Phillip H. Pekala

There are 5 included publications by Phillip H. Pekala :

TitleDateViewsBrief Description
Ectopic expression of Hel-N1 an RNA-binding protein increases glucose transporter (GLUT1) expression in 3T3-L1 adipocytes. 2011 56348 3T3-L1 preadipocytes ectopically expressing the mammalian RNA-binding protein Hel-N1 expressed up to 10-fold more glucose transporter (GLUT1) protein and exhibited elevated rates of basal glucose uptake. Hel-N1 is a member of the ELAV-like family of ...
HuR binds to a single site on the C/EBP - beta mRNA of 3T3-L1 Adipocytes 2011 56348 HuR is a ligand for nuclear mRNAs containing adenylate-uridylate rich elements in the 3'- untranslated region. Once bound to the mRNA HuR is recognized by adapter proteins which then facilitate nuclear export of the complex. In the cytosol HuR is tho...
Insulin responsiveness in skeletal muscle is determined by glucose transporter (Glut4) protein level. 2011 56348 Glucose transport in skeletal muscle is mediated by two distinct transporter isoforms designated muscle/adipose glucose transporter (Glut4) and erythrocyte/HepG2/brain glucose transporter (Glutl) which differ in both abundance and membrane distributi...
Lipid mediators of insulin resistance: ceramide signalling down-regulates GLUT4 gene transcription in 3T3-L1 adipocytes. 2011 56348 We have previously demonstrated that chronic exposure of 3T3- L1 adipocytes to tumour necrosis factor-α (TNF) resulted in a marked decrease (~90%) in cellular GLUT4 (insulin-responsive glucose transporter) mRNA content as a result of a decreased tra...
Tumour necrosis factor-alpha regulates expression of the CCAAT-enhancer-binding proteins (C/EBPs) alpha and beta and determines the occupation of the C/EBP site in the promoter of the insulin-responsive glucose-transporter gene in 3T3-L1 adipocytes. 2011 56348 We have demonstrated previously that treatment of 3T3-L1 adipocytes with tumour necrosis factor-alpha (TNF) results in a rapid (4 h) and significant (75–80%) reduction in the rate of transcription of the GLUT4 gene. Control of GLUT4 gene transcript...