YWHAG Monoclonal Antibody, Clone HS23

Total Page：16

File Type：pdf, Size：1020Kb

YWHAG monoclonal antibody, clone Gene Alias: 14-3-3GAMMA HS23 Gene Summary: This gene product belongs to the 14-3-3 family of proteins which mediate signal Catalog Number: MAB2288 transduction by binding to phosphoserine-containing proteins. This highly conserved protein family is found in Regulatory Status: For research use only (RUO) both plants and mammals, and this protein is 100% Product Description: Mouse monoclonal antibody identical to the rat ortholog. It is induced by growth raised against YWHAG. factors in human vascular smooth muscle cells, and is also highly expressed in skeletal and heart muscles, Clone Name: HS23 suggesting an important role for this protein in muscle tissue. It has been shown to interact with RAF1 and Immunogen: N-terminus of human YWHAG. protein kinase C, proteins involved in various signal transduction pathways. [provided by RefSeq] Host: Mouse References: Reactivity: Bovine,Chicken,Human,Mouse,Rat,Zebra 1. Elucidation of the function of type 1 human methionine fish aminopeptidase during cell cycle progression. Hu X, Addlagatta A, Lu J, Matthews BW, Liu JO. Proc Natl Applications: ICC, IF, WB-Ce Acad Sci U S A. 2006 Nov 28;103(48):18148-53. Epub (See our web site product page for detailed applications 2006 Nov 17. information) Protocols: See our web site at http://www.abnova.com/support/protocols.asp or product page for detailed protocols Specificity: This antibody is specific to human 14-3-3 gamma. Form: Liquid Isotype: IgG1, kappa Recommend Usage: Immunocytochemistry (1:50-1:200) Immunofluorescence (1:50-1:200) Western Blot (1:1000) The optimal working dilution should be determined by the end user. Storage Buffer: In ascites (0.02% sodium azide) Storage Instruction: Store at 4°C for short term. For long term storage store at -20°C. Aliquot to avoid repeated freezing and thawing. Entrez GeneID: 7532 Gene Symbol: YWHAG Page 1/1 Powered by TCPDF (www.tcpdf.org).

Copy Link

Recommended publications

14-3-3Sigma Negatively Regulates the Stability and Subcellular Localization of Cop1
The Texas Medical Center Library DigitalCommons@TMC The University of Texas MD Anderson Cancer Center UTHealth Graduate School of The University of Texas MD Anderson Cancer Biomedical Sciences Dissertations and Theses Center UTHealth Graduate School of (Open Access) Biomedical Sciences 12-2010 14-3-3SIGMA NEGATIVELY REGULATES THE STABILITY AND SUBCELLULAR LOCALIZATION OF COP1 Chun-Hui Su Follow this and additional works at: https://digitalcommons.library.tmc.edu/utgsbs_dissertations Part of the Biology Commons Recommended Citation Su, Chun-Hui, "14-3-3SIGMA NEGATIVELY REGULATES THE STABILITY AND SUBCELLULAR LOCALIZATION OF COP1" (2010). The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access). 101. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/101 This Dissertation (PhD) is brought to you for free and open access by the The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences at DigitalCommons@TMC. It has been accepted for inclusion in The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access) by an authorized administrator of DigitalCommons@TMC. For more information, please contact [email protected]. 14-3-3SIGMA NEGATIVELY REGULATES THE STABILITY AND SUBCELLULAR LOCALIZATION OF COP1 By Chun-Hui Su, M.S. APPROVED: ______________________________ Mong-Hong Lee, Supervisory Professor ______________________________ Randy
[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]
YWHAG Antibody (Center) Purified Rabbit Polyclonal Antibody (Pab) Catalog # Ap2939c
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 YWHAG Antibody (Center) Purified Rabbit Polyclonal Antibody (Pab) Catalog # AP2939c Specification YWHAG Antibody (Center) - Product Information Application WB, IHC-P, FC,E Primary Accession P61981 Other Accession Q6NRY9, Q6PCG0, P61983, P61982, Q5F3W6, P68252, P68253 Reactivity Human, Mouse Predicted Bovine, Chicken, Rat, Sheep, Xenopus Host Rabbit Clonality Polyclonal Isotype Rabbit Ig Calculated MW 28303 Western blot analysis of YWHAG Antibody Antigen Region 136-164 (Center) (Cat. #AP2939c) in mouse cerebellum tissue lysates (35ug/lane). YWHAG Antibody (Center) - Additional YWHAG (arrow) was detected using the Information purified Pab. Gene ID 7532 Other Names 14-3-3 protein gamma, Protein kinase C inhibitor protein 1, KCIP-1, 14-3-3 protein gamma, N-terminally processed, YWHAG Target/Specificity This YWHAG antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 136-164 amino acids from the Central region of human YWHAG. Dilution Western blot analysis of YWHAG (arrow) WB~~1:1000 using rabbit polyclonal YWHAG Antibody IHC-P~~1:50~100 (Center) (Cat. #AP2939c). 293 cell lysates (2 FC~~1:10~50 ug/lane) either nontransfected (Lane 1) or transiently transfected (Lane 2) with the Format YWHAG gene. Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. Page 1/3 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 Storage Maintain refrigerated at 2-8°C for up to 2 weeks.
[Show full text]
Mir-222 Inhibited OS Via YWHAG
European Review for Medical and Pharmacological Sciences 2018; 22: 2588-2597 MicroRNA-222 contributed to cell proliferation, invasion and migration via regulating YWHAG in osteosarcoma Y.-W. CHU1, C.-R. WANG1, F.-B. WENG1, Z.-J. YAN1, C. WANG2 1Department of Orthopedic, First People’s Hospital of Wujiang District, Affiliated Hospital of Nantong University Medical School, Suzhou, China 2Department of Orthopedic, The Third People’s Hospital of Yancheng, Affiliated Yancheng Hospital of Southeast University Medical School, Yancheng, China Yawei Chu and Churong Wang contributed equally to this work Abstract. – OBJECTIVE: The aim of this study Introduction was to investigate the role of microRNA-222 (miR-222) in osteosarcoma (OS), and to further Osteosarcoma (OS) is a common malignant explore the potential molecular mechanism. osteogenic tumor, which is predisposed to attack PATIENTS AND METHODS: We measured the the adolescence, and has a poor prognosis with a level of miR-222 in OS tissues and cell lines using high degree of malignancy1. The current 5-year quantitative Real-time polymerase chain reaction. Synthesized miR-222 mimics or inhibitors were survival rate is only about 55% to 68%, with the obtained to up-regulate or down-regulate the ex- vast majority of patients eventually occurring 2 pression of miR-222 in U2OS or Saos2 cells. Cell tumor metastasis . Therefore, looking for new counting kit-8 (CCK8) and colony formation assay and effective prevention and control measures to were employed to detect the ability of cell prolif- improve the quality of life and survival of pa- eration, and transwell assay was used to confirm tients and to prevent or delay the transfer of OS the ability of cell invasion.
[Show full text]
Differential Expression of 14-3-3 Isoforms in Human Alcoholic Brain
Published in final edited form as: Alcohol Clin Exp Res. 2011 June ; 35(6): 1041±1049. doi:10.1111/j.1530-0277.2011.01436.x. Differential expression of 14-3-3 isoforms in human alcoholic brain Rachel K. MacKay, M.MolBiol1, Natalie J. Colson, PhD1, Peter R. Dodd, PhD2, and Joanne M. Lewohl, PhD1 1Griffith Health Institute and School of Medical Sciences, Griffith University, Gold Coast Campus, Southport, Australia 2School of Chemistry and Molecular Biosciences, University of Queensland, Brisbane, Australia Abstract Background—Neuropathological damage due to chronic alcohol abuse often results in impairment of cognitive function. The damage is particularly marked in the frontal cortex. The 14-3-3 protein family consists of 7 proteins, β, γ, ε, ζ, η, θ and σ, encoded by 7 distinct genes. They are highly conserved molecular chaperones with roles in regulation of metabolism, signal transduction, cell-cycle control, protein trafficking, and apoptosis. They may also play an important role in neurodegeneration in chronic alcoholism. Methods—We used Real-Time PCR to measure the expression of 14-3-3 mRNA transcripts in both the dorsolateral prefrontal cortex and motor cortex of human brains obtained at autopsy. Results—We found significantly lower 14-3-3β, γ and θ expression in both cortical areas of alcoholics; but no difference in 14-3-3η expression, and higher expression of 14-3-3σ, in both areas. Levels of 14-3-3ζ and ε transcripts were significantly lower only in alcoholic motor cortex. Conclusions—Altered 14-3-3 expression could contribute to synaptic dysfunction and altered neurotransmission in chronic alcohol misuse by human subjects.
[Show full text]
Evidence for the Role of Ywha in Mouse Oocyte Maturation
EVIDENCE FOR THE ROLE OF YWHA IN MOUSE OOCYTE MATURATION A thesis submitted To Kent State University in partial Fulfillment of the requirements for the Degree of Master of Science By Ariana Claire Detwiler August, 2015 © Copyright All rights reserved Except for previously published materials Thesis written by Ariana Claire Detwiler B.S., Pennsylvania State University, 2012 M.S., Kent State University, 2015 Approved by ___________________________________________________________ Douglas W. Kline, Professor, Ph.D., Department of Biological Sciences, Masters Advisor ___________________________________________________________ Laura G. Leff, Professor, PhD., Chair, Department of Biological Sciences ___________________________________________________________ James L. Blank, Professor, Dean, College of Arts and Sciences i TABLE OF CONTENTS List of Figures ……………………………………………………………………………………v List of Tables ……………………………………………………………………………………vii Acknowledgements …………………………………………………………………………….viii Abstract ……………………………………………………………………………………….....1 Chapter I Introduction…………………………………………………………………………………..2 1.1 Introduction …………………………………………………………………………..2 1.2 Ovarian Function ……………………………………………………………………..2 1.3 Oogenesis and Folliculogenesis ………………………………………………………3 1.4 Oocyte Maturation ……………………………………………………………………5 1.5 Maternal to Embryonic Messenger RNA Transition …………………………………8 1.6 Meiotic Spindle Formation …………………………………………………………...9 1.7 YWHA Isoforms and Oocyte Maturation …………………………………………...10 Aim…………………………………………………………………………………………..15 Chapter II Methods……………………………………………………………………………………...16
[Show full text]
The Kinesin Spindle Protein Inhibitor Filanesib Enhances the Activity of Pomalidomide and Dexamethasone in Multiple Myeloma
Plasma Cell Disorders SUPPLEMENTARY APPENDIX The kinesin spindle protein inhibitor filanesib enhances the activity of pomalidomide and dexamethasone in multiple myeloma Susana Hernández-García, 1 Laura San-Segundo, 1 Lorena González-Méndez, 1 Luis A. Corchete, 1 Irena Misiewicz- Krzeminska, 1,2 Montserrat Martín-Sánchez, 1 Ana-Alicia López-Iglesias, 1 Esperanza Macarena Algarín, 1 Pedro Mogollón, 1 Andrea Díaz-Tejedor, 1 Teresa Paíno, 1 Brian Tunquist, 3 María-Victoria Mateos, 1 Norma C Gutiérrez, 1 Elena Díaz- Rodriguez, 1 Mercedes Garayoa 1* and Enrique M Ocio 1* 1Centro Investigación del Cáncer-IBMCC (CSIC-USAL) and Hospital Universitario-IBSAL, Salamanca, Spain; 2National Medicines Insti - tute, Warsaw, Poland and 3Array BioPharma, Boulder, Colorado, USA *MG and EMO contributed equally to this work ©2017 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol. 2017.168666 Received: March 13, 2017. Accepted: August 29, 2017. Pre-published: August 31, 2017. Correspondence: [email protected] MATERIAL AND METHODS Reagents and drugs. Filanesib (F) was provided by Array BioPharma Inc. (Boulder, CO, USA). Thalidomide (T), lenalidomide (L) and pomalidomide (P) were purchased from Selleckchem (Houston, TX, USA), dexamethasone (D) from Sigma-Aldrich (St Louis, MO, USA) and bortezomib from LC Laboratories (Woburn, MA, USA). Generic chemicals were acquired from Sigma Chemical Co., Roche Biochemicals (Mannheim, Germany), Merck & Co., Inc. (Darmstadt, Germany). MM cell lines, patient samples and cultures. Origin, authentication and in vitro growth conditions of human MM cell lines have already been characterized (17, 18). The study of drug activity in the presence of IL-6, IGF-1 or in co-culture with primary bone marrow mesenchymal stromal cells (BMSCs) or the human mesenchymal stromal cell line (hMSC–TERT) was performed as described previously (19, 20).
[Show full text]
Rare Copy Number Variants Are an Important Cause of Epileptic Encephalopathies
ORIGINAL ARTICLE Rare Copy Number Variants Are an Important Cause of Epileptic Encephalopathies Heather C. Mefford, MD, PhD,1 Simone C. Yendle, BSc,2 Cynthia Hsu, BS,1 Joseph Cook, MS,1 Eileen Geraghty, BA,1 Jacinta M. McMahon, BSc,2 Orvar Eeg-Olofsson, MD, PhD,3 Lynette G. Sadleir, MBChB, MD,4 Deepak Gill, MBBS, BSc,5 Bruria Ben-Zeev, MD,6,7 Tally Lerman-Sagie, MD,7,8 Mark Mackay, MBBS,9,10 Jeremy L. Freeman, MBBS,10 Eva Andermann, MD, PhD,11 James T. Pelakanos, MBBS,12 Ian Andrews, MBBS,13 Geoffrey Wallace, MBBS,14 Evan E. Eichler, PhD,15,16 Samuel F. Berkovic, MD,2 and Ingrid E. Scheffer, MBBS, PhD2,9,10,17 Objective: Rare copy number variants (CNVs)—deletions and duplications—have recently been established as important risk factors for both generalized and focal epilepsies. A systematic assessment of the role of CNVs in epileptic encephalopathies, the most devastating and often etiologically obscure group of epilepsies, has not been performed. Methods: We evaluated 315 patients with epileptic encephalopathies characterized by epilepsy and progressive cognitive impairment for rare CNVs using a high-density, exon-focused, whole-genome oligonucleotide array. Results: We found that 25 of 315 (7.9%) of our patients carried rare CNVs that may contribute to their phenotype, with at least one-half being clearly or likely pathogenic. We identified 2 patients with overlapping deletions at 7q21 and 2 patients with identical duplications of 16p11.2. In our cohort, large deletions were enriched in affected individuals compared to controls, and 4 patients harbored 2 rare CNVs.
[Show full text]
Mutations and Protein Interaction Landscape Reveal Key Cellular Events Perturbed in Upper Motor Neurons with HSP and PLS
brain sciences Article Mutations and Protein Interaction Landscape Reveal Key Cellular Events Perturbed in Upper Motor Neurons with HSP and PLS Oge Gozutok 1, Benjamin Ryan Helmold 1 and P. Hande Ozdinler 1,2,3,4,* 1 Department of Neurology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Ave, Chicago, IL 60611, USA; [email protected] (O.G.); [email protected] (B.R.H.) 2 Center for Molecular Innovation and Drug Discovery, Center for Developmental Therapeutics, Chemistry of Life Processes Institute, Northwestern University, Evanston, IL 60611, USA 3 Mesulam Center for Cognitive Neurology and Alzheimer’s Disease, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA 4 Feinberg School of Medicine, Les Turner ALS Center at Northwestern University, Chicago, IL 60611, USA * Correspondence: [email protected]; Tel.: +1-(312)-503-2774 Abstract: Hereditary spastic paraplegia (HSP) and primary lateral sclerosis (PLS) are rare motor neuron diseases, which affect mostly the upper motor neurons (UMNs) in patients. The UMNs display early vulnerability and progressive degeneration, while other cortical neurons mostly remain functional. Identiﬁcation of numerous mutations either directly linked or associated with HSP and PLS begins to reveal the genetic component of UMN diseases. Since each of these mutations are identiﬁed on genes that code for a protein, and because cellular functions mostly depend on protein- protein interactions, we hypothesized that the mutations detected in patients and the alterations in Citation: Gozutok, O.; Helmold, B.R.; protein interaction domains would hold the key to unravel the underlying causes of their vulnerability. Ozdinler, P.H. Mutations and Protein In an effort to bring a mechanistic insight, we utilized computational analyses to identify interaction Interaction Landscape Reveal Key Cellular Events Perturbed in Upper partners of proteins and developed the protein-protein interaction landscape with respect to HSP Motor Neurons with HSP and PLS.
[Show full text]
Peripheral Nerve Single-Cell Analysis Identifies Mesenchymal Ligands That Promote Axonal Growth
Research Article: New Research Development Peripheral Nerve Single-Cell Analysis Identifies Mesenchymal Ligands that Promote Axonal Growth Jeremy S. Toma,1 Konstantina Karamboulas,1,ª Matthew J. Carr,1,2,ª Adelaida Kolaj,1,3 Scott A. Yuzwa,1 Neemat Mahmud,1,3 Mekayla A. Storer,1 David R. Kaplan,1,2,4 and Freda D. Miller1,2,3,4 https://doi.org/10.1523/ENEURO.0066-20.2020 1Program in Neurosciences and Mental Health, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada, 2Institute of Medical Sciences University of Toronto, Toronto, Ontario M5G 1A8, Canada, 3Department of Physiology, University of Toronto, Toronto, Ontario M5G 1A8, Canada, and 4Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5G 1A8, Canada Abstract Peripheral nerves provide a supportive growth environment for developing and regenerating axons and are es- sential for maintenance and repair of many non-neural tissues. This capacity has largely been ascribed to paracrine factors secreted by nerve-resident Schwann cells. Here, we used single-cell transcriptional profiling to identify ligands made by different injured rodent nerve cell types and have combined this with cell-surface mass spectrometry to computationally model potential paracrine interactions with peripheral neurons. These analyses show that peripheral nerves make many ligands predicted to act on peripheral and CNS neurons, in- cluding known and previously uncharacterized ligands. While Schwann cells are an important ligand source within injured nerves, more than half of the predicted ligands are made by nerve-resident mesenchymal cells, including the endoneurial cells most closely associated with peripheral axons. At least three of these mesen- chymal ligands, ANGPT1, CCL11, and VEGFC, promote growth when locally applied on sympathetic axons.
[Show full text]
Phenotype Informatics
Freie UniversitätBerlin Department of Mathematics and Computer Science Phenotype informatics: Network approaches towards understanding the diseasome Sebastian Kohler¨ Submitted on: 12th September 2012 Dissertation zur Erlangung des Grades eines Doktors der Naturwissenschaften (Dr. rer. nat.) am Fachbereich Mathematik und Informatik der Freien Universitat¨ Berlin ii 1. Gutachter Prof. Dr. Martin Vingron 2. Gutachter: Prof. Dr. Peter N. Robinson 3. Gutachter: Christopher J. Mungall, Ph.D. Tag der Disputation: 16.05.2013 Preface This thesis presents research work on novel computational approaches to investigate and characterise the association between genes and pheno- typic abnormalities. It demonstrates methods for organisation, integra- tion, and mining of phenotype data in the field of genetics, with special application to human genetics. Here I will describe the parts of this the- sis that have been published in peer-reviewed journals. Often in modern science different people from different institutions contribute to research projects. The same is true for this thesis, and thus I will itemise who was responsible for specific sub-projects. In chapter 2, a new method for associating genes to phenotypes by means of protein-protein-interaction networks is described. I present a strategy to organise disease data and show how this can be used to link diseases to the corresponding genes. I show that global network distance measure in interaction networks of proteins is well suited for investigat- ing genotype-phenotype associations. This work has been published in 2008 in the American Journal of Human Genetics. My contribution here was to plan the project, implement the software, and finally test and evaluate the method on human genetics data; the implementation part was done in close collaboration with Sebastian Bauer.
[Show full text]
Generative Modeling of Multi-Mapping Reads with Mhi-C
Manuscript submitted to eLife 1 Generative Modeling of 2 Multi-mapping Reads with mHi-C 3 Advances Analysis of Hi-C Studies 1 2,3 1,4* 4 Ye Zheng , Ferhat Ay , Sündüz Keleş *For correspondence: [email protected] (SK) 1 2 5 Department of Statistics, University of Wisconsin-Madison, Madison, WI 53706, USA; La 3 6 Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA; School of Medicine, 4 7 University of California San Diego, La Jolla, CA 92093, USA; Department of Biostatistics 8 and Medical Informatics, University of Wisconsin-Madison, Madison, WI 53706, USA 9 10 Abstract Current Hi-C analysis approaches are unable to account for reads that align to multiple 11 locations, and hence underestimate biological signal from repetitive regions of genomes. We 12 developed and validated mHi-C,amulti-read mapping strategy to probabilistically allocate Hi-C 13 multi-reads. mHi-C exhibited superior performance over utilizing only uni-reads and heuristic 14 approaches aimed at rescuing multi-reads on benchmarks. Specifically, mHi-C increased the 15 sequencing depth by an average of 20% resulting in higher reproducibility of contact matrices and 16 detected interactions across biological replicates. The impact of the multi-reads on the detection of 17 significant interactions is influenced marginally by the relative contribution of multi-reads to the 18 sequencing depth compared to uni-reads, cis-to-trans ratio of contacts, and the broad data quality 19 as reflected by the proportion of mappable reads of datasets. Computational experiments 20 highlighted that in Hi-C studies with short read lengths, mHi-C rescued multi-reads can emulate the 21 effect of longer reads.
[Show full text]