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Chromosome 12 open reading frame 5

TIGAR, TP53-induced glycolysis and apoptosis regulator, C12orf5
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: p53, Ros, V1a, CAN, SCO2
Papers on TIGAR
Oncogenic role of the TP53-induced glycolysis and apoptosis regulator in nasopharyngeal carcinoma through NF-κB pathway modulation.
Yang et al., China. In Int J Oncol, Feb 2016
The TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene, which functions to suppress reactive oxygen species (ROS) damage and protect cells from apoptosis.
Opposing effects of TIGAR- and RAC1-derived ROS on Wnt-driven proliferation in the mouse intestine.
Vousden et al., Glasgow, United Kingdom. In Genes Dev, Feb 2016
However, APC loss also increased the expression of TIGAR, which functions to limit ROS.
Reduced Nicotinamide Adenine Dinucleotide Phosphate, a Pentose Phosphate Pathway Product, Might Be a Novel Drug Candidate for Ischemic Stroke.
Qin et al., Shanghai, China. In Stroke, Jan 2016
BACKGROUND AND PURPOSE: Our previous study has defined a role of TP53-induced glycolysis and apoptosis regulator in neuroprotection against ischemic injury through increasing the flow of pentose phosphate pathway.
Downregulation of caveolin‑1 upregulates the expression of growth factors and regulators in co‑culture of fibroblasts with cancer cells.
Li et al., Nanchang, China. In Mol Med Report, Jan 2016
Tumor protein 53‑induced glycolysis and apoptosis regulator (TIGAR) was upregulated in the BT474 cells under the condition of co‑culture with Cav‑1 siRNA fibroblasts, while levels of reactive oxygen species (ROS) were decreased, resulting in apoptosis inhibition in the breast cancer cells.
Identification of the TP53-induced glycolysis and apoptosis regulator in various stages of colorectal cancer patients.
Ahmad et al., Riyadh, Saudi Arabia. In Oncol Rep, Jan 2016
UNASSIGNED: The TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene known to regulate glycolysis by acting as fructose bis-phosphatase (FBPase) and modulate reactive oxygen species.
Novel therapeutic interventions for p53-altered tumors through manipulation of its family members, p63 and p73.
Flores et al., Houston, United States. In Cell Cycle, Jan 2016
We report that inhibition of both ΔNp63 and ΔNp73 in combination results in upregulation of three key metabolic regulators, IAPP, GLS2, and TIGAR resulting in an increase in apoptosis and tumor regression in ΔNp63/ΔNp73/p53 deficient thymic lymphomas.
CK2 induced RIG-I drives metabolic adaptations in IFNγ-treated glioma cells.
Sen et al., India. In Cytokine, Dec 2015
While RIG-I had no effect on glioma cell survival, it increased expression of p53 and its downstream target TP53 induced glycolysis and apoptosis regulator (TIGAR).
ROS and Autophagy: Interactions and Molecular Regulatory Mechanisms.
Zhang et al., Tianjin, China. In Cell Mol Neurobiol, Jul 2015
The internal regulatory mechanisms of autophagy by ROS can be summarized as transcriptional and post-transcriptional regulation, which includes various molecular signal pathways such as ROS-FOXO3-LC3/BNIP3-autophagy, ROS-NRF2-P62-autophagy, ROS-HIF1-BNIP3/NIX-autophagy, and ROS-TIGAR-autophagy. Autophagy also may regulate ROS levels through several pathways such as chaperone-mediated autophagy pathway, mitophagy pathway, and P62 delivery pathway, which might provide a further theoretical basis for the pathogenesis of the related diseases and still need further research.
Upregulation of energy metabolism-related, p53-target TIGAR and SCO2 in HuH-7 cells with p53 mutation by geranylgeranoic acid treatment.
Shidoji et al., Nagasaki, Japan. In Biomed Res, 2014
Here, we show that a branched-chain C-20 polyunsaturated fatty acid, geranylgeranoic acid (GGA), induces upregulation of the cellular protein levels of TP53-induced glycolysis and apoptosis regulator (TIGAR) and synthesis of cytochrome c oxidase 2 (SCO2) in human hepatoma-derived HuH-7cells harboring the mutant TP53 gene, suggesting that GGA may shift an energetic state of the tumor cells from aerobic glycolysis to mitochondrial respiration.
American Pancreatic Association Practice Guidelines in Chronic Pancreatitis: evidence-based report on diagnostic guidelines.
Vege et al., Boston, United States. In Pancreas, 2014
Furthermore, a nomenclature is suggested to further characterize patients with established chronic pancreatitis based on TIGAR-O (toxic, idiopathic, genetic, autoimmune, recurrent, and obstructive) etiology, gland morphology (Cambridge criteria), and physiologic state (exocrine, endocrine function) for uniformity across future multicenter research collaborations.
To be, or not to be: functional dilemma of p53 metabolic regulation.
Gu et al., New York City, United States. In Curr Opin Oncol, 2014
Specifically, Tp53-induced glycolysis and apoptosis regulator (TIGAR) has been thought to promote tumor suppression through metabolic fine-tuning, yet, TIGAR-deficient mice display reduction in tumorigenesis.
Regulatory role of p53 in cancer metabolism via SCO2 and TIGAR in human breast cancer.
Lee et al., Seoul, South Korea. In Hum Pathol, 2012
These results suggest that p53 can modulate the metabolic pathways via the proteins SCO2 and TIGAR in human breast cancer.
SP1 plays a pivotal role for basal activity of TIGAR promoter in liver cancer cell lines.
Fan et al., Shanghai, China. In Mol Cell Biochem, 2012
SP1 can interact with the SP1-binding site within TIGAR promoter in vitro and in vivo. Conclusively, SPl is indispensable for basal activity of TIGAR promoter.
Regulation of glucose metabolism by p53: emerging new roles for the tumor suppressor.
Mahdi et al., Lucknow, India. In Oncotarget, 2011
p53 regulates aerobic respiration at the glycolytic and oxidative phosphorylation (OXPHOS) steps via transcriptional regulation of its downstream genes TP53-induced glycolysis regulator (TIGAR) and synthesis of cytochrome c oxidase (SCO2).
TP53 induced glycolysis and apoptosis regulator (TIGAR) knockdown results in radiosensitization of glioma cells.
Manzano et al., Barcelona, Spain. In Radiother Oncol, 2011
TIGAR abrogation provides a novel adjunctive therapeutic strategy against glial tumors by increasing radiation-induced cell impairment, thus allowing the use of lower radiotherapeutic doses.
Inhibition of c-Met downregulates TIGAR expression and reduces NADPH production leading to cell death.
Mills et al., Hong Kong, Hong Kong. In Oncogene, 2011
Inhibition of TIGAR by c-Met results in reduction of cellular NADPH and cell death.
Control of glycolysis through regulation of PFK1: old friends and recent additions.
Vousden et al., Glasgow, United Kingdom. In Cold Spring Harb Symp Quant Biol, 2010
TIGAR, a recently identified F2,6 bisphosphatase (F2,6BPase), could also contribute to this complexity and participate in shaping the metabolic profile of the cell.
Modulation of intracellular ROS levels by TIGAR controls autophagy.
Vousden et al., Glasgow, United Kingdom. In Embo J, 2009
TIGAR can modulate reactive oxygen species in response to nutrient starvation or metabolic stress, and functions to inhibit autophagy.
TIGAR, a p53-inducible regulator of glycolysis and apoptosis.
Vousden et al., Glasgow, United Kingdom. In Cell, 2006
The decrease of intracellular ROS levels in response to TIGAR may also play a role in the ability of p53 to protect from the accumulation of genomic damage.
p53 and metabolism: Inside the TIGAR.
Chipuk et al., Memphis, United States. In Cell, 2006
The p53 tumor suppressor pathway coordinates DNA repair, cell-cycle arrest, apoptosis, and senescence to preserve genomic stability and prevent tumor formation.
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