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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 (3) and many more products for this protein.
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simultaneous mutations at all four acetylation sites completely abolish its ability to regulate metabolic targets, such as TIGAR and SLC7A11 (show SLC7A11 Antibodies). Moreover, p53 (show TP53 Antibodies)(4KR) is still capable of inducing the p53 (show TP53 Antibodies)-Mdm2 (show MDM2 Antibodies) feedback loop, but p53 (show TP53 Antibodies)-dependent ferroptotic responses are markedly abrogated
High TIGAR expression was an independent predictor of poor survival and high incidence of relapse in adult patients with CN-AML (show RUNX1 Antibodies). TIGAR also showed high expression in multiple human leukemia cell lines and knockdown of TIGAR activated glycolysis through PFKFB3 (show PFKFB3 Antibodies) upregulation in human leukemia cells.
the upregulation of hsamiR101 in ccRCC was induced by hypoxia. Its expression deceased the protein expression of TIGAR and promoted glycolysis. This regulatory pathway may represent a novel mechanism of carcinogenesis and requires further investigation.
TIGAR expression in breast carcinoma cells promotes metabolic compartmentalization and tumor growth with a mitochondrial metabolic phenotype with lactate and glutamine (show GFPT1 Antibodies) catabolism.
we investigate the crosstalk between PFKFB3 (show PFKFB3 Antibodies) and TIGAR (TP53-Induced Glycolysis and Apoptosis Regulator), a protein known to protect cells from oxidative stress. Our results show consistent TIGAR induction in HeLa cells in response to PFKFB3 (show PFKFB3 Antibodies) knockdown
The study showed that miR (show MLXIP Antibodies)-101 inhibited viability, induced apoptosis, pushed glucose metabolism flux from the pentose phosphate pathway into glycolysis in prostate cancer PC3 (show PCSK1 Antibodies) cell line by decreasing NADPH (show NQO1 Antibodies) levels by throughly directly binding to 3'-UTR (show UTS2R Antibodies) of TIGAR mRNA and repressing TIGAR expression.
This study demonstrated that a high p53 (show TP53 Antibodies) expression could be associated with the promotion of glycolysis in gastric cancer via the modulation of TIGAR expression.
TIGAR expression may be used as a bio-marker for detection of colorectal cancer and can be used as a target for developing therapeutics for the treatment of colorectal cancer.
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 contributes to ischemic tolerance induced by cerebral preconditioning through scavenging of reactive oxygen species and inhibition of apoptosis.
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