目录号 | 产品详情 | 靶点 | |
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T35683 | |||
2-deoxy-D-Glucose-13C6is intended for use as an internal standard for the quantification of 2-deoxy-D-glucose by GC- or LC-MS. 2-deoxy-D-Glucose is a glucose antimetabolite and an inhibitor of glycolysis.1,2It inhibits hexokinase, the enzyme that converts glucose to glucose-6-phosphate, as well as phosphoglucose isomerase, the enzyme that converts glucose-6-phosphate to fructose-6-phosphate.32-deoxy-D-Glucose (16 mM) induces apoptosis in SK-BR-3 cells, as well as inhibits the growth of 143B osteosarcoma cells cultured under hypoxic conditions when used at a concentration of 2 mg/ml.4,5In vivo, 2-deoxy-D-glucose (500 mg/kg) reduces tumor growth in 143B osteosarcoma and MV522 non-small cell lung cancer mouse xenograft models when used alone or in combination with doxorubicin or paclitaxel .6 1.Kang, H.T., and Hwang, E.S.2-Deoxyglucose: An anticancer and antiviral therapeutic, but not any more a low glucose mimeticLife Sci.78(12)1392-1399(2006) 2.Aft, R.L., Zhang, F.W., and Gius, D.Evaluation of 2-deoxy-D-glucose as a chemotherapeutic agent: Mechanism of cell deathBr. J. Cancer87(7)805-812(2002) 3.Ralser, M., Wamelink, M.M., Struys, E.A., et al.A catabolic block does not sufficiently explain how 2-deoxy-D-glucose inhibits cell growthProc. Natl. Acad. Sci. USA105(46)17807-17811(2008) 4.Liu, H., Savaraj, N., Priebe, W., et al.Hypoxia increases tumor cell sensitivity to glycolytic inhibitors: A strategy for solid tumor therapy (Model C)Biochem. Pharmacol.64(12)1745-1751(2002) 5.Zhang, X.D., Deslandes, E., Villedieu, M., et al.Effect of 2-deoxy-D-glucose on various malignant cell lines in vitroAnticancer Res.26(5A)3561-3566(2006) 6.Maschek, G., Savaraj, N., Priebe, W., et al.2-deoxy-D-glucose increases the efficacy of adriamycin and paclitaxel in human osteosarcoma and non-small cell lung cancers in vivoCancer Res.64(1)31-34(2004) |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-02646 | NSE/ENO2 Protein, Human, Recombinant (His) | Human | E. coli | ||
The combination of silencing ENO2 and 2-deoxyglucose (2-DG) synergistically inhibited leukemia cell survival. ENO2 may be a biological marker for monitoring chemotherapeutic efficacy and relapse in ALL. Reduced ENO2 expression may be a biomarker for a subset of autistic children. Neuron specific enolase (ENO2, gamma-enolase) has been used as a biomarker to help identify neuroendocrine differentiation in breast cancer.
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TMPY-03407 | NQO1 Protein, Human, Recombinant (His) | Human | E. coli | ||
NQO1 gene is a member of the NAD(P)H dehydrogenase (quinone) family and encodes a cytoplasmic 2-electron reductase. NQO1 forms homodimers and reduces quinones to hydroquinones. NQO1's enzymatic activity prevents the one-electron reduction of quinones that results in the production of radical species. Mutations in the NQO1 gene have been associated with tardive dyskinesia (TD), an increased risk of hematotoxicity after exposure to benzene, and susceptibility to various forms of cancer. Altered expression of NQO1 has been seen in many tumors and is also associated with Alzheimer's disease (AD). Alternate transcriptional splice variants, encoding different isoforms, have been characterized. Recent pharmacological research suggests the feasibility of genotype-directed redox chemotherapeutic intervention targeting NQO1 breast cancer, a common missense genotype encoding a functionally impaired NQO1 protein.
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TMPH-01211 | DGUOK Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Phosphorylates deoxyguanosine and deoxyadenosine in the mitochondrial matrix, with the highest efficiency for deoxyguanosine. In non-replicating cells, where cytosolic dNTP synthesis is down-regulated, mtDNA synthesis depends solely on DGUOK and TK2. Phosphorylates certain nucleoside analogs. Widely used as target of antiviral and chemotherapeutic agents.
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TMPY-03048 | PRAP1 Protein, Human, Recombinant (mFc) | Human | HEK293 | ||
PRAP1 is a protein interacting partner of MAD1 and that PRAP1 is able to down-regulate MAD1 and suppress mitotic checkpoint signalling in HCC. PRAP1 is a novel p53 target gene. The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment. PRAP1 appears to protect cells from apoptosis by inducing cell-cycle arrest, suggesting that the induction of PRAP1 expression by p53 in response to DNA-damaging agents contributes to cancer cell survival.
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TMPJ-01145 | ABCB5 Protein, Human, Recombinant (Trx) | Human | E. coli | ||
ATP-binding cassette sub-family B member 5(ABCB5) is a plasma membrane-spanning protein. ABCB5 is principally expressed in physiological skin and human malignant melanoma. ABCB5 has been suggested to regulate skin progenitor cell fusion and mediate chemotherapeutic drug resistance in stem-like tumor cell subpopulations in human malignant melanoma. It is commonly over-expressed on circulating melanoma tumour cells. Furthermore, the ABCB5+ melanoma- initiating cells were demonstrated to express FLT1 (VEGFR1) receptor tyrosine kinase which was functionally required for efficient xenograft tumor formation, as demonstrated by shRNA knockdown experiments.
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TMPY-00999 | UNC5A Protein, Human, Recombinant (His) | Human | HEK293 | ||
The netrin-1 receptor Uncoordinated Phenotype-5A, or UNC5A, plays an important role in predicting response to DNA damage induced by chemotherapeutic drug and regulating cell death in bladder cancer. Moreover, UNC5A is cumulatively downregulated by the unfolding protein response (UPR) at the transcriptional level in vitro and at the translational level both in vitro and in vivo. Also, UNC5A is a novel transcriptional target of p53 and plays a role in p53-dependent apoptosis.
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TMPY-03076 | PRAP1 Protein, Human, Recombinant (His) | Human | HEK293 | ||
PRAP1 is a protein interacting partner of MAD1 and that PRAP1 is able to down-regulate MAD1 and suppress mitotic checkpoint signalling in HCC. PRAP1 is a novel p53 target gene. The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment. PRAP1 appears to protect cells from apoptosis by inducing cell-cycle arrest, suggesting that the induction of PRAP1 expression by p53 in response to DNA-damaging agents contributes to cancer cell survival.
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TMPY-00648 | UNC5A Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
The netrin-1 receptor Uncoordinated Phenotype-5A, or UNC5A, plays an important role in predicting response to DNA damage induced by chemotherapeutic drug and regulating cell death in bladder cancer. Moreover, UNC5A is cumulatively downregulated by the unfolding protein response (UPR) at the transcriptional level in vitro and at the translational level both in vitro and in vivo. Also, UNC5A is a novel transcriptional target of p53 and plays a role in p53-dependent apoptosis.
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TMPH-00607 | Cytosine deaminase Protein, E. coli, Recombinant (His & SUMO) | E. coli | E. coli | ||
Catalyzes the hydrolytic deamination of cytosine to uracil. Is involved in the pyrimidine salvage pathway, which allows the cell to utilize cytosine for pyrimidine nucleotide synthesis. Is also able to catalyze deamination of isoguanine, a mutagenic oxidation product of adenine in DNA, and of isocytosine. To a lesser extent, also catalyzes the conversion of 5-fluorocytosine (5FC) to 5-fluorouracil (5FU); this activity allows the formation of a cytotoxic chemotherapeutic agent from a non-cytotoxic precursor.
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TMPY-03329 | DPEP1 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Dehydropeptidase-I, also known as DPEP1, is a kidney membrane enzyme. Its expression in normal colonic mucosa is very low, but it is highly expressed in colorectal adenoma and cancer specimens and is negatively correlated with parameters of pathological aggressiveness and poor prognosis. The overexpression of DPEP1 suppressed tumor cells invasiveness and increased sensitivity to chemotherapeutic agent Gemcitabine. Growth factor EGF treatment decreased DPEP1 expression. Dehydropeptidase-I may be a candidate target in PDAC for designing improved treatments. It uses zinc as a cofactor and acts as a disulfide-linked homodimer.
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TMPJ-00922 | DCK Protein, Human, Recombinant (His & T7) | Human | E. coli | ||
Deoxycytidine Kinase (DCK) is a member of the DCK/DGK family. DCK exists as a homodimer and is localized to the nucleus. DCK is required for the phosphorylation of the deoxyribonucleosides deoxycytidine (dC), deoxyguanosine (dG), and deoxyadenosine (dA). DCK has broad substrate specificity, and does not display selectivity based on the chirality of the substrate. In addition, DCK is also an essential enzyme for the phosphorylation of numerous nucleoside analogs widely employed as antiviral and chemotherapeutic agents. DCK is clinically important because of its relationship to drug resistance and sensitivity.
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TMPY-00924 | SMAC Protein, Human, Recombinant (His) | Human | E. coli | ||
Apoptosis is an essential processes required for normal development and homeostasis of all metazoan organisms. Second Mitochondria-Derived Activator of Caspases (Smac) or Direct IAP Binding Protein with low isoelectric point, pI (Diablo) is a proapoptogenic mitochondrial protein that is released to the cytosol in response to diverse apoptotic stimuli, including commonly used chemotherapeutic drugs. The current knowlege about structure and function of Smac/Diablo during programmed cell death, both in mitochondrial and receptor pathways are presented. It has been shown that Diablo mainly interacts with IAPs in the cytochrome c/Apaf-1/caspase-9 pathway, and promotes apoptosis. Diablo is released from the mitochondria into the cytosol occurring downstream of cytochrome c release in response to apoptotic stimuli such as irradiation, DNA damage or cytotoxic drugs. In the cytosol, Smac/Diablo interacts and antagonizes inhibitors of apoptosis proteins (IAPs), thus allowing the activation of caspases and apoptosis. This activity has prompted the synthesis of peptidomimetics that could potentially be used in cancer therapy. The role of Smac/DIABLO in colorectal carcinogenesis is ill defined. Data continues to accumulate to suggest that decreased levels of Smac/DIABLO may be important in chemoradiation-resistance to apoptosis in advanced colon cancer.
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