目录号 | 产品详情 | 靶点 | |
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T79735 | |||
DHFR-IN-9(化合物8A)是一种二氢叶酸还原酶(DHFR)抑制剂,通过干扰细胞内嘌呤和胸苷酸的生物合成而影响细胞生长和增殖。该化合物对抗耐甲氧西林金黄色葡萄球菌(MRSA)ATCC 43300展现出显著的抑制效果(IC50=0.25 μg/mL),并在全身及大腿感染的小鼠模型中显示出抗感染能力(剂量:2.5 mg/kg,5 mg/kg;ip)。此外,DHFR-IN-9在乳腺癌小鼠模型中展示了超过紫杉醇(Y-B0015)的抗癌活性(剂量:2.5 mg/kg;ip;每3天1次)。 | |||
T36844 | |||
Inostamycin A is a bacterial metabolite that has been found inStreptomycesand has anticancer activity.1It is an inhibitor of CDP-diacylglycerol:inositol 3-phosphatidyltransferase (IC50= 0.02 μg/ml in A431 cell membranes) and is selective for CDP-diacylglycerol:inositol 3-phosphatidyltransferase over phospholipase C (PLC) and phosphatidylinositol kinase at 10 μg/ml.2Inostamycin A decreases viability of YCU-T892, KCC-TC873, KB, HSC-4, and YCU-T891 oral squamous cell carcinoma (OSCC) cells in a concentration-dependent manner.3It induces cell cycle arrest in the G1phase in HSC-4 cells when used at a concentration of 250 ng/ml and induces apoptosis in Ms-1 small cell lung cancer cells at 300 ng/ml.3,4Inostamycin A also reduces levels of matrix metalloproteinase-2 (MMP-2) and MMP-9 and inhibits EGF-induced migration of HSC-4 cells.5 1.Imoto, M., Umezawa, K., Takahashi, Y., et al.Isolation and structure determination of inostamycin, a novel inhibitor of phosphatidylinositol turnoverJ. Nat. Prod.53(4)825-829(1990) 2.Imoto, M., Taniguchi, Y., and Umezawa, K.Inhibition of CDP-DG: inositol transferase by inostamycinJ. Biochem.112(2)299-302(1992) 3.Baba, Y., Tsukuda, M., Mochimatsu, I., et al.Cytostatic effect of inostamycin, an inhibitor of cytidine 5'-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): inositol transferase, on oral squamous cell carcinoma cell linesCell Biol. Int.25(7)613-620(2001) 4.Imoto, M., Tanabe, K., Simizu, S., et al.Inhibition of cyclin D1 expression and induction of apoptosis by inostamycin in small cell lung carcinoma cellsJpn. J. Cancer Res.89(3)315-322(1998) 5.Baba, Y., Tsukuda, M., Mochimatsu, I., et al.Inostamycin, an inhibitor of cytidine 5'-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): Inositol transferase, suppresses invasion ability by reducing productions of matrix metalloproteinase-2 and -9 and cell motility in HSC-4 tongue carcinoma cell lineClin. Exp. Metastasis18(3)273-279(2000) | |||
T83786 | |||
8-Chloroadenosine-5’-triphosphate(8-chloro ATP)是抗癌剂8-chloro cAMP的活性代谢物,也是核苷酸腺苷5’-三磷酸(ATP)的衍生物。它通过8-chloro cAMP、8-chloroadenosine以及一磷酸和二磷酸中间体形成。应用8-chloro cAMP或8-chloroadenosine后,8-chloro ATP可累积长达12小时,与细胞生长抑制、内源性ATP水平下降以及患者源多发性骨髓瘤细胞中RNA合成减少(但DNA合成不受影响)相关。在1.5至8 mM浓度范围内,它抑制topoisomerase II-α依赖的超螺旋pUC19 DNA放松,同时在1 mM时减少了K562人髓性白血病细胞中topoisomerase II-α催化的ATP水解50%。 | |||
T83898 | |||
S-(N-Methylsulfinylbutylthiocarbamoyl)-L-cysteine (SFN-Cys) 是一种异硫氰酸酯衍生物及第一类和第二类组蛋白去乙酰化酶(HDAC)抑制剂和抗癌剂硫代硫酸烯醇醚的活性代谢产物。它通过巯基乙酸途径酶从硫代硫酸烯醇醚经DL-硫代硫酸烯醇醚谷胱甘肽和硫代硫酸烯醇醚半胱氨酸甘肽中间体形成。SFN-Cys (20 µM) 通过创伤愈合和腔室分析实验,分别减少了U87MG和U373 MG胶质母细胞瘤细胞的侵袭和迁移。在45 µM的浓度下,它降低了对紫杉醇耐药的A549肺癌细胞(A549/T)中的α-微管蛋白、βIII-微管蛋白、司他敏1和X连锁抑制剂的凋亡(XIAP)的水平,并减少了细胞密度。使用30 µM浓度的SFN-Cys诱导U87MG和U373 MG细胞凋亡和G2/M期细胞周期停滞。 | |||
T35624 | |||
Ajoene is a disulfide that has been found inA. sativumand has diverse biological activities, including antibacterial, anticancer, antiplatelet, and antioxidant properties.1,2,3,4It is active against Gram-positive (MICs = 5-160 µg/ml) and Gram-negative bacteria (MICs = 136-200 µg/ml), as well as yeasts (MICs = 10-20 µg/ml).1Ajoene is cytotoxic to mouse melanoma cells (IC50= 18 µM), as well as human colon, lung, mammary, and pancreatic cancer cells (IC50s = 7-41 µM).2It reduces tumor growth in a B16/BL6 mouse model of melanoma when administered at a dose of 25 mg/kg every other day and decreases the number of lung metastases when administered prior to tumor cell inoculation at doses ranging from 1-25 mg/kg. It inhibits ADP- or collagen-induced platelet aggregation in isolated baboon platelets when used at concentrations ranging from 75 to 150 µg/ml and in platelet-rich plasma isolated from baboons when administered at a dose of 25 mg/kg.3Ajoene (25 mg/kg) prevents thrombus formation on damaged arterial walls in heparinized pigs in anin situmodel of thrombogenesis.5It also reduces high-fat diet-induced hepatic steatosis, histopathological markers of liver damage, thiobarbituric acid reactive substances (TBARS) formation, and protein oxidation in a mouse model of non-alcoholic fatty liver disease (NAFLD).4 1.Naganawa, R., Iwata, N., Ishikawa, K., et al.Inhibition of microbial growth by ajoene, a sulfur-containing compound derived from garlicAppl. Environ. Microbiol.62(11)4238-4242(1996) 2.Taylor, P., Noriega, R., Farah, C., et al.Ajoene inhibits both primary tumor growth and metastasis of B16/BL6 melanoma cells in C57BL/6 miceCancer Lett.239(2)298-304(2006) 3.Teranishi, K., Apitz-Castro, R., Robson, S.C., et al.Inhibition of baboon platelet aggregation in vitro and in vivo by the garlic derivative, ajoeneXenotransplantation10(4)374-379(2003) 4.Han, C.Y., Ki, S.H., Kim, Y.W., et al.Ajoene, a stable garlic by-product, inhibits high fat diet-induced hepatic steatosis and oxidative injury through LKB1-dependent AMPK activationAntioxid. Redox Signal.14(2)187-202(2011) 5.Apitz-Castro, R., Badimon, J.J., and Badimon, L.A garlic derivative, ajoene, inhibits platelet deposition on severely damaged vessel wall in an in vivo porcine experimental modelThromb. Res.75(3)243-249(1994) | |||
T35629 | |||
ATRA-BA hybrid is a mutual prodrug form of all-transretinoic acid and butyric acid .1ATRA-BA hybrid is cleaved to release ATRA and BA in isolated mouse plasma. It inhibits the growth of MDA-MB-231 breast and PC3 prostate cancer cells with GI50values of 0.01 and 1.02 μM, respectively. ATRA-BA (20 μM) has 15-fold greater antiproliferative activity in PC3 cells compared to an equimolar concentration of ATRA and BA. 1.Gediya, L.K., Khandelwal, A., Patel, J., et al.Design, synthesis, and evaluation of novel mutual prodrugs (hybrid drugs) of all-trans-retinoic acid and histone deacetylase inhibitors with enhanced anticancer activities in breast and prostate cancer cells in vitroJ. Med. Chem.51(13)3895-3904(2008) | |||
T83680 | |||
Azurin (50-77)是一种含铜细菌蛋白azurin的肽段,存在于P. aeruginosa中,具有细胞周期停滞、抑制癌细胞增殖和调节血管生成活性。作为VEGFR2的抑制剂(IC20约为10.7 µM),Azurin (50-77)(20 µM)能在MCF-7乳腺癌细胞中诱导G2/M期的细胞周期停滞。在50 µM的浓度下,减少MCF-7和ZR-75-1乳腺癌细胞的增殖。Azurin (50-77)以25 µM的浓度减少VEGF-A诱导的毛细管管腔形成(IC50 = 12 µM),降低人脐静脉内皮细胞(HUVECs)中与细胞膜相关的F-actin、焦点粘附激酶(FAK)和paxillin的水平,并增加胞外的血小板内皮细胞粘附分子-1(PECAM-1)的水平。在体内,Azurin (50-77)(每日10 mg/kg)在MCF-7小鼠异种移植模型中减少肿瘤体积。 | |||
T36108 | |||
YW3-56 is an inhibitor of protein arginine deiminase 2 (PAD2) and PAD4 (IC50s = 0.5-1 and 1-5 μM, respectively).1It inhibits the growth of U2OS osteosarcoma cells (IC50= ~2.5 μM) in a p53-dependent mannerviainduction of SESN2 and subsequent inhibition of mTORC1. YW3-56 (10 mg/kg) reduces tumor growth in an S-180 murine sarcoma tumor model. It also inhibits tumor growth in the 1883 MDA-MB-231 breast cancer bone metastasis mouse xenograft model.2 1.Wang, Y., Li, P., Wang, S., et al.Anticancer peptidylarginine deiminase (PAD) inhibitors regulate the autophagy flux and the mammalian target of rapamycin complex 1 activityThe Journal of Biological Chemisty287(31)25941-25952(2012) 2.Wang, S., Chen, X.A., Hu, J., et al.ATF4 gene network mediates cellular response to the anticancer PAD inhibitor YW3-56 in triple-negative breast cancer cellsMol. Cancer Ther.14(4)877-888(2015) | |||
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-05033 | 5T4/TPBG Protein, Human, Recombinant (aa 60-345, His) | Human | HEK293 | ||
Trophoblast glycoprotein (TPBG), also known as 5T4, is the therapeutic target of several anticancer agents currently in clinical development, largely due to its high expression in tumors and low expression in normal adult tissues.
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TMPY-04644 | PDGFB Protein, Human, Recombinant (His) | Human | Yeast | ||
Platelet-derived growth factor-B (PDGFB) is necessary for normal cardiovascular development. The administration of PDGFB alone normalized tumor vasculature by increasing periendothelial coverage and vascular functionality. Interestingly, this effect exerted by PDGFB was also observed in the presence of DAPT. So PDGFB is able to improve tumor vascularity and allows the anticancer action of DAPT in the tumor.
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TMPY-06191 | 5T4/TPBG Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Trophoblast glycoprotein (TPBG), also known as 5T4, is the therapeutic target of several anticancer agents currently in clinical development, largely due to its high expression in tumors and low expression in normal adult tissues.
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TMPY-06214 | 5T4/TPBG Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
Trophoblast glycoprotein (TPBG), also known as 5T4, is the therapeutic target of several anticancer agents currently in clinical development, largely due to its high expression in tumors and low expression in normal adult tissues.
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TMPY-06317 | 5T4/TPBG Protein, Human, Recombinant (aa 1-355, His) | Human | HEK293 | ||
Trophoblast glycoprotein (TPBG), also known as 5T4, is the therapeutic target of several anticancer agents currently in clinical development, largely due to its high expression in tumors and low expression in normal adult tissues.
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TMPK-01310 | Syndecan-1 Protein, Rabbit, Recombinant (His) | Rabbit | HEK293 | ||
CD138 (syndecan-1, Sdc-1) is a member of the syndecan family that comprises heparan sulfate proteoglycans. CD138 is significant for cell-cell and cell-matrix interactions.CD138 plays a crucial role in carcinogenesis and is an attractive target for anticancer treatment with heparanase inhibitors and anti-CD138 antibodies for immunotherapy.
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TMPY-05077 | PDGFB Protein, Rhesus, Recombinant (His) | Rhesus | Yeast | ||
Platelet-derived growth factor-B (PDGFB) is necessary for normal cardiovascular development. The administration of PDGFB alone normalized tumor vasculature by increasing periendothelial coverage and vascular functionality. Interestingly, this effect exerted by PDGFB was also observed in the presence of DAPT. So PDGFB is able to improve tumor vascularity and allows the anticancer action of DAPT in the tumor.
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TMPY-04877 | PDGFB Protein, Mouse, Recombinant (His) | Mouse | Yeast | ||
Platelet-derived growth factor-B (PDGFB) is necessary for normal cardiovascular development. The administration of PDGFB alone normalized tumor vasculature by increasing periendothelial coverage and vascular functionality. Interestingly, this effect exerted by PDGFB was also observed in the presence of DAPT. So PDGFB is able to improve tumor vascularity and allows the anticancer action of DAPT in the tumor.
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TMPY-02395 | PDGFB Protein, Cynomolgus, Recombinant (mFc) | Cynomolgus | HEK293 | ||
Platelet-derived growth factor-B (PDGFB) is necessary for normal cardiovascular development. The administration of PDGFB alone normalized tumor vasculature by increasing periendothelial coverage and vascular functionality. Interestingly, this effect exerted by PDGFB was also observed in the presence of DAPT. So PDGFB is able to improve tumor vascularity and allows the anticancer action of DAPT in the tumor.
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TMPK-00721 | CX3CL1/Fractalkine Protein, Mouse, Recombinant (His & Avi), Biotinylated | Mouse | HEK293 | ||
Fractalkine/CX3C chemokine ligand 1 (CX3CL1) is a chemokine involved in the anticancer function of lymphocytes-mainly NK cells, T cells and dendritic cells. Its increased levels in tumors improve the prognosis for cancer patients, although it is also associated with a poorer prognosis in some types of cancers, such as pancreatic ductal adenocarcinoma.
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TMPY-05076 | PDGFB Protein, Canine, Recombinant (His) | Canine | Yeast | ||
Platelet-derived growth factor-B (PDGFB) is necessary for normal cardiovascular development. The administration of PDGFB alone normalized tumor vasculature by increasing periendothelial coverage and vascular functionality. Interestingly, this effect exerted by PDGFB was also observed in the presence of DAPT. So PDGFB is able to improve tumor vascularity and allows the anticancer action of DAPT in the tumor.
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TMPK-00060 | IL-17B Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
IL-17A, the prototypic member of the IL-17 family, several experimental findings strongly support the role of the IL-17B/IL-17 receptor B (IL-17RB) pathway in tumorigenesis and resistance to anticancer therapies. IL-17B/IL-17RB expression patterns and biological activities in cancer and highlight issues that remain to be addressed to better characterize IL-17B and its receptor as potential targets for enhancing the effectiveness of the existing cancer therapies.
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TMPK-00710 | Claudin-4 Protein-VLP, Human, Recombinant | Human | HEK293 | ||
Claudin-4 (CLDN4) is a key component of tight junctions (TJs) in epithelial cells. CLDN4 is overexpressed in many epithelial malignancies and correlates with cancer progression. Changes in CLDN4 expression have been associated with epigenetic factors (such as hypomethylation of promoter DNA), inflammation associated with infection and cytokines, and growth factor signaling. CLDN4 helps to maintain the tumor microenvironment by forming TJs and acts as a barrier to the entry of anticancer drugs into tumors.
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TMPH-01711 | ABCC1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Mediates export of organic anions and drugs from the cytoplasm. Mediates ATP-dependent transport of glutathione and glutathione conjugates, leukotriene C4, estradiol-17-beta-o-glucuronide, methotrexate, antiviral drugs and other xenobiotics. Confers resistance to anticancer drugs by decreasing accumulation of drug in cells, and by mediating ATP- and GSH-dependent drug export. Hydrolyzes ATP with low efficiency. Catalyzes the export of sphingosine 1-phosphate from mast cells independently of their degranulation. Participates in inflammatory response by allowing export of leukotriene C4 from leukotriene C4-synthezing cells.
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TMPJ-00247 | METAP1 Protein, Human, Recombinant | Human | E. coli | ||
Methionine Aminopeptidase 1 is a member of the M24 family of metalloproteases. METAP1 plays an important role in G(2)/M phase regulation of the cell cycle and may serve as a promising target for the discovery and development of new anticancer agents. METAP1 and METAP2 have different substrate specificity due to the differences in both size and shape of the active sites. The proteolytic removal of N-terminal methionine from nascent peptides is catalyzed by a family of enzymes known as methionine aminopeptidases (MetAPs) and is essential for cell growth. Inhibition of METAPs provides a novel strategy in developing anti-cancer drugs.
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TMPY-00324 | METAP1 Protein, Human, Recombinant (His) | Human | Baculovirus-Insect Cells | ||
Processing of the N-terminal initiator methionine or formylated methionine is an essential cellular process conserved from prokaryotes to eukaryotes. The proteolytic removal of N-terminal methionine from nascent peptides is catalyzed by a family of enzymes known as methionine aminopeptidases (MetAPs) and is essential for cell growth. METAP1 and METAP2 have different substrate specificity due to the differences in both size and shape of the active sites. As a member of the M24 family of metalloproteases, METAP1 plays an important role in G(2)/M phase regulation of the cell cycle and may serve as a promising target for the discovery and development of new anticancer agents.
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TMPY-00883 | METAP1 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Processing of the N-terminal initiator methionine or formylated methionine is an essential cellular process conserved from prokaryotes to eukaryotes. The proteolytic removal of N-terminal methionine from nascent peptides is catalyzed by a family of enzymes known as methionine aminopeptidases (MetAPs) and is essential for cell growth. METAP1 and METAP2 have different substrate specificity due to the differences in both size and shape of the active sites. As a member of the M24 family of metalloproteases, METAP1 plays an important role in G(2)/M phase regulation of the cell cycle and may serve as a promising target for the discovery and development of new anticancer agents.
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TMPY-01865 | BLMH Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
The papain superfamily member bleomycin hydrolase (BLMH) is a cytoplasmic cysteine peptidase that is highly conserved through evolution. The only known activity of the enzyme is metabolic inactivation of the glycopeptide bleomycin (BLM), an essential component of combination chemotherapy regimens for cancer. The papain superfamily member bleomycin hydrolase (BLMH) is a neutral cysteine protease with structural similarity to a 20S proteasome. Bleomycin (BLM), a clinically used glycopeptide anticancer agent. BLMH is an essential protectant against BLM-induced death and has an important role in neonatal survival and in maintaining epidermal integrity. Sequencing revealed several putative sites phosphorylated by different types of protein kinases, but no signal sequence, transmembrane domain, N-linked glycosylation site or DNA-binding motif.
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TMPY-04143 | Chemerin/RARRES2 Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
Retinoic acid receptor responder protein 2 (RARRES2) is a small secreted protein involved in multiple cancers, including adrenocortical carcinoma (ACC). Serum RARRES2 may be used as a novel prognostic marker for ACC. Retinoic acid receptor responder 2 (RARRES2) is transcriptionally downregulated in multiple cancer types. Previous studies suggested that it can serve as an immune-dependent tumor suppressor by acting as a chemoattractant to recruit anticancer immune cells expressing its receptor, the chemerin chemokine receptor 1 (CMKLR1), to sites of tumor. Mechanistically, RARRES2 overexpression in ACC cells inhibited Wnt/beta-catenin pathway activity by promoting beta-catenin phosphorylation and degradation, it also inhibited the phosphorylation of p38 mitogen-activated protein kinase. Thus RARRES2 is a novel tumor suppressor for ACC, which can function through an immune-independent mechanism.
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TMPY-00367 | Chemerin/RARRES2 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Retinoic acid receptor responder protein 2 (RARRES2) is a small secreted protein involved in multiple cancers, including adrenocortical carcinoma (ACC). Serum RARRES2 may be used as a novel prognostic marker for ACC. Retinoic acid receptor responder 2 (RARRES2) is transcriptionally downregulated in multiple cancer types. Previous studies suggested that it can serve as an immune-dependent tumor suppressor by acting as a chemoattractant to recruit anticancer immune cells expressing its receptor, the chemerin chemokine receptor 1 (CMKLR1), to sites of tumor. Mechanistically, RARRES2 overexpression in ACC cells inhibited Wnt/beta-catenin pathway activity by promoting beta-catenin phosphorylation and degradation, it also inhibited the phosphorylation of p38 mitogen-activated protein kinase. Thus RARRES2 is a novel tumor suppressor for ACC, which can function through an immune-independent mechanism.
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TMPY-02072 | HSF1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Heat shock factor protein 1, also known as heat shock transcription factor 1, HSF1, and HSTF1, is a cytoplasm and nucleus protein that belongs to the HSF family. HSF1 is the major transcription factor of HSPs (heat shock proteins) in response to various stresses. Wild type HSF1 (heat shock transcriptional factor 1) is normally inactive. HSF1 / HSTF1 is a DNA-binding protein that specifically binds heat shock promoter elements (HSE) and activates transcription. In higher eukaryotes, HSF is unable to bind to the HSE unless the cells are heat shocked. HSF1 / HSTF1 protects cells and organisms against various types of stress, either by triggering a complex response that promotes cell survival or by triggering cell death when stress-induced alterations cannot be rescued. HSF1 / HSTF1 is the key protein in regulating the stress response. It can be activated under heat, oxidative, or other stress conditions. Dominant-positive and dominant-negative HSF1 are two types of HSF1 mutants. Both of them gain DNA binding activity in the absence of stress. Also, dominant-positive HSF1 acquires transcriptional activity, which dominant-negative HSF1 does not acquire. HSF1 / HSTF1 was also reported to contribute to cell resistance against genotoxic stress, such as that caused by doxorubicin, an anticancer drug in common clinical use.
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TMPY-02076 | PIN1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Peptidyl-prolyl cis-trans isomerase Pin1, also known as Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1, Rotamase Pin1 and PIN1, peptidyl-prolyl cis/trans isomerase (PPIase), is a nucleus protein. PIN1 is a peptidyl-prolyl isomerase that can alter the conformation of phosphoproteins and so affect protein function and/or stability. PIN1 regulates a number of proteins important for cell-cycle progression and is presumed to operate as a molecular timer of this important process. PIN1 is an essential PPIase that regulates mitosis presumably by interacting with NIMA and attenuating its mitosis-promoting activity. PIN1 displays a preference for an acidic residue N-terminal to the isomerized proline bond. Alterations in the level of PIN1 can influence hyperproliferative diseases such as cancer. PIN1 has been implicated in multiple aspects of cell cycle regulation. It has been suggested that PIN1 function is required for both normal mitotic progression and reentry into the cell cycle from quiescence. PIN1 is also a target of several oncogenic pathways and is overexpressed in human breast cancer. Its overexpression can lead to upregulation of cyclin-D1 and transformation of breast epithelial cells in collaboration with the oncogenic pathways. PIN1 plays a pivotal role in breast development and may be a promising new anticancer target. Pin1 activity regulates the outcome of proline-directed kinase (e.g. MAPK, CDK or GSK3) signalling and consequently regulates cell proliferation (in part through control of cyclin D1 levels and stability) and cell survival. Recent data also implicate Pin1 as playing an important role in immune responses, at least in part by increasing the stability of cytokine mRNAs by influencing the protein complexes to which they bind.
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TMPY-02114 | PIN1 Protein, Human, Recombinant | Human | E. coli | ||
Peptidyl-prolyl cis-trans isomerase Pin1, also known as Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1, Rotamase Pin1 and PIN1, peptidyl-prolyl cis/trans isomerase (PPIase), is a nucleus protein. PIN1 is a peptidyl-prolyl isomerase that can alter the conformation of phosphoproteins and so affect protein function and/or stability. PIN1 regulates a number of proteins important for cell-cycle progression and is presumed to operate as a molecular timer of this important process. PIN1 is an essential PPIase that regulates mitosis presumably by interacting with NIMA and attenuating its mitosis-promoting activity. PIN1 displays a preference for an acidic residue N-terminal to the isomerized proline bond. Alterations in the level of PIN1 can influence hyperproliferative diseases such as cancer. PIN1 has been implicated in multiple aspects of cell cycle regulation. It has been suggested that PIN1 function is required for both normal mitotic progression and reentry into the cell cycle from quiescence. PIN1 is also a target of several oncogenic pathways and is overexpressed in human breast cancer. Its overexpression can lead to upregulation of cyclin-D1 and transformation of breast epithelial cells in collaboration with the oncogenic pathways. PIN1 plays a pivotal role in breast development and may be a promising new anticancer target. Pin1 activity regulates the outcome of proline-directed kinase (e.g. MAPK, CDK or GSK3) signalling and consequently regulates cell proliferation (in part through control of cyclin D1 levels and stability) and cell survival. Recent data also implicate Pin1 as playing an important role in immune responses, at least in part by increasing the stability of cytokine mRNAs by influencing the protein complexes to which they bind.
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