolase; cartilage 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 intermediate layer protein 1; HsT18872; cartilage intermediate-layer protein; cartilage intermediate layer protein 1 C1; cartilage intermediate layer protein 1 C2; CILP-1; Entrez Gene ID 8483 mRNA Refseq NM_003613 Protein Refseq NP_003604 UniProt ID O75339 Chromosome Location 15q22 Function NOT alkaline phosphatase activity; NOT nucleotide diphosphatase activity; 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 2 © Creative Diagnostics All Rights Reserved.

Copy Link

Recommended publications

Metastatic Adrenocortical Carcinoma Displays Higher Mutation Rate and Tumor Heterogeneity Than Primary Tumors
ARTICLE DOI: 10.1038/s41467-018-06366-z OPEN Metastatic adrenocortical carcinoma displays higher mutation rate and tumor heterogeneity than primary tumors Sudheer Kumar Gara1, Justin Lack2, Lisa Zhang1, Emerson Harris1, Margaret Cam2 & Electron Kebebew1,3 Adrenocortical cancer (ACC) is a rare cancer with poor prognosis and high mortality due to metastatic disease. All reported genetic alterations have been in primary ACC, and it is 1234567890():,; unknown if there is molecular heterogeneity in ACC. Here, we report the genetic changes associated with metastatic ACC compared to primary ACCs and tumor heterogeneity. We performed whole-exome sequencing of 33 metastatic tumors. The overall mutation rate (per megabase) in metastatic tumors was 2.8-fold higher than primary ACC tumor samples. We found tumor heterogeneity among different metastatic sites in ACC and discovered recurrent mutations in several novel genes. We observed 37–57% overlap in genes that are mutated among different metastatic sites within the same patient. We also identiﬁed new therapeutic targets in recurrent and metastatic ACC not previously described in primary ACCs. 1 Endocrine Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. 2 Center for Cancer Research, Collaborative Bioinformatics Resource, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. 3 Department of Surgery and Stanford Cancer Institute, Stanford University, Stanford, CA 94305, USA. Correspondence and requests for materials should be addressed to E.K. (email: [email protected]) NATURE COMMUNICATIONS | (2018) 9:4172 | DOI: 10.1038/s41467-018-06366-z | www.nature.com/naturecommunications 1 ARTICLE NATURE COMMUNICATIONS | DOI: 10.1038/s41467-018-06366-z drenocortical carcinoma (ACC) is a rare malignancy with types including primary ACC from the TCGA to understand our A0.7–2 cases per million per year1,2.
[Show full text]
Mouse Cilp Knockout Project (CRISPR/Cas9)
https://www.alphaknockout.com Mouse Cilp Knockout Project (CRISPR/Cas9) Objective: To create a Cilp knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Cilp gene (NCBI Reference Sequence: NM_173385 ; Ensembl: ENSMUSG00000042254 ) is located on Mouse chromosome 9. 10 exons are identified, with the ATG start codon in exon 3 and the TAA stop codon in exon 10 (Transcript: ENSMUST00000048762). Exon 3~9 will be selected as target site. Cas9 and gRNA will be co-injected into fertilized eggs for KO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Exon 3 starts from the coding region. Exon 3~9 covers 31.63% of the coding region. The size of effective KO region: ~8960 bp. The KO region does not have any other known gene. Page 1 of 8 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 3 4 5 6 7 8 9 10 Legends Exon of mouse Cilp Knockout region Page 2 of 8 https://www.alphaknockout.com Overview of the Dot Plot (up) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 1191 bp section upstream of Exon 3 is aligned with itself to determine if there are tandem repeats. Tandem repeats are found in the dot plot matrix. The gRNA site is selected outside of these tandem repeats. Overview of the Dot Plot (down) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 1809 bp section downstream of Exon 9 is aligned with itself to determine if there are tandem repeats.
[Show full text]
Locating Potentially Lethal Genes Using the Abnormal Distributions of Genotypes
www.nature.com/scientificreports OPEN Locating potentially lethal genes using the abnormal distributions of genotypes Received: 29 January 2019 Xiaojun Ding & Xiaoshu Zhu Accepted: 10 July 2019 Genes are the basic functional units of heredity. Diferences in genes can lead to various congenital Published: xx xx xxxx physical conditions. One kind of these diferences is caused by genetic variations named single nucleotide polymorphisms (SNPs). An SNP is a variation in a single nucleotide that occurs at a specifc position in the genome. Some SNPs can afect splice sites and protein structures and cause gene abnormalities. SNPs on paired chromosomes may lead to fatal diseases so that a fertilized embryo cannot develop into a normal fetus or the people born with these abnormalities die in childhood. The distributions of genotypes on these SNP sites are diferent from those on other sites. Based on this idea, we present a novel statistical method to detect the abnormal distributions of genotypes and locate the potentially lethal genes. The test was performed on HapMap data and 74 suspicious SNPs were found. Ten SNP maps “reviewed” genes in the NCBI database. Among them, 5 genes were related to fatal childhood diseases or embryonic development, 1 gene can cause spermatogenic failure, and the other 4 genes were associated with many genetic diseases. The results validated our method. The method is very simple and is guaranteed by a statistical test. It is an inexpensive way to discover potentially lethal genes and the mutation sites. The mined genes deserve further study. Genes are the most important genetic materials that determine the health of a person.
[Show full text]
Genetic and Environmental Perturbations Lead to Regulatory
RESEARCH COMMUNICATION Genetic and environmental perturbations lead to regulatory decoherence Amanda Lea1,2†, Meena Subramaniam3†, Arthur Ko4, Terho Lehtima¨ ki5,6, Emma Raitoharju6, Mika Ka¨ ho¨ nen6,7, Ilkka Seppa¨ la¨ 6, Nina Mononen6, Olli T Raitakari8,9, Mika Ala-Korpela10,11,12,13,14,15, Pa¨ ivi Pajukanta16, Noah Zaitlen3‡, Julien F Ayroles1,2‡* 1Department of Ecology and Evolution, Princeton University, Princeton, United States; 2Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, United States; 3Department of Medicine, Lung Biology Center, University of California, San Francisco, San Francisco, United States; 4Department of Medicine, David Geffen School of Medicine at UCLA, University of California, Los Angeles, Los Angeles, United States; 5Department of Clinical Chemistry, Fimlab Laboratories, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland; 6Finnish Cardiovascular Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland; 7Department of Clinical Physiology, Tampere University, Tampere University Hospital, Tampere, Finland; 8Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland; 9Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Turku, Finland; 10Systems Epidemiology, Baker Heart and Diabetes Institute, Melbourne, Australia; 11Computational Medicine, Faculty of Medicine, Biocenter Oulu, University of Oulu, Oulu, Finland; 12NMR Metabolomics Laboratory,
[Show full text]
Homozygosity Mapping Approach Identifies a Missense Mutation in Equine Cyclophilin B (PPIB) Associated with HERDA in the American Quarter Horse ⁎ Robert C
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Genomics 90 (2007) 93–102 www.elsevier.com/locate/ygeno Homozygosity mapping approach identifies a missense mutation in equine cyclophilin B (PPIB) associated with HERDA in the American Quarter Horse ⁎ Robert C. Tryon a, Stephen D. White b, Danika L. Bannasch a, a Department of Population Health and Reproduction, School of Veterinary Medicine, University of California-Davis, One Shields Ave., Davis, CA 9516, USA b Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California-Davis, One Shields Ave., Davis, CA 9516, USA Received 3 February 2007; accepted 19 March 2007 Available online 11 May 2007 Abstract Hereditary equine regional dermal asthenia (HERDA), a degenerative skin disease that affects the Quarter Horse breed, was localized to ECA1 by homozygosity mapping. Comparative genomics allowed the development of equine gene-specific markers which were used with a set of affected horses to detect a homozygous, identical-by-descent block spanning ∼2.5 Mb, suggesting a recent origin for the HERDA mutation. We report a mutation in cyclophilin B (PPIB) as a novel, causal candidate gene for HERDA. A c.115G>A missense mutation in PPIB alters a glycine residue that has been conserved across vertebrates. The mutation was homozygous in 64 affected horses and segregates concordant with inbreeding loops apparent in the genealogy of 11 affected horses. Screening of control Quarter Horses indicates a 3.5% carrier frequency. The development of a test that can detect affected horses prior to development of clinical signs and carriers of HERDA will allow Quarter Horse breeders to eliminate this debilitating disease.
[Show full text]
(12) United States Patent (10) Patent No.: US 6,960,562 B2 Jay (45) Date of Patent: Nov
USOO6960562B2 (12) United States Patent (10) Patent No.: US 6,960,562 B2 Jay (45) Date of Patent: Nov. 1, 2005 (54) TRIBONECTIN POLYPEPTIDES AND USES J.P. Caron (1992) “Understanding the Pathogenesis of THEREOF Equine Osteoarthritis”, Br. Vet.J.Sci. USA, Vol. 149, pp. 369-371. (75) Inventor: Gregory D. Jay, Norfolk, MA (US) Flannery et al. (1999) “Articular Cartilage Superficial Zone (73) Assignee: Rhode Island Hospital, A Lifespan Protein (SZP) is Homologous to Megakaryocyte Stimulating Factor Precursor and is a Multifunctional Proteoglycan with Partner, Providence, RI (US) Potential Growth-Promoting, Cytoprotective, anmd Lubri (*) Notice: Subject to any disclaimer, the term of this cating Properties in Cartilage Metabolism”, Biochemical patent is extended or adjusted under 35 and Biophysical Communications, vol. 254, pp. 535-541. U.S.C. 154(b) by 430 days. Garg et al (1979) “The Structure of the O-Glycosylically linked Oligosacharide Chains of LPG-I, A Glycoprotein (21) Appl. No.: 09/897,188 Present in Articular Lubricating Fraction of Bovine Synovial Fluid” Carbohydrate Research, vol. 78, pp. 79-88. (22) Filed: Jul. 2, 2001 Jay (1992) “Characterization of a Bovine Synovial Fluid (65) Prior Publication Data Lubricating Factor. I. Chemical, Surface Activity and Lubri US 2004/0072741 A1 Apr. 15, 2004 cating Properties' Connective Tissue Research, vol. 28, pp. 71-88. Related U.S. Application Data Jay et al. (1992) “Characterization of a Bovine Synovial (63) Continuation-in-part of application No. 09/556,246, filed on Fluid Lubricating Factor. II. Comparison with Purified Ocu Apr. 24, 2000, and a continuation-in-part of application No.
[Show full text]
Supplementary Material Peptide-Conjugated Oligonucleotides Evoke Long-Lasting Myotonic Dystrophy Correction in Patient-Derived C
Supplementary material Peptide-conjugated oligonucleotides evoke long-lasting myotonic dystrophy correction in patient-derived cells and mice Arnaud F. Klein1†, Miguel A. Varela2,3,4†, Ludovic Arandel1, Ashling Holland2,3,4, Naira Naouar1, Andrey Arzumanov2,5, David Seoane2,3,4, Lucile Revillod1, Guillaume Bassez1, Arnaud Ferry1,6, Dominic Jauvin7, Genevieve Gourdon1, Jack Puymirat7, Michael J. Gait5, Denis Furling1#* & Matthew J. A. Wood2,3,4#* 1Sorbonne Université, Inserm, Association Institut de Myologie, Centre de Recherche en Myologie, CRM, F-75013 Paris, France 2Department of Physiology, Anatomy and Genetics, University of Oxford, South Parks Road, Oxford, UK 3Department of Paediatrics, John Radcliffe Hospital, University of Oxford, Oxford, UK 4MDUK Oxford Neuromuscular Centre, University of Oxford, Oxford, UK 5Medical Research Council, Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, UK 6Sorbonne Paris Cité, Université Paris Descartes, F-75005 Paris, France 7Unit of Human Genetics, Hôpital de l'Enfant-Jésus, CHU Research Center, QC, Canada † These authors contributed equally to the work # These authors shared co-last authorship Methods Synthesis of Peptide-PMO Conjugates. Pip6a Ac-(RXRRBRRXRYQFLIRXRBRXRB)-CO OH was synthesized and conjugated to PMO as described previously (1). The PMO sequence targeting CUG expanded repeats (5′-CAGCAGCAGCAGCAGCAGCAG-3′) and PMO control reverse (5′-GACGACGACGACGACGACGAC-3′) were purchased from Gene Tools LLC. Animal model and ASO injections. Experiments were carried out in the “Centre d’études fonctionnelles” (Faculté de Médecine Sorbonne University) according to French legislation and Ethics committee approval (#1760-2015091512001083v6). HSA-LR mice are gift from Pr. Thornton. The intravenous injections were performed by single or multiple administrations via the tail vein in mice of 5 to 8 weeks of age.
[Show full text]
Gene Modules Associated with Human Diseases Revealed by Network
bioRxiv preprint doi: https://doi.org/10.1101/598151; this version posted June 15, 2019. 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. Gene modules associated with human diseases revealed by network analysis Shisong Ma1,2*, Jiazhen Gong1†, Wanzhu Zuo1†, Haiying Geng1, Yu Zhang1, Meng Wang1, Ershang Han1, Jing Peng1, Yuzhou Wang1, Yifan Wang1, Yanyan Chen1 1. Hefei National Laboratory for Physical Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China 2. School of Data Science, University of Science and Technology of China, Hefei, Anhui 230027, China * To whom correspondence should be addressed. Email: [email protected] † These authors contribute equally. 1 bioRxiv preprint doi: https://doi.org/10.1101/598151; this version posted June 15, 2019. 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. ABSTRACT Despite many genes associated with human diseases have been identified, disease mechanisms often remain elusive due to the lack of understanding how disease genes are connected functionally at pathways level. Within biological networks, disease genes likely map to modules whose identification facilitates etiology studies but remains challenging. We describe a systematic approach to identify disease-associated gene modules.
[Show full text]
Analysis of RHOA Mutations and Their Significance in the Proliferation and Transcriptome of Digestive Tract Cancer Cells
ONCOLOGY LETTERS 22: 735, 2021 Analysis of RHOA mutations and their significance in the proliferation and transcriptome of digestive tract cancer cells NAOKI IKARI1,2, AKIKO SERIZAWA1, ETSUKO TANJI2, MASAKAZU YAMAMOTO1 and TORU FURUKAWA1‑3 1Department of Surgery, Institute of Gastroenterology; 2Institute for Integrated Medical Sciences, Tokyo Women's Medical University, Shinjuku‑ku, Tokyo 162‑8666; 3Department of Investigative Pathology, Tohoku University Graduate School of Medicine, Aoba‑ku, Sendai 980‑8575, Japan Received April 23, 2021; Accepted July 14, 2021 DOI: 10.3892/ol.2021.12996 Abstract. The ras homolog family member A (RHOA) gene showed that the genes associated with small molecule metabolic encodes a member of the Rho family of small GTPases and is process, oxidation‑reduction processes, protein kinase activity, known to function in reorganization of the actin cytoskeleton, transport, and cell junction were commonly downregulated in which is associated with regulation of cell shape, attachment cells whose proliferation was attenuated by the knockdown of and motility. RHOA has been found to be recurrently mutated RHOA. These results suggested that certain RHOA mutations in gastrointestinal cancer; however, the functional signifi‑ may result in upregulation of lnc‑DERA‑1 and genes associated cance of the mutated RHOA protein in digestive tract cancers with cellular metabolism and proliferation in digestive tract remains to be uncovered. The aim of the present study was cancers. to understand the role of mutant RHOA in the proliferation and transcriptome of digestive tract cancer cells. Mutations of Introduction RHOA in one esophageal cancer cell line, OE19, eight gastric cancer cell lines, namely, AGS, GCIY, HGC‑27, KATO III, The ras homolog family member A (RHOA) gene encodes a MKN1, MKN45, SNU16 and SNU719, as well as two colon member of the Rho family of small GTPases and is known cancer cell lines, CCK‑81 and SW948, were determined using to function in reorganization of the actin cytoskeleton, which Sanger sequencing.
[Show full text]
You Can Check If Genes Are Captured by the Agilent Sureselect V5 Exome
IIHG Clinical Exome Sequencing Test Gene Coverage • Whole Exome Sequencing is a targeted capture platform which does not capture the entire exome. Regions not captured by the exome will not be analyzed. o Please note, it is important to understand the absence of a reportable variant in a given gene does not mean there are not pathogenic variants in that gene. • Data sensitivity and specificity for exome testing is variable as gene coverage is not uniform throughout the exome. • The Agilent SureSelect XT Human All Exon v5 kit captures ~98% of Refseq coding base pairs, and >94% of the captured coding bases in the exome are covered at our depth-of-coverage minimum threshold (30 reads). • All test reports include the following information: o Regions of the Symptom Candidate Gene List which were not captured by the current exome capture platform. o Regions of the Symptom Candidate Gene List which were not sequenced to a sufficient depth of coverage to make a clinical diagnosis. • You can check if genes are captured by the Agilent Agilent SureSelect v5 exome capture, and how well those genes are typically covered here. • Explanations for the headings; • Symbol: Gene symbol • Chr: Chromosome • % Captured: the minimum portion of the gene captured by the Agilent SureSelect XT Human All Exon v5 kit. This includes all transcripts for a given gene. o 100.00% = the entire gene is captured o 0.00% = none of the gene is captured • % Covered: the minimum portion of the gene that has at least 30x average coverage when sequenced on the Illumina HiSeq2000 with 100 base pair (bp) paired-end reads for eight CEPH samples.
[Show full text]
1 Supplementary Material Figure S1. Volcano Plot of Differentially
Supplementary material Figure S1. Volcano Plot of differentially expressed genes between preterm infants fed own mother’s milk (OMM) or pasteurized donated human milk (DHM). Table S1. The 10 most representative biological processes filtered for enrichment p- value in preterm infants. Biological Processes p-value Quantity of DEG* Transcription, DNA-templated 3.62x10-24 189 Regulation of transcription, DNA-templated 5.34x10-22 188 Transport 3.75x10-17 140 Cell cycle 1.03x10-13 65 Gene expression 3.38x10-10 60 Multicellular organismal development 6.97x10-10 86 1 Protein transport 1.73x10-09 56 Cell division 2.75x10-09 39 Blood coagulation 3.38x10-09 46 DNA repair 8.34x10-09 39 Table S2. Differential genes in transcriptomic analysis of exfoliated epithelial intestinal cells between preterm infants fed own mother’s milk (OMM) and pasteurized donated human milk (DHM). Gene name Gene Symbol p-value Fold-Change (OMM vs. DHM) (OMM vs. DHM) Lactalbumin, alpha LALBA 0.0024 2.92 Casein kappa CSN3 0.0024 2.59 Casein beta CSN2 0.0093 2.13 Cytochrome c oxidase subunit I COX1 0.0263 2.07 Casein alpha s1 CSN1S1 0.0084 1.71 Espin ESPN 0.0008 1.58 MTND2 ND2 0.0138 1.57 Small ubiquitin-like modifier 3 SUMO3 0.0037 1.54 Eukaryotic translation elongation EEF1A1 0.0365 1.53 factor 1 alpha 1 Ribosomal protein L10 RPL10 0.0195 1.52 Keratin associated protein 2-4 KRTAP2-4 0.0019 1.46 Serine peptidase inhibitor, Kunitz SPINT1 0.0007 1.44 type 1 Zinc finger family member 788 ZNF788 0.0000 1.43 Mitochondrial ribosomal protein MRPL38 0.0020 1.41 L38 Diacylglycerol
[Show full text]
Supplementary Methods
Supplementary Methods Patient Cohorts and Clinicopathological Review AOCS and Clinical Cohort AOCS is a population-based, case control study of ovarian cancer which recruited eligible women aged 18-79 years with newly diagnosed epithelial ovarian cancer (including primary peritoneal and fallopian tube cancer) through 20 gynaecologic oncology units across all Australian states, between January 2002 and June 2006. Women who were unable to provide informed consent due to illness, language difficulties or mental incapacity were excluded, as were those whose diagnosis was not histopathologically confirmed. Detailed clinical and follow-up data was obtained from medical records at predefined intervals: post surgery, post primary chemotherapy, at 6-monthly intervals to 5 years and annually thereafter. All treatment details and clinical assessments were recorded on case report forms using Good Clinical Practice (GCP) guidelines (ICH E6: Good Clinical Practice: Consolidated Guidance. 1996; http://www.fda.gov/oc/gcp/guidance.html), and included chemotherapy regimen, imaging details and pre- and post-treatment serum CA125 levels. The CA125 assay type and upper limit of normal for each measurement were recorded and assignment of relapse date was based on Gynecologic Cancer Intergroup (GCIG) criteria1. Clinical details for the cases from The Royal Brisbane Hospital, and Westmead Hospital were obtained retrospectively from medical records. The majority of patients with invasive ovarian cancer (n= 267) underwent laparotomy for diagnosis, staging and debulking and subsequently received first-line platinum/taxane based chemotherapy. In most cases, tumor examined was excised at the time of primary surgery, prior to the administration of chemotherapy. Eighteen patients who had neoadjuvant, platinum based chemotherapy were also included in the study as were 18 patients with low malignant potential disease.
[Show full text]