Product Details

Purity

>96% as determined by SDS-PAGE.

Endotoxin

Less than 1.0 EU/μg as determined by LAL method.

Activity

Fully biologically active when compared to standard. The biological activity determined by its ability to protect U2OS cells from apoptosis induced by hydrogen peroxide is in a concentration range of 0.1-5.0 μg/ml, after pretreating with rHuTIGAR-TAT for 4 hours.

Target Names

TIGAR

Uniprot No.

Q9NQ88

Research Area

Cell Biology

Alternative Names

6-bisphosphatase TIGAR; C12ORF5; chromosome 12 open reading frame 5; FR2BP; Fructose-2,6-bisphosphatase TIGAR; Fructose-2,6-bisphosphate 2-phosphatase; Probable fructose 2,6 bisphosphatase TIGAR; Probable fructose-2; tigar; TIGAR_HUMAN; TP53 induced glycolysis and apoptosis regulator; TP53 induced glycolysis regulatory phosphatase; TP53-induced glycolysis and apoptosis regulator; Transactivated by NS3TP2 protein

Species

Homo sapiens (Human)

Source

E.coli

Expression Region

1-270aa

Complete Sequence

MARFALTVVRHGETRFNKEKIIQGQGVDEPLSETGFKQAAAAGIFLNNVKFTHAFSSDLMRTKQTMHGILERSKFCKDMTVKYDSRLRERKYGVVEGKALSELRAMAKAAREECPVFTPPGGETLDQVKMRGIDFFEFLCQLILKEADQKEQFSQGSPSNCLETSLAEIFPLGKNHSSKVNSDSGIPGLAASVLVVSHGAYMRSLFDYFLTDLKCSLPATLSRSELMSVTPNTGMSLFIINFEEGREVKPTVQCICMNLQDHLNGLTETR+GGYGRKKRRQ

Mol. Weight

31.7 kDa

Protein Length

Full Length

Tag Info

C-terminal TAT-tagged

Form

Lyophilized powder

Buffer

Lyophilized from a 0.2 m filtered 30 % Acetonitrile, 0.1% TFA

Reconstitution

We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.

Troubleshooting and FAQs

Protein FAQs

Storage Condition

Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.

Shelf Life

The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.

Lead Time

5-10 business days

Notes

Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Datasheet & COA

Please contact us to get it.

Description

To generate a recombinant human fructose-2,6-bisphosphatase TIGAR protein in E. coli, the full-length human TIGAR gene is inserted into an expression vector containing a C-terminal TAT-tag. The recombinant plasmid is then transformed into E. coli cells for protein production. Following expression, the cells are harvested, and the recombinant TIGAR protein is purified the cell lysate. The purity of the recombinant TIGAR protein exceeds 96% as determined by both SDS-PAGE and HPLC analysis. The activity of the recombinant TIGAR protein is assessed by its ability to protect U2OS cells from apoptosis induced by hydrogen peroxide. After pretreatment with the purified rHuTIGAR-TAT protein for 4 hours, the concentration range of 0.1-5.0 μg/ml demonstrates this recombinant TIGAR protein's efficacy in preserving cell viability. Its endotoxin is less than 1.0 EU/μg as determined by the LAL method.

Target Background

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.

Gene References into Functions

Knockdown of TP53 induced glycolysis and apoptosis(TIGAR) was able to radiosensitize thioredoxin reductase-1-overexpressing gliomas by inhibiting irradiation -induced thioredoxin-1 nuclear transport. PMID: 28338004
findings demonstrate that the HTLV-1 latency-maintenance factor p30(II) induces the TP53-induced glycolysis and apoptosis regulator (TIGAR) and counters the oxidative stress, mitochondrial damage, and cytotoxicity caused by the viral oncoproteins Tax and HBZ PMID: 29777913
simultaneous mutations at all four acetylation sites completely abolish its ability to regulate metabolic targets, such as TIGAR and SLC7A11. Moreover, p53(4KR) is still capable of inducing the p53-Mdm2 feedback loop, but p53-dependent ferroptotic responses are markedly abrogated PMID: 27705786
High TIGAR expression was an independent predictor of poor survival and high incidence of relapse in adult patients with CN-AML. TIGAR also showed high expression in multiple human leukemia cell lines and knockdown of TIGAR activated glycolysis through PFKFB3 upregulation in human leukemia cells. PMID: 27884166
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. PMID: 28138701
TIGAR expression in breast carcinoma cells promotes metabolic compartmentalization and tumor growth with a mitochondrial metabolic phenotype with lactate and glutamine catabolism. PMID: 27803158
we investigate the crosstalk between PFKFB3 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 knockdown PMID: 27491040
The study showed that miR-101 inhibited viability, induced apoptosis, pushed glucose metabolism flux from the pentose phosphate pathway into glycolysis in prostate cancer PC3 cell line by decreasing NADPH levels by throughly directly binding to 3'-UTR of TIGAR mRNA and repressing TIGAR expression. PMID: 28384067
This study demonstrated that a high p53 expression could be associated with the promotion of glycolysis in gastric cancer via the modulation of TIGAR expression. PMID: 27499152
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. PMID: 26675982
TIGAR knockdown reduced tumor growth rate. PMID: 26691054
Geranylgeranoic acid induced upregulation of the TIGAR gene, which might inhibit the glycolysis in HuH-7 cells with p53 mutation. PMID: 26700591
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. PMID: 26191173
The Cdk5-AMT signal pathway involved in regulation of DDR by TIGAR. PMID: 25928429
miR-144 targeted TIGAR, inhibited proliferation, enhanced apoptosis, and increased autophagy in A549 and H460 cells PMID: 25660220
Results revealed that TIGAR inhibits both apoptosis and autophagy. PMID: 25085248
TIGAR is correlated with maximal standardized uptake value on FDG-PET and survival in non-small cell lung cancer. PMID: 24363807
Data show targeting MUC1-C is synergistic with bortezomib (BTZ) in suppressing p53-inducible regulator of glycolysis and apoptosis (TIGAR)-mediated regulation of reactive oxygen species levels for combining GO-203 with BTZ in BTZ resistance. PMID: 24632713
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. PMID: 24423178
CREB regulates TIGAR expression via a CRE-binding site at the TIGAR promoter. PMID: 24036271
oroxylin A could increase protein and mRNA expression of TP53-induced glycolysis and apoptosis regulator (TIGAR) and synthesis of cytochrome c oxidase 2 (SCO2), which are the key metabolic modulators regulated by p53. PMID: 23612020
TIGAR gene expression is down regulated by oxidative stress through the mediation of reactive oxygen species PMID: 23832602
TIGAR regulates akt and erk phosphorylation but hase no effect on NF-kappa B activation in neocazinostatin-treated cells. PMID: 23640457
data provide the first evidence that targeted silencing of TIGAR induces apoptotic and autophagic cell death in HepG2 cells PMID: 23817040
TIGAR has roles in efficient intestinal regeneration and tumorigenesis PMID: 23726973
The ability of TIGAR to function as a Fru-2,6-BPase was independent of hexokinase 2 binding and mitochondrial localization, although activities can contribute to the activity of TIGAR in limiting mitochondrial ROS levels and protecting from cell death. PMID: 23185017
TIGAR regulates the expression of genes involved in cell-cycle progression. PMID: 22782351
Tp53-induced glycolysis and apoptosis regulator (TIGAR) protects glioma cells from starvation-induced cell death by up-regulating respiration and improving cellular redox homeostasis PMID: 22887998
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. PMID: 21761199
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. PMID: 21864926
These results suggest that p53 can modulate the metabolic pathways via the proteins SCO2 and TIGAR in human breast cancer. PMID: 21820150
Inhibition of TIGAR by c-Met results in reduction of cellular NADPH and cell death. PMID: 21057531
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. PMID: 16839880
correlation between the recently described p53-inducible apoptosis gene TIGAR and both sensitivity to fludarabine and hENT2 expression in chronic lymphocytic leukemia cells. PMID: 18945750
TIGAR can modulate reactive oxygen species in response to nutrient starvation or metabolic stress, and functions to inhibit autophagy. PMID: 19713938

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Subcellular Location

Cytoplasm. Nucleus. Mitochondrion.

Protein Families

Phosphoglycerate mutase family

Tissue Specificity

Expressed in the brain. Expressed in breast tumors. Expressed in glioblastomas.

Database Links

HGNC: 1185

OMIM: 610775

KEGG: hsa:57103

STRING: 9606.ENSP00000179259

UniGene: Hs.504545

Code	CSB-AP000111HU
Abbreviation	Recombinant Human TIGAR protein (Active)
MSDS	MSDS Datasheet
Size	$142
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Recombinant Human Fructose-2,6-bisphosphatase TIGAR protein (TIGAR) (Active)

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