YWHAG Antibody

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Product Datasheet YWHAG antibody Catalog No: #38549 Orders: [email protected] Description Support: [email protected] Product Name YWHAG antibody Host Species Rabbit Clonality Polyclonal Purification Antibodies were purified by affinity purification using immunogen. Applications WB,IHC Species Reactivity Human,Mouse,Rat Specificity The antibody detects endogenous level of total YWHAG antibody. Immunogen Type Peptide Immunogen Description A synthetic peptide of human YWHAG. Target Name YWHAG Other Names 14-3-3GAMMA Accession No. Swiss-Prot#: P61981NCBI Gene ID: 7532 SDS-PAGE MW 28kd Concentration 1.0mg/ml Formulation Supplied at 1.0mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Storage Store at -20°C Application Details WB 1:500 - 1:2000IHC 1:50 - 1:200 Images Western blot analysis of extracts of various cell lines, using YWHAG at 1:500 dilution. Background This gene product belongs to the 14-3-3 family of proteins which mediate signal transduction by binding to phosphoserine-containing proteins. This highly conserved protein family is found in both plants and mammals, and this protein is 100% identical to the rat ortholog. It is induced by growth factors in human vascular smooth muscle cells, and is also highly expressed in skeletal and heart muscles, suggesting an important role for this protein in muscle tissue. It has been shown to interact with RAF1 and protein kinase C, proteins involved in various signal transduction pathways. Address: 8400 Baltimore Ave., Suite 302, College Park, MD 20740, USA http://www.sabbiotech.com 1 Note: This product is for in vitro research use only and is not intended for use in humans or animals. Address: 8400 Baltimore Ave., Suite 302, College Park, MD 20740, USA http://www.sabbiotech.com 2.

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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
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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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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.
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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.
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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.
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YWHAG Monoclonal Antibody, Clone HS23
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