Human TIGAR protein (Recombinant) (N-His) (STJP009477)
SPECIFICATIONS
HostE.coli
ImmunogenHomo sapiens (Human)
General Information
| Short Description | Recombinant-Human TIGAR-N-His protein was developed from e.coli for the region N-His. For use in research applications. |
| Applications | ELISA/Immunogen/SDS-PAGE/WB |
| Host | E.coli |
| Note | STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS. |
Product Properties
| Dilution Range | Reconstitute in sterile water for a stock solution. A copy of datasheet will be provided with the products, please refer to it for details. |
| Formulation | Lyophilized from a solution in PBS pH 7.4, 0.02% NLS, 1mM EDTA, 4% Trehalose, 1% Mannitol. |
| Storage Instruction | Use a manual defrost freezer and avoid repeated freeze thaw cycles. Store at 2 to 8°C for frequent use. Store at-20 to-80°C for twelve months from the date of receipt. |
Target Information
| Gene Symbol | TIGAR |
| Gene ID | 57103 |
| Uniprot ID | TIGAR_HUMAN |
| Immunogen | Homo sapiens (Human) |
| Immunogen Region | Met1-Arg270 |
Additional Info
| Function | Fructose-bisphosphatase hydrolyzing fructose-2,6-bisphosphate as well as fructose-1,6-bisphosphate. Acts as a negative regulator of glycolysis by lowering intracellular levels of fructose-2,6-bisphosphate in a p53/TP53-dependent manner, resulting in the pentose phosphate pathway (PPP) activation and NADPH production. Contributes to the generation of reduced glutathione to cause a decrease in intracellular reactive oxygen species (ROS) content, correlating with its ability to protect cells from oxidative or metabolic stress-induced cell death. Plays a role in promoting protection against cell death during hypoxia by decreasing mitochondria ROS levels in a HK2-dependent manner through a mechanism that is independent of its fructose-bisphosphatase activity. In response to cardiac damage stress, mediates p53-induced inhibition of myocyte mitophagy through ROS levels reduction and the subsequent inactivation of BNIP3. Reduced mitophagy results in an enhanced apoptotic myocyte cell death, and exacerbates cardiac damage. Plays a role in adult intestinal regeneration.contributes to the growth, proliferation and survival of intestinal crypts following tissue ablation. Plays a neuroprotective role against ischemic brain damage by enhancing PPP flux and preserving mitochondria functions. Protects glioma cells from hypoxia- and ROS-induced cell death by inhibiting glycolysis and activating mitochondrial energy metabolism and oxygen consumption in a TKTL1-dependent and p53/TP53-independent manner. Plays a role in cancer cell survival by promoting DNA repair through activating PPP flux in a CDK5-ATM-dependent signaling pathway during hypoxia and/or genome stress-induced DNA damage responses. Involved in intestinal tumor progression. |
| Protein Name | Fructose-2 -6-Bisphosphatase TigarTp53-Induced Glycolysis And Apoptosis RegulatorTp53-Induced Glycolysis Regulatory Phosphatase |
| Database Links | Reactome: R-HSA-5628897 |
| Cellular Localisation | CytoplasmNucleusMitochondrionTranslocated To The Mitochondria During Hypoxia In A Hif1a-Dependent MannerColocalizes With Hk2 In The Mitochondria During HypoxiaTranslocated To The Nucleus During Hypoxia And/Or Genome Stress-Induced Dna Damage Responses In Cancer CellsTranslocation To The Mitochondria Is Enhanced In Ischemic Cortex After Reperfusion And/Or During Oxygen And Glucose Deprivation (Ogd)/Reoxygenation Insult In Primary Neurons |
| Alternative Protein Names | Fructose-2 -6-Bisphosphatase Tigar proteinTp53-Induced Glycolysis And Apoptosis Regulator proteinTp53-Induced Glycolysis Regulatory Phosphatase proteinTIGAR proteinC12orf5 protein |
Information sourced from Uniprot.org