SAR1B Antibody Cat

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SAR1B Antibody Cat. No.: 55-163 SAR1B Antibody Flow cytometric analysis of 293 cells (right histogram) Western blot analysis in MCF-7,MDA-MB453 cell line compared to a negative control cell (left histogram).FITC- lysates (35ug/lane). conjugated goat-anti-rabbit secondary antibodies were used for the analysis. Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human Predicted species reactivity based on immunogen sequence: Bovine, Hamster, Mouse, Pig, HOMOLOGY: Rat This SAR1B antibody is generated from rabbits immunized with a KLH conjugated IMMUNOGEN: synthetic peptide between 89-116 amino acids from the Central region of human SAR1B. TESTED APPLICATIONS: Flow, IHC-P, WB September 26, 2021 1 https://www.prosci-inc.com/sar1b-antibody-55-163.html For IHC-P starting dilution is: 1:50~100 APPLICATIONS: For WB starting dilution is: 1:1000 For FACS starting dilution is: 1:10~50 PREDICTED MOLECULAR 22 kDa WEIGHT: Properties This antibody is purified through a protein A column, followed by peptide affinity PURIFICATION: purification. CLONALITY: Polyclonal ISOTYPE: Rabbit Ig CONJUGATE: Unconjugated PHYSICAL STATE: Liquid BUFFER: Supplied in PBS with 0.09% (W/V) sodium azide. CONCENTRATION: batch dependent Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies STORAGE CONDITIONS: care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Additional Info OFFICIAL SYMBOL: SAR1B ALTERNATE NAMES: GTP-binding protein SAR1b, GTP-binding protein B, GTBPB, SAR1B, SARA2, SARB ACCESSION NO.: Q9Y6B6 PROTEIN GI NO.: 14285769 GENE ID: 51128 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References The protein encoded by this gene is a small GTPase that acts as a homodimer. The encoded protein is activated by the guanine nucleotide exchange factor PREB and is involved in protein transport from the endoplasmic reticulum to the Golgi. This protein is BACKGROUND: part of the COPII coat complex. Defects in this gene are a cause of chylomicron retention disease (CMRD), also known as Anderson disease (ANDD). Two transcript variants encoding the same protein have been found for this gene. September 26, 2021 2 https://www.prosci-inc.com/sar1b-antibody-55-163.html REFERENCES: 1) Cefalu, A.B., et al. Metab. Clin. Exp. 59(4):463-467(2010) 2) Silvain, M., et al. Clin. Genet. 74(6):546-552(2008) 3) Charcosset, M., et al. Mol. Genet. Metab. 93(1):74-84(2008) 4) Jardim, D.L., et al. J. Biochem. Mol. Biol. 38(3):328-333(2005) ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. September 26, 2021 3 https://www.prosci-inc.com/sar1b-antibody-55-163.html.

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Chylomicron Retention Disease)
Molecular analysis and intestinal expression of SAR1 genes and proteins in Anderson's disease (Chylomicron retention disease). Amandine Georges, Jessica Bonneau, Dominique Bonnefont-Rousselot, Jacqueline Champigneulle, Jean Rabès,Marianne Abifadel, Thomas Aparicio, Jean Guenedet, Eric Bruckert, Catherine Boileau, et al. To cite this version: Amandine Georges, Jessica Bonneau, Dominique Bonnefont-Rousselot, Jacqueline Champigneulle, Jean Rabès,et al.. Molecular analysis and intestinal expression of SAR1 genes and proteins in Anderson's disease (Chylomicron retention disease).. Orphanet Journal of Rare Diseases, BioMed Central, 2011, 6 (1), pp.1. <10.1186/1750-1172-6-1>. <inserm-00663694> HAL Id: inserm-00663694 http://www.hal.inserm.fr/inserm-00663694 Submitted on 27 Jan 2012 HAL is a multi-disciplinary open access L'archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinéeau dépôtet àla diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiésou non, lished or not. The documents may come from émanant des établissements d'enseignement et de teaching and research institutions in France or recherche fran¸caisou étrangers,des laboratoires abroad, or from public or private research centers. publics ou privés. Georges et al. Orphanet Journal of Rare Diseases 2011, 6:1 http://www.ojrd.com/content/6/1/1 RESEARCH Open Access Molecular analysis and intestinal expression of SAR1 genes and proteins in Anderson’s disease (Chylomicron retention disease) Amandine Georges1, Jessica Bonneau2, Dominique Bonnefont-Rousselot3, Jacqueline Champigneulle4, Jean P Rabès2,8, Marianne Abifadel2, Thomas Aparicio5, Jean C Guenedet4,9, Eric Bruckert6, Catherine Boileau2,8, Alain Morali1, Mathilde Varret2, Lawrence P Aggerbeck7, Marie E Samson-Bouma2* Abstract Background: Anderson’s disease (AD) or chylomicron retention disease (CMRD) is a very rare hereditary lipid malabsorption syndrome.
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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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SAR1B Gene Secretion Associated Ras Related Gtpase 1B
SAR1B gene secretion associated Ras related GTPase 1B Normal Function The SAR1B gene provides instructions for making a protein that is produced in a variety of tissues. Most research involving the SAR1B protein has studied its role in the digestive tract. The SAR1B protein is needed for the transport of molecules called chylomicrons. During digestion, chylomicrons are formed within cells called enterocytes that line the small intestine and absorb nutrients. Chylomicrons are needed to absorb fat-soluble vitamins ( vitamins K, E, and D) and carry fats and cholesterol from the small intestine into the bloodstream. Within enterocytes, SAR1B proteins help transport immature chylomicrons from a cell structure called the endoplasmic reticulum to another cell structure called the Golgi apparatus. Immature chylomicrons are processed within the Golgi apparatus, resulting in mature chylomicrons. These mature chylomicrons are then released from enterocytes into the bloodstream so the body can use the fats and fat-soluble vitamins they carry. Sufficient levels of fats, cholesterol, and vitamins are necessary for normal growth and development. In other tissues, such as the heart and other muscles, the SAR1B protein is likely involved in transporting calcium within cells. Health Conditions Related to Genetic Changes Chylomicron retention disease More than 20 mutations in the SAR1B gene have been found to cause chylomicron retention disease. This is an inherited disorder that impairs the normal absorption of fats, cholesterol, and fat-soluble vitamins from food. Most of the mutations change one protein building block (amino acid) in the SAR1B protein. Other mutations lead to the production of an abnormally small version of the protein that cannot function properly.
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