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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. Zusätzlich bieten wir Ihnen Chromosome 12 Open Reading Frame 5 Proteine (3) und viele weitere Produktgruppen zu diesem Protein an.
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simultaneous mutations at all four acetylation sites completely abolish its ability to regulate metabolic targets, such as TIGAR and SLC7A11 (zeige SLC7A11 Antikörper). Moreover, p53 (zeige TP53 Antikörper)(4KR) is still capable of inducing the p53 (zeige TP53 Antikörper)-Mdm2 (zeige MDM2 Antikörper) feedback loop, but p53 (zeige TP53 Antikörper)-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 (zeige RUNX1 Antikörper). TIGAR also showed high expression in multiple human leukemia cell lines and knockdown of TIGAR activated glycolysis through PFKFB3 (zeige PFKFB3 Antikörper) 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 (zeige GFPT1 Antikörper) catabolism.
we investigate the crosstalk between PFKFB3 (zeige PFKFB3 Antikörper) 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 (zeige PFKFB3 Antikörper) knockdown
The study showed that miR (zeige MLXIP Antikörper)-101 inhibited viability, induced apoptosis, pushed glucose metabolism flux from the pentose phosphate pathway into glycolysis in prostate cancer PC3 (zeige PCSK1 Antikörper) cell line by decreasing NADPH (zeige NQO1 Antikörper) levels by throughly directly binding to 3'-UTR (zeige UTS2R Antikörper) of TIGAR mRNA and repressing TIGAR expression.
This study demonstrated that a high p53 (zeige TP53 Antikörper) 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 (zeige TP53 Antikörper) 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 (zeige TP53 Antikörper) or TAp73 (zeige TP73 Antikörper).
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 (zeige TXN Antikörper) nuclear translocation.
TIGAR protects ischemic brain injury and preserves mitochodrial function.
TIGAR has roles in efficient intestinal regeneration and tumorigenesis
p53 (zeige TP53 Antikörper)/TIGAR-mediated inhibition of myocyte mitophagy is responsible for impairment of mitochondrial integrity and subsequent apoptosis.
p53 (zeige TP53 Antikörper) and TIGAR inhibit glycolysis in hypoxic myocytes and that inhibition of glycolysis is closely involved in apoptosis, suggesting that p53 (zeige TP53 Antikörper) 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