Effect of Slc35b4 knockdown on total and O-glycosylated cellular proteins in HepG2 cell line. (c2012)

LAUR Repository

Show simple item record

dc.contributor.author Antonios, Gregory
dc.date.accessioned 2015-09-18T04:43:17Z
dc.date.available 2015-09-18T04:43:17Z
dc.date.copyright 2012 en_US
dc.date.issued 2015-09-18
dc.date.submitted 2012-09-21
dc.identifier.uri http://hdl.handle.net/10725/2151
dc.description.abstract Diabetes is considered a Non-Communicable Disease (NCD). Type II diabetes is caused by the lack of insulin production from liver beta cells in the aftermath of insulin resistance. Slc35b4 encodes a protein that transports UDP-xylose and UDP-N-acetylglucosamine from the cytosol into the golgi. UDP-N-acetylglucosamine then serves as both a substrate for O-linked glycosylation (O-GlcNAC) and as a negative feedback inhibitor of the Hexosamine Biosynthesis Pathway (HBP) pathway. Solute receptor SLC35b4 has been identified, using both genetic and functional studies, as a regulator of obesity, insulin resistance and gluconeogenesis by Yazbek et al. Over 600 proteins are modified with the addition of an O-GlcNAC moiety and may therefore contribute to the phenotype. This study employs One Dimensional (1D) and Two Dimensional (2D) electrophoresis to investigate differentially expressed O-glycosylated and total proteins in a HepG2 (Human liver carcinoma cell line) SLC35b4 knockdown cell line. Western blot analysis, using a primary antibody against O-glycosylated proteins, showed one differentially expressed O-glycosylated protein in a HepG2 cell line knockdown of SLC35b4. Its size was estimated to be 67.5 kDa. The 2D electrophoresis study of SLC35b4 knockdown resulted in the differential expression of 10 proteins, more than 2 fold, as compared to control siRNA. Moreover, 3 of the differentially expressed proteins (corresponding to Spots SSP 6203, 6204 and 8102) have very close matches in O-glycosylated proteins of the insulin resistance pathway where O-glycosylation might play a role in glucose synthesis. The identification of the differentially expressed protein is a must in order to assess SLC35b4 role in the insulin resistance (IR) pathway using its knockdown. en_US
dc.language.iso en en_US
dc.subject Non-insulin-dependent diabetes en_US
dc.subject Glycoproteins -- Synthesis en_US
dc.subject Insulin resistance en_US
dc.subject Glycosyltransferases en_US
dc.subject Lebanese American University -- Dissertations en_US
dc.subject Dissertations, Academic en_US
dc.title Effect of Slc35b4 knockdown on total and O-glycosylated cellular proteins in HepG2 cell line. (c2012) en_US
dc.type Thesis en_US
dc.term.submitted Summer II en_US
dc.author.degree MS in Molecular Biology en_US
dc.author.school SAS en_US
dc.author.idnumber 200904351 en_US
dc.author.commembers Yazbek, Soha
dc.author.commembers Tokajian, Sima
dc.author.woa OA en_US
dc.author.department Biology en_US
dc.description.embargo N/A en_US
dc.description.physdesc 1 hard copy: xv, 55 leaves; col. ill.; 31 cm. available at RNL. en_US
dc.author.advisor Wex, Brigitte
dc.keywords Type II diabetes en_US
dc.keywords Two Dimensional electrophoresis en_US
dc.keywords SLC35b4 en_US
dc.keywords O-glycosylated proteins en_US
dc.description.bibliographiccitations Includes bibliographical references (leaves 49-55). en_US
dc.identifier.doi https://doi.org/10.26756/th.2012.41 en_US
dc.publisher.institution Lebanese American University en_US

Files in this item

This item appears in the following Collection(s)

Show simple item record

Search LAUR

Advanced Search


My Account