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C12orf5 is regulated as part of the p53 tumor suppressor pathway and encodes a protein with sequence similarity to the bisphosphate domain of the glycolytic enzyme that degrades fructose-2,6-bisphosphate. Additionally we are shipping Chromosome 12 Open Reading Frame 5 Proteins (19) and Chromosome 12 Open Reading Frame 5 Kits (3) and many more products for this protein.
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Human Polyclonal C12orf5 Primary Antibody for EIA, IHC (p) - ABIN500909
Corcoran, Huang, Sheikh: The regulation of energy generating metabolic pathways by p53. in Cancer biology & therapy 2007
Show all 3 references for ABIN500909
Human Polyclonal C12orf5 Primary Antibody for EIA, IHC (p) - ABIN500907
Guimaraes, Hainaut: TP53: a key gene in human cancer. in Biochimie 2002
Show all 3 references for ABIN500907
TIGAR knockdown reduced tumor growth rate.
Geranylgeranoic acid induced upregulation of the TIGAR gene, which might inhibit the glycolysis in HuH-7 cells with p53 (show TP53 Antibodies) mutation.
TIGAR over-expression could diminish the radiosensitivity of Hs 917.T cells, and the autophagy level induced by ionizing radiation (IR) was also decreased by TIGAR transfection.
The Cdk5 (show CDK5 Antibodies)-AMT (show AMT Antibodies) signal pathway involved in regulation of DDR (show DDR1 Antibodies) by TIGAR.
miR (show MLXIP Antibodies)-144 targeted TIGAR, inhibited proliferation, enhanced apoptosis, and increased autophagy in A549 and H460 cells
Results revealed that TIGAR inhibits both apoptosis and autophagy.
TIGAR is correlated with maximal standardized uptake value on FDG (show SMUG1 Antibodies)-PET and survival in non-small cell lung cancer.
Data show targeting MUC1 (show MUC1 Antibodies)-C is synergistic with bortezomib (BTZ (show CASC3 Antibodies)) in suppressing p53 (show TP53 Antibodies)-inducible regulator of glycolysis and apoptosis (TIGAR)-mediated regulation of reactive oxygen species levels for combining GO-203 with BTZ (show CASC3 Antibodies) in BTZ (show CASC3 Antibodies) resistance.
The kinetic properties and the structural similarity of the best substrates of TIGAR make it unlikely that TIGAR modulates cellular fructose 2,6-bisphosphate levels directly.
CREB (show CREB1 Antibodies) regulates TIGAR expression via a CRE-binding site at the TIGAR promoter.
Results suggest that TIGAR expression changes during development and its expression level may be correlated with the vulnerability of neurons to ischemic injury.
Although mouse TIGAR expression is clearly induced in the intestines of mice following DNA-damaging stress of ionizing radiation, that was not dependent on p53 (show TP53 Antibodies) or TAp73 (show TP73 Antibodies).
TIGAR protein expression in brain is increased following ischemia reperfusion injury.
Therefore, we conclude that TIGAR knockdown-induced radiosensitization of glioma cells may be dependent on the inhibition of TRX1 (show TXN Antibodies) nuclear translocation.
TIGAR protects ischemic brain injury and preserves mitochodrial function.
TIGAR has roles in efficient intestinal regeneration and tumorigenesis
p53 (show TP53 Antibodies)/TIGAR-mediated inhibition of myocyte mitophagy is responsible for impairment of mitochondrial integrity and subsequent apoptosis.
p53 (show TP53 Antibodies) and TIGAR inhibit glycolysis in hypoxic myocytes and that inhibition of glycolysis is closely involved in apoptosis, suggesting that p53 (show TP53 Antibodies) and TIGAR are significant mediators of cellular energy homeostasis and cell death under ischemic stress.
This gene is regulated as part of the p53 tumor suppressor pathway and encodes a protein with sequence similarity to the bisphosphate domain of the glycolytic enzyme that degrades fructose-2,6-bisphosphate. The protein functions by blocking glycolysis and directing the pathway into the pentose phosphate shunt. Expression of this protein also protects cells from DNA damaging reactive oxygen species and provides some protection from DNA damage-induced apoptosis. The 12p13.32 region that includes this gene is paralogous to the 11q13.3 region.
TP53-induced glycolysis and apoptosis regulator
, fructose-2,6-bisphosphatase TIGAR
, probable fructose-2,6-bisphosphatase TIGAR
, chromosome 12 open reading frame 5
, fructose-2,6-bisphosphate 2-phosphatase
, transactivated by NS3TP2 protein