Anti-KIF20A Monoclonal Antibody (DCABH-15860) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

Total Page：16

File Type：pdf, Size：1020Kb

Anti-KIF20A monoclonal antibody (DCABH-15860) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description Mitotic kinesin required for chromosome passenger complex (CPC)-mediated cytokinesis. Following phosphorylation by PLK1, involved in recruitment of PLK1 to the central spindle. Interacts with guanosine triphosphate (GTP)-bound forms of RAB6A and RAB6B. May act as a motor required for the retrograde RAB6 regulated transport of Golgi membranes and associated vesicles along. Immunogen A synthetic peptide of human KIF20A is used for rabbit immunization. Isotype IgG Source/Host Rabbit Species Reactivity Human Purification Protein A Conjugate Unconjugated Applications Western Blot (Transfected lysate); ELISA Size 1 ea Buffer In 1x PBS, pH 7.4 Preservative None Storage Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. GENE INFORMATION Gene Name KIF20A kinesin family member 20A [ Homo sapiens ] Official Symbol KIF20A Synonyms KIF20A; kinesin family member 20A; RAB6 interacting, kinesin like (rabkinesin6) , RAB6KIFL; kinesin-like protein KIF20A; GG10_2; rabkinesin-6; mitotic kinesin-like protein 2; rab6-interacting kinesin-like protein; RAB6 interacting, kinesin-like (rabkinesin6); MKLP2; RAB6KIFL; FLJ21151; Entrez Gene ID 10112 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 Protein Refseq NP_005724 UniProt ID O95235 Chromosome Location 5q31 Pathway Aurora B signaling, organism-specific biosystem; Cell Cycle, organism-specific biosystem; Cell Cycle, Mitotic, organism-specific biosystem; DNA Replication, organism-specific biosystem; Factors involved in megakaryocyte development and platelet production Function ATP binding; microtubule motor activity; nucleotide binding; protein kinase binding; transporter 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

Uwaterloo Latex Thesis Template
New Algorithms for Predicting Conformational Polymorphism and Inferring Direct Couplings for Side Chains of Proteins by Laleh Soltan Ghoraie A thesis presented to the University of Waterloo in fulfillment of the thesis requirement for the degree of Doctor of Philosophy in Computer Science Waterloo, Ontario, Canada, 2015 c Laleh Soltan Ghoraie 2015 I hereby declare that I am the sole author of this thesis. This is a true copy of the thesis, including any required final revisions, as accepted by my examiners. I understand that my thesis may be made electronically available to the public. ii Abstract Protein crystals populate diverse conformational ensembles. Despite much evidence that there is widespread conformational polymorphism in protein side chains, most of the x- ray crystallography data are modelled by single conformations in the Protein Data Bank. The ability to extract or to predict these conformational polymorphisms is of crucial im- portance, as it facilitates deeper understanding of protein dynamics and functionality. This dissertation describes a computational strategy capable of predicting side-chain poly- morphisms. The applied approach extends a particular class of algorithms for side-chain prediction by modelling the side-chain dihedral angles more appropriately as continuous rather than discrete variables. Employing a new inferential technique known as particle belief propagation (PBP), we predict residue-specific distributions that encode informa- tion about side-chain polymorphisms. The predicted polymorphisms are in relatively close agreement with results from a state-of-the-art approach based on x-ray crystallography data. This approach characterizes the conformational polymorphisms of side chains us- ing electron density information, and has successfully discovered previously unmodelled conformations.
[Show full text]
Comprehensive Analyses of 723 Transcriptomes Enhance Genetic and Biological Interpretations for Complex Traits in Cattle
Downloaded from genome.cshlp.org on October 3, 2021 - Published by Cold Spring Harbor Laboratory Press Resource Comprehensive analyses of 723 transcriptomes enhance genetic and biological interpretations for complex traits in cattle Lingzhao Fang,1,2,3,4,8 Wentao Cai,2,5,8 Shuli Liu,1,5,8 Oriol Canela-Xandri,3,4,8 Yahui Gao,1,2 Jicai Jiang,2 Konrad Rawlik,3 Bingjie Li,1 Steven G. Schroeder,1 Benjamin D. Rosen,1 Cong-jun Li,1 Tad S. Sonstegard,6 Leeson J. Alexander,7 Curtis P. Van Tassell,1 Paul M. VanRaden,1 John B. Cole,1 Ying Yu,5 Shengli Zhang,5 Albert Tenesa,3,4 Li Ma,2 and George E. Liu1 1Animal Genomics and Improvement Laboratory, Henry A. Wallace Beltsville Agricultural Research Center, Agricultural Research Service, USDA, Beltsville, Maryland 20705, USA; 2Department of Animal and Avian Sciences, University of Maryland, College Park, Maryland 20742, USA; 3The Roslin Institute, Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Midlothian EH25 9RG, United Kingdom; 4Medical Research Council Human Genetics Unit at the Medical Research Council Institute of Genetics and Molecular Medicine, The University of Edinburgh, Edinburgh EH4 2XU, United Kingdom; 5College of Animal Science and Technology, China Agricultural University, Beijing 100193, China; 6Acceligen, Eagan, Minnesota 55121, USA; 7Fort Keogh Livestock and Range Research Laboratory, Agricultural Research Service, USDA, Miles City, Montana 59301, USA By uniformly analyzing 723 RNA-seq data from 91 tissues and cell types, we built a comprehensive gene atlas and studied tissue specificity of genes in cattle. We demonstrated that tissue-specific genes significantly reflected the tissue-relevant biol- ogy, showing distinct promoter methylation and evolution patterns (e.g., brain-specific genes evolve slowest, whereas testis- specific genes evolve fastest).
[Show full text]
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.
[Show full text]
High-Throughput Discovery of Novel Developmental Phenotypes
High-throughput discovery of novel developmental phenotypes The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Dickinson, M. E., A. M. Flenniken, X. Ji, L. Teboul, M. D. Wong, J. K. White, T. F. Meehan, et al. 2016. “High-throughput discovery of novel developmental phenotypes.” Nature 537 (7621): 508-514. doi:10.1038/nature19356. http://dx.doi.org/10.1038/nature19356. Published Version doi:10.1038/nature19356 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:32071918 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Nature. Manuscript Author Author manuscript; Manuscript Author available in PMC 2017 March 14. Published in final edited form as: Nature. 2016 September 22; 537(7621): 508–514. doi:10.1038/nature19356. High-throughput discovery of novel developmental phenotypes A full list of authors and affiliations appears at the end of the article. Abstract Approximately one third of all mammalian genes are essential for life. Phenotypes resulting from mouse knockouts of these genes have provided tremendous insight into gene function and congenital disorders. As part of the International Mouse Phenotyping Consortium effort to generate and phenotypically characterize 5000 knockout mouse lines, we have identified 410 Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms #Corresponding author: [email protected].
[Show full text]
RAB6B Polyclonal Antibody
For Research Use Only RAB6B Polyclonal antibody Catalog Number:10340-1-AP 2 Publications www.ptgcn.com Catalog Number: GenBank Accession Number: Recommended Dilutions: Basic Information 10340-1-AP BC002510 WB 1:500-1:2000 Size: GeneID (NCBI): IP 0.5-4.0 ug for IP and 1:500-1:2000 450 μg/ml 51560 for WB IHC 1:20-1:200 Source: Full Name: IF 1:10-1:100 Rabbit RAB6B, member RAS oncogene family Isotype: Calculated MW: IgG 23 kDa Purification Method: Observed MW: Antigen affinity purification 24 kDa Immunogen Catalog Number: AG0322 Applications Tested Applications: Positive Controls: IF, IHC, IP, WB,ELISA WB : mouse brain tissue; C6 cells, rat brain tissue Cited Applications: IP : mouse brain tissue; IF, WB IHC : human gliomas tissue; Species Specificity: human, mouse, rat IF : C6 cells; Cited Species: mouse, rat Note-IHC: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0 The human RAB genes share structural and biochemical properties with the Ras gene superfamily. Accumulating Background Information data suggests an important role for RAB proteins either in endocytosis or in biosynthetic protein transport. The transport of newly synthesized proteins from endoplasmic reticulum to the Golgi complex and to secretory vesicles involves the movement of carrier vesicles, a process that appears to involve RAB protein function. Rab6A has been shown to be a regulator of membrane traffic from the Golgi apparatus towards the endoplasmic reticulum (ER). Rab6B is encoded by an independent gene which is located on chromosome 3 region q21-q23.
[Show full text]
Identification of Conserved Genes Triggering Puberty in European Sea
Blázquez et al. BMC Genomics (2017) 18:441 DOI 10.1186/s12864-017-3823-2 RESEARCHARTICLE Open Access Identification of conserved genes triggering puberty in European sea bass males (Dicentrarchus labrax) by microarray expression profiling Mercedes Blázquez1,2* , Paula Medina1,2,3, Berta Crespo1,4, Ana Gómez1 and Silvia Zanuy1* Abstract Background: Spermatogenesisisacomplexprocesscharacterized by the activation and/or repression of a number of genes in a spatio-temporal manner. Pubertal development in males starts with the onset of the first spermatogenesis and implies the division of primary spermatogonia and their subsequent entry into meiosis. This study is aimed at the characterization of genes involved in the onset of puberty in European sea bass, and constitutes the first transcriptomic approach focused on meiosis in this species. Results: European sea bass testes collected at the onset of puberty (first successful reproduction) were grouped in stage I (resting stage), and stage II (proliferative stage). Transition from stage I to stage II was marked by an increase of 11ketotestosterone (11KT), the main fish androgen, whereas the transcriptomic study resulted in 315 genes differentially expressed between the two stages. The onset of puberty induced 1) an up-regulation of genes involved in cell proliferation, cell cycle and meiosis progression, 2) changes in genes related with reproduction and growth, and 3) a down-regulation of genes included in the retinoic acid (RA) signalling pathway. The analysis of GO-terms and biological pathways showed that cell cycle, cell division, cellular metabolic processes, and reproduction were affected, consistent with the early events that occur during the onset of puberty.
[Show full text]
1 Supplementary Materials and Methods Gene Set Enrichment Analysis for Gene Expression Data We Compared the Gene Expression Leve
Supplementary Materials and Methods Gene set enrichment analysis for gene expression data We compared the gene expression levels from 2 different phenotypes (i.e., drug sensitive versus resistant) and picked up the genes which had significant different expression for Gene set enrichment analysis (GSEA) by using Molecular Signatures Database(V3.0). Gene set enrichment analysis was carried out by computing overlaps with canonical pathways(CP) and gene ontology (GO) gene sets(C5), obtained from the Broad Institute [1]. Genes in Gene Set (K), Genes in Overlap (k), k/K and P value were used to rank the pathways enriched in each phenotype. We used with 10363 genes in 2334 pathways as the gene set in this study. Supplementary References 1.Subramanian A, Tamayo P, Mootha VK, et al. Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles. Proc Natl Acad Sci U S A 2005;102:15545– 50. 1 Supplementary Results Other drug response-genotype associations in this study Cells with wild genotype were more sensitive to irinotecan than those with TGFβR2 mutation and deletion together (P=0.03) (Supplementary Table S6). PC cells with wild genotype in ADAM gene family were more sensitive to gemcitabine and docetaxel than those with mutation in this family (p<0.05) (Supplementary Table S6). PC cells with wild genotype were more sensitive to docetaxel than those with DEPDC or TTN mutation (p<0.05) (Supplementary Table S6). PC cells with BAI3 mutation were more sensitive to cisplatin than those with wild genotype (p=0.02) (Supplementary Table S6).
[Show full text]
Prognostic Significance of Autophagy-Relevant Gene Markers in Colorectal Cancer
ORIGINAL RESEARCH published: 15 April 2021 doi: 10.3389/fonc.2021.566539 Prognostic Signiﬁcance of Autophagy-Relevant Gene Markers in Colorectal Cancer Qinglian He 1, Ziqi Li 1, Jinbao Yin 1, Yuling Li 2, Yuting Yin 1, Xue Lei 1 and Wei Zhu 1* 1 Department of Pathology, Guangdong Medical University, Dongguan, China, 2 Department of Pathology, Dongguan People’s Hospital, Southern Medical University, Dongguan, China Background: Colorectal cancer (CRC) is a common malignant solid tumor with an extremely low survival rate after relapse. Previous investigations have shown that autophagy possesses a crucial function in tumors. However, there is no consensus on the value of autophagy-associated genes in predicting the prognosis of CRC patients. Edited by: This work screens autophagy-related markers and signaling pathways that may Fenglin Liu, Fudan University, China participate in the development of CRC, and establishes a prognostic model of CRC Reviewed by: based on autophagy-associated genes. Brian M. Olson, Emory University, United States Methods: Gene transcripts from the TCGA database and autophagy-associated gene Zhengzhi Zou, data from the GeneCards database were used to obtain expression levels of autophagy- South China Normal University, China associated genes, followed by Wilcox tests to screen for autophagy-related differentially Faqing Tian, Longgang District People's expressed genes. Then, 11 key autophagy-associated genes were identiﬁed through Hospital of Shenzhen, China univariate and multivariate Cox proportional hazard regression analysis and used to Yibing Chen, Zhengzhou University, China establish prognostic models. Additionally, immunohistochemical and CRC cell line data Jian Tu, were used to evaluate the results of our three autophagy-associated genes EPHB2, University of South China, China NOL3, and SNAI1 in TCGA.
[Show full text]
Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement.
[Show full text]
Supplementary Materials
Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine
[Show full text]
Inhibition of Mitochondrial Complex II in Neuronal Cells Triggers Unique
www.nature.com/scientificreports OPEN Inhibition of mitochondrial complex II in neuronal cells triggers unique pathways culminating in autophagy with implications for neurodegeneration Sathyanarayanan Ranganayaki1, Neema Jamshidi2, Mohamad Aiyaz3, Santhosh‑Kumar Rashmi4, Narayanappa Gayathri4, Pulleri Kandi Harsha5, Balasundaram Padmanabhan6 & Muchukunte Mukunda Srinivas Bharath7* Mitochondrial dysfunction and neurodegeneration underlie movement disorders such as Parkinson’s disease, Huntington’s disease and Manganism among others. As a corollary, inhibition of mitochondrial complex I (CI) and complex II (CII) by toxins 1‑methyl‑4‑phenylpyridinium (MPP+) and 3‑nitropropionic acid (3‑NPA) respectively, induced degenerative changes noted in such neurodegenerative diseases. We aimed to unravel the down‑stream pathways associated with CII inhibition and compared with CI inhibition and the Manganese (Mn) neurotoxicity. Genome‑wide transcriptomics of N27 neuronal cells exposed to 3‑NPA, compared with MPP+ and Mn revealed varied transcriptomic profle. Along with mitochondrial and synaptic pathways, Autophagy was the predominant pathway diferentially regulated in the 3‑NPA model with implications for neuronal survival. This pathway was unique to 3‑NPA, as substantiated by in silico modelling of the three toxins. Morphological and biochemical validation of autophagy markers in the cell model of 3‑NPA revealed incomplete autophagy mediated by mechanistic Target of Rapamycin Complex 2 (mTORC2) pathway. Interestingly, Brain Derived Neurotrophic Factor
[Show full text]
The Rab6-Regulated KIF1C Kinesin Motor Domain Contributes to Golgi Organization Peter L Lee, Maikke B Ohlson†, Suzanne R Pfeffer*
RESEARCH ARTICLE elifesciences.org The Rab6-regulated KIF1C kinesin motor domain contributes to Golgi organization Peter L Lee, Maikke B Ohlson†, Suzanne R Pfeffer* Department of Biochemistry, Stanford University School of Medicine, Stanford, United States Abstract Most kinesins transport cargoes bound to their C-termini and use N-terminal motor domains to move along microtubules. We report here a novel function for KIF1C: it transports Rab6A-vesicles and can influence Golgi complex organization. These activities correlate with KIF1C’s capacity to bind the Golgi protein Rab6A directly, both via its motor domain and C-terminus. Rab6A binding to the motor domain inhibits microtubule interaction in vitro and in cells, decreasing the amount of motile KIF1C. KIF1C depletion slows protein delivery to the cell surface, interferes with vesicle motility, and triggers Golgi fragmentation. KIF1C can protect Golgi membranes from fragmentation in cells lacking an intact microtubule network. Rescue of fragmentation requires sequences that enable KIF1C to bind Rab6A at both ends, but not KIF1C motor function. Rab6A binding to KIF1C’s motor domain represents an entirely new mode of regulation for a kinesin motor, and likely has important consequences for KIF1C’s cellular functions. DOI: 10.7554/eLife.06029.001 *For correspondence: pfeffer@ stanford.edu Introduction Kinesin superfamily proteins (KIFs) are microtubule-based motors that are responsible for the Present address: †Genentech, motility of membrane-bound compartments and transport vesicles (Hirokawa et al., 2009b; South San Francisco, United States Verhey and Hammond, 2009). Of fundamental interest is how these motor proteins link to specific membrane cargoes and how they are regulated.
[Show full text]