Search results for: TIGAR Antibody
#30267647 
2018/09/26
To Up
TIGAR inclusion pathology is specific for Lewy body diseases.
We previously reported up-regulation of tigarb (the zebrafish orthologue of human TIGAR, TP53 - Induced Glycolysis and Apoptosis Regulator) in a zebrafish pink1 model of Parkinson's disease (PD). Genetic inactivation of tigarb led to the rescue of dopaminergic neurons and mitochondrial function in pink zebrafish. The aim of this study was to determine the relevance of TIGAR for human PD, investigate its disease specificity and identify relevant upstream and downstream mechanisms.Karla L Robles López, Julie E Simpson, Lisa C Watson, Heather Mortiboys, Guillaume M Hautbergue, Oliver Bandmann, J Robin Highley
1506 related Products with: TIGAR inclusion pathology is specific for Lewy body diseases.
250 ml100 TESTS0.2 mg1 LITRE0.1 mg100 ml25 µg0.1 ml1 ml0.25 mg0.1 mg25 µg
Related Pathways
#26212201 2015/07/23
To Up
Resveratrol inhibits TIGAR to promote ROS induced apoptosis and autophagy.
Resveratrol has been shown to exhibit its anti-cancer effect through a variety of mechanisms. Here, TIGAR (TP53-Induced Glycolysis and Apoptosis Regulator) was identified as an important target of resveratrol for exhibiting ROS-dependent-consequences on apoptosis and autophagy. Resveratrol treatment decreased TIGAR protein irrespective of cell line used. Down-regulated TIGAR protein triggered a drop in reduced-glutathione levels which resulted in sustained ROS, responsible for apoptosis and autophagy. Over-expression and silencing experiments demonstrated the importance of TIGAR in affecting the ROS-dependent anti-cancer effects of resveratrol. Resveratrol treated cells exhibited autophagy to escape apoptosis, however, chloroquine treatment along with resveratrol, blocked protective autophagy and facilitated apoptosis. Collectively, results unravel the effects of resveratrol on TIGAR in mediating its ROS dependent influence and suggest a better combination therapy of resveratrol and chloroquine for probable cancer treatment.Bhupender Kumar, Mohammad Askandar Iqbal, Rajnish Kumar Singh, Rameshwar N K Bamezai
1445 related Products with: Resveratrol inhibits TIGAR to promote ROS induced apoptosis and autophagy.
2 Pieces/Box 25 G100 extractions0.1 mg5 mg 1000 ml 96 Tests n2.5 mg1 module100ug100ug Lyophilized
Related Pathways
#22591674 2012/05/16
To Up
Small molecule inhibition of 6-phosphofructo-2-kinase suppresses t cell activation.
T cell activation is associated with a rapid increase in intracellular fructose-2,6-bisphosphate (F2,6BP), an allosteric activator of the glycolytic enzyme, 6-phosphofructo-1-kinase. The steady state concentration of F2,6BP in T cells is dependent on the expression of the bifunctional 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFKFB1-4) and the fructose-2,6-bisphosphatase, TIGAR. Of the PFKFB family of enzymes, PFKFB3 has the highest kinase:bisphosphatase ratio and has been demonstrated to be required for T cell proliferation. A small molecule antagonist of PFKFB3, 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO), recently has been shown to reduce F2,6BP synthesis, glucose uptake and proliferation in transformed cells. We hypothesized that the induction of PFKFB3 expression may be required for the stimulation of glycolysis in T cells and that exposure to the PFKFB3 antagonist, 3PO, would suppress T cell activation.Sucheta Telang, Brian F Clem, Alden C Klarer, Amy L Clem, John O Trent, Richard Bucala, Jason Chesney
1753 related Products with: Small molecule inhibition of 6-phosphofructo-2-kinase suppresses t cell activation.
Related Pathways
#21864926 2011/08/22
To Up
TP53 induced glycolysis and apoptosis regulator (TIGAR) knockdown results in radiosensitization of glioma cells.
The TP53 induced glycolysis and apoptosis regulator (TIGAR) functions to lower fructose-2,6-bisphosphate (Fru-2,6-P(2)) levels in cells, consequently decreasing glycolysis and leading to the scavenging of reactive oxygen species (ROS), which correlate with a higher resistance to cell death. The decrease in intracellular ROS levels in response to TIGAR may also play a role in the ability of p53 to protect from the accumulation of genomic lesions. Given these good prospects of TIGAR for metabolic regulation and p53-response modulation, we analyzed the effects of TIGAR knockdown in U87MG and T98G glioblastoma-derived cell lines.Miguel A Peña-Rico, María Nieves Calvo-Vidal, Ruth Villalonga-Planells, Fina Martínez-Soler, Pepita Giménez-Bonafé, Àurea Navarro-Sabaté, Avelina Tortosa, Ramon Bartrons, Anna Manzano