Product Name: C1orf21 Polyclonal Antibody, ALEXA FLUOR® 594 Conjugated Catalog No

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Product Name: C1orf21 Polyclonal Antibody, ALEXA FLUOR® 594 Conjugated Catalog No. : TAP01-84943R-A594 Intended Use: For Research Use Only. Not for used in diagnostic procedures. Size 100ul Concentration 1ug/ul Gene ID 81563 ISO Type Rabbit IgG Clone N/A Immunogen Range Conjugation ALEXA FLUOR® 594 Subcellular Locations Applications IF(IHC-P) Cross Reactive Species Human, Mouse, Rat Source KLH conjugated synthetic peptide derived from human C1orf21 Applications with IF(IHC-P)(1:50-200) Dilutions Purification Purified by Protein A. Background Chromosome 1 is the largest human chromosome spanning about 260 million base pairs and making up 8% of the human genome. There are about 3,000 genes on chromosome 1, and considering the great number of genes there are also a large number of diseases associated with chromosome 1. Notably, the rare aging disease Hutchinson-Gilford progeria is associated with the LMNA gene which encodes lamin A. When defective, the LMNA gene product can build up in the nucleus and cause characteristic nuclear blebs. The mechanism of rapidly enhanced aging is unclear and is a topic of continuing exploration. The MUTYH gene is located on chromosome 1 and is partially responsible for familial adenomatous polyposis. Stickler syndrome, Parkinsons, Gaucher disease and Usher syndrome are also associated with chromosome 1. A breakpoint has been identified in 1q which disrupts the DISC1 gene and is linked to schizophrenia. Aberrations in chromosome 1 are found in a variety of cancers including head and neck cancer, malignant melanomaand multiple myeloma. The C1orf21 gene product has been provisionally designated C1orf21 pending further characterization. Synonyms C1orf21; CA021_HUMAN; Cell proliferation-inducing gene 13 protein; PIG13; RP4-768P8.1; Uncharacterized protein C1orf21. Storage Aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Store at 4°C for 12 months. If unexpected results are observed which cannot be explained by variations in laboratory procedures and a problem with the reagent is suspected, contact Technical Support at [email protected] or your distributor service. .

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C1orf21 CRISPR/Cas9 KO Plasmid (H): Sc-417269
SANTA CRUZ BIOTECHNOLOGY, INC. C1orf21 CRISPR/Cas9 KO Plasmid (h): sc-417269 BACKGROUND APPLICATIONS The Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) and C1orf21 CRISPR/Cas9 KO Plasmid (h) is recommended for the disruption of CRISPR-associated protein (Cas9) system is an adaptive immune response gene expression in human cells. defense mechanism used by archea and bacteria for the degradation of foreign genetic material (4,6). This mechanism can be repurposed for other 20 nt non-coding RNA sequence: guides Cas9 functions, including genomic engineering for mammalian systems, such as to a speciﬁc target location in the genomic DNA gene knockout (KO) (1,2,3,5). CRISPR/Cas9 KO Plasmid products enable the U6 promoter: drives gRNA scaffold: helps Cas9 identification and cleavage of specific genes by utilizing guide RNA (gRNA) expression of gRNA bind to target DNA sequences derived from the Genome-scale CRISPR Knock-Out (GeCKO) v2 library developed in the Zhang Laboratory at the Broad Institute (3,5). Termination signal Green Fluorescent Protein: to visually REFERENCES verify transfection CRISPR/Cas9 Knockout Plasmid CBh (chicken β-Actin 1. Cong, L., et al. 2013. Multiplex genome engineering using CRISPR/Cas hybrid) promoter: drives expression of Cas9 systems. Science 339: 819-823. 2A peptide: allows production of both Cas9 and GFP from the 2. Mali, P., et al. 2013. RNA-guided human genome engineering via Cas9. same CBh promoter Science 339: 823-826. Nuclear localization signal 3. Ran, F.A., et al. 2013. Genome engineering using the CRISPR-Cas9 system. Nuclear localization signal SpCas9 ribonuclease Nat. Protoc. 8: 2281-2308.
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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.
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PRODUCT SPECIFICATION Prest Antigen C1orf21 Product Datasheet
PrEST Antigen C1orf21 Product Datasheet PrEST Antigen PRODUCT SPECIFICATION Product Name PrEST Antigen C1orf21 Product Number APrEST71329 Gene Description chromosome 1 open reading frame 21 Alternative Gene PIG13 Names Corresponding Anti-C1orf21 (HPA026831) Antibodies Description Recombinant protein fragment of Human C1orf21 Amino Acid Sequence Recombinant Protein Epitope Signature Tag (PrEST) antigen sequence: AKHVATVQNEEEAQKGKNYQNGDVFGDEYRIKPVEEVKYMKNGAEEEQKI AARNQENLEKSASSNVRLKTNKEVPGLVHQPRANMHISESQQEFFRMLDE KIEKGRDYCSEE Fusion Tag N-terminal His6ABP (ABP = Albumin Binding Protein derived from Streptococcal Protein G) Expression Host E. coli Purification IMAC purification Predicted MW 31 kDa including tags Usage Suitable as control in WB and preadsorption assays using indicated corresponding antibodies. Purity >80% by SDS-PAGE and Coomassie blue staining Buffer PBS and 1M Urea, pH 7.4. Unit Size 100 µl Concentration Lot dependent Storage Upon delivery store at -20°C. Avoid repeated freeze/thaw cycles. Notes Gently mix before use. Optimal concentrations and conditions for each application should be determined by the user. 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. Atlas Antibodies AB's sole liability is limited to replacement of the product or refund of the purchase price.
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www.nature.com/scientificreports OPEN Genome-wide association study identifes loci for arterial stifness index in 127,121 UK Biobank Received: 1 February 2019 Accepted: 5 June 2019 participants Published: xx xx xxxx Kenneth Fung1, Julia Ramírez 2, Helen R. Warren2,3, Nay Aung 1, Aaron M. Lee1, Evan Tzanis2,3, Stefen E. Petersen 1,3 & Patricia B. Munroe2,3 Arterial stifness index (ASI) is a non-invasive measure of arterial stifness using infra-red fnger sensors (photoplethysmography). It is a well-suited measure for large populations as it is relatively inexpensive to perform, and data can be acquired within seconds. These features raise interest in using ASI as a tool to estimate cardiovascular disease risk as prior work demonstrates increased arterial stifness is associated with elevated systolic blood pressure, and ASI is predictive of cardiovascular disease and mortality. We conducted genome-wide association studies (GWASs) for ASI in 127,121 UK Biobank participants of European-ancestry. Our primary analyses identifed variants at four loci reaching genome-wide signifcance (P < 5 × 10−8): TEX41 (rs1006923; P = 5.3 × 10−12), FOXO1 (rs7331212; P = 2.2 × 10−11), C1orf21 (rs1930290, P = 1.1 × 10−8) and MRVI1 (rs10840457, P = 3.4 × 10−8). Gene- based testing revealed three signifcant genes, the most signifcant gene was COL4A2 (P = 1.41 × 10−8) encoding type IV collagen. Other candidate genes at associated loci were also involved in smooth muscle tone regulation. Our fndings provide new information for understanding the development of arterial stifness. Arterial stifness measures have been reported as independent markers of vascular ageing1,2, hypertension3,4, car- diovascular disease (CVD)5,6 and mortality6,7.
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Neurosurg Focus 35 (6):E3, 2013 ©AANS, 2013 Genomic and transcriptome analysis revealing an oncogenic functional module in meningiomas XIAO CHANG, PH.D.,1 LINGLING SHI, PH.D.,2 FAN GAO, PH.D.,1 JONATHAN RUssIN, M.D.,3 LIYUN ZENG, PH.D.,1 SHUHAN HE, B.S.,3 THOMAS C. CHEN, M.D.,3 STEVEN L. GIANNOTTA, M.D.,3 DANIEL J. WEISENBERGER, PH.D.,4 GAbrIEL ZADA, M.D.,3 KAI WANG, PH.D.,1,5,6 AND WIllIAM J. MAck, M.D.1,3 1Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California; 2GHM Institute of CNS Regeneration, Jinan University, Guangzhou, China; 3Department of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California; 4USC Epigenome Center, Keck School of Medicine, University of Southern California, Los Angeles, California; 5Department of Psychiatry, Keck School of Medicine, University of Southern California, Los Angeles, California; and 6Division of Bioinformatics, Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California Object. Meningiomas are among the most common primary adult brain tumors. Although typically benign, roughly 2%–5% display malignant pathological features. The key molecular pathways involved in malignant trans- formation remain to be determined. Methods. Illumina expression microarrays were used to assess gene expression levels, and Illumina single- nucleotide polymorphism arrays were used to identify copy number variants in benign, atypical, and malignant me- ningiomas (19 tumors, including 4 malignant ones). The authors also reanalyzed 2 expression data sets generated on Affymetrix microarrays (n = 68, including 6 malignant ones; n = 56, including 3 malignant ones).
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Alma Mater Studiorum – Università di Bologna DOTTORATO DI RICERCA IN Scienze della terra, della vita e dell’ambiente Ciclo XXX Settore Concorsuale: 05/B1 - Zoologia e Antropologia Settore Scientifico Disciplinare: BIO/08 - Antropologia Unraveling the combined effects of demography and natural selection in shaping the genomic background of Southern Himalayan populations Presentata da Guido Alberto Gnecchi Ruscone Coordinatore Dottorato Supervisore Prof. Giulio Viola Dott. Marco Sazzini Esame finale anno 2018 Table of contents Abstract 1 1. Introduction 3 1.1 Molecular Anthropology and the study of the genetic bases of human biodiversity 3 1.1.1 Studies based on uniparental genetic markers 3 1.1.2 Studies based on autosomal genome-wide markers 5 1.2 The Southern route hypothesis and the first peopling of the Asian continent 7 1.3 The genetic history of South Asian populations 8 1.4 The peopling of East Asia: southern and northern routes 11 1.5 Historical migrations in East Asia 13 1.6 The spread of Tibeto-Burman populations 15 1.7 The peopling of the Tibetan Plateau and its adaptive implications 19 1.7.1 Archeological evidence for the peopling of the Tibetan Plateau 19 1.7.2 Genetic evidence for the peopling of the Tibetan Plateau 21 1.7.3 Adaptive implications related to the peopling of the Tibetan Plateau 22 1.8 The Nepalese Tibeto-Burman populations 23 1.9 High altitude adaptation: the Himalayan case study 24 2. Aim of the study 29 3. Materials and Methods 31 3.1 Sampling campaigns and populations studied 31 3.2 Molecular analyses 35
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Insulin and Glucose Alter Death-Associated Protein Kinase 3 (DAPK3) DNA Methylation
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