isotype
IgG2b
biological source
mouse
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
9C10, monoclonal
form
buffered aqueous solution
mol wt
antigen ~30 kDa
species reactivity
monkey, human
packaging
antibody small pack of 25 μL
concentration
~1.0 mg/mL
technique(s)
immunoprecipitation (IP): suitable, indirect ELISA: suitable, western blot: 2-4 μg/mL using HeLa nuclear extract
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... C12orf5(57103)
General description
Monoclonal Anti-TIGAR (mouse IgG2b isotype) is derived from the hybridoma 9C10 produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice immunized with a peptide corresponding to a fragment in exon 6-encoding region of human TIGAR . TIGAR expression was found to correlate with fludarabine sensitivity in chronic lymphocytic leukemia (CLL) cells.
TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene mapped to human chromosome 12p13-3. The gene contains six exons and it is characterized with two possible p53 binding sites, one upstream of the first exon (BS1) and one within the first intron (BS2).
Application
Monoclonal Anti-TIGAR antibody produced in mouse has been used in:
- enzyme linked immuno sorbent assay (ELISA)
- immunoblotting
- immunoprecipitation
Biochem/physiol Actions
TP53-induced glycolysis and apoptosis regulator (TIGAR) inhibits glycolysis by decreasing the fructose-2, 6-bisphosphate levels in cells. This p53 induced protein also plays a vital role in regulation of intracellular reactive oxygen species (ROS) levels. TIGAR expression is associated with oncogenesis and development of several human cancers. Overexpression of TIGAR is observed in colorectal cancer patients. Thus, TIGAR expression might function as a potential biomarker for diagnosis of colorectal cancer and it can act as a target for developing therapeutics for the treatment of colorectal cancer. Nullified expression of TIGAR, increases the radiosensitivity of tumor cells and also enhances the autophagy activity in cells with nutrient starvation or metabolic stress. TIGAR increases cancer cell survival rate in response to tumor chemotherapy by inhibiting both apoptosis and autophagy.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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存储类别
10 - Combustible liquids
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
法规信息
常规特殊物品
此项目有
Z-B Hu et al.
Cancer gene therapy, 15(3), 173-182 (2007-12-25)
Oncolytic adenoviruses, also called conditionally replicating adenoviruses (CRADs), have been widely applied in cancer gene therapy. However, the construction of CRADs is still time-consuming. In this study, we attempted to establish a simplified method of generating CRADs based on AdEasy
Guomei Tai et al.
International journal of clinical and experimental pathology, 8(5), 4823-4829 (2015-07-21)
Our previous study proved that TP53-induced glycolysis and apoptosis regulator (TIGAR) abrogation is able to radiosensitize glioma cells. Whether TIGAR over-expression has radio-protective effect in human parotid gland cells is still unknown. In this study human parotid gland fibroblast Hs
Khayal Al-Khayal et al.
Oncology reports, 35(3), 1281-1286 (2015-12-18)
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. TIGAR expression has been implicated in oncogenesis and progression of several human cancers.
Mónica López-Guerra et al.
Haematologica, 93(12), 1843-1851 (2008-10-24)
The nucleoside analogue fludarabine is used in the treatment of chronic lymphocytic leukemia. It triggers p53-mediated apoptosis, although the mutational status of p53 does not fully account for heterogeneity in responsiveness to treatment. The aim of this study was to
Karim Bensaad et al.
Cell, 126(1), 107-120 (2006-07-15)
The p53 tumor-suppressor protein prevents cancer development through various mechanisms, including the induction of cell-cycle arrest, apoptosis, and the maintenance of genome stability. We have identified a p53-inducible gene named TIGAR (TP53-induced glycolysis and apoptosis regulator). TIGAR expression lowered fructose-2,6-bisphosphate
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