2,6-dihydroxyl-4-methoxyl-chalcone/2',6'-Dihydroxy-4'-methoxy-trans-chalkon/DIHYDROXY-4'-METHOXYCHALCONE,2',6'/(2E)-1-(2,6-Dihydroxy-4-methoxyphenyl)-3-phenyl-2-propen-1-one/2-Propen-1-one, 1-(2,6-dihydroxy-4-methoxyphenyl)-3-phenyl-, (2E)-/2-Propen-1-one, 1-(2,6-dihydroxy-4-methoxyphenyl)-3-phenyl-, (E)-/Pistrobin chalcone/Pinostrobin chalcone/2',6'-dihydroxy-4'-methoxy-trans-chalcone/Chalcone, 2',6'-dihydroxy-4'-methoxy-/plnostrobin chalcone/(2E)-1-(2,6-Dihydroxy-4-methoxyphenyl)-3-phenylprop-2-en-1-one
Methanol; Ethyl Acetate; Acetontrile; DMSO
521.1±50.0 °C at 760 mmHg
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For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:18956-15-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Kansenone is a triterpene from the root of the traditional Chinese medicine, Euphorbia kansui. However, kansenone exerts serious toxicity, but the exact mechanism was not clear. In this work, the effects of kansenone on cell proliferation, cell cycle, cell damage, and cell apoptosis were investigated. The suppression of cell proliferation was assessed via the colorimetric MTT assay, and cell morphology was visualized via inverted microscopy after IEC-6 cells were incubated with different concentrations of kansenone. Reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA) content were detected for evaluating cell damage. RNase/propidium iodide (PI) labeling for evaluation of cell cycle distribution was performed by flow cytometry analysis. Annexin V-fluorescein isothiocyanate (FITC)/PI and Hoechst 33342/Annexin V-FITC/PI staining assay for cell apoptosis detection were performed using confocal laser scanning microscopy and high content screening. Moreover, apoptosis induction was further confirmed by transmission electron microscope (TEM) and JC-1 mitochondrial membrane potential, western blot and RT-PCR analysis. The results demonstrated that kansenone exerted high cytotoxicity, induced cell arrest at G0/G1 phase, and caused mitochondria damage. In addition, kansenone could up-regulate the apoptotic proteins Bax, AIF, Apaf-1, cytochrome c, caspase-3, caspase-9, caspase-8, FasR, FasL, NF-κB, and TNFR1 mRNA expression levels, and down-regulate the anti-apoptotic Bcl-2 family proteins, revealing that kansenone induces apoptosis through both the death receptor and mitochondrial pathways.
kansenone, cell proliferation, cell damage, cell cycle, cell apoptosis, death receptor pathway, mitochondrial pathway
A Natural Triterpene Derivative from Euphorbia kansui Inhibits Cell Proliferation and Induces Apoptosis against Rat Intestinal Epithelioid Cell Line in Vitro
Fangfang Cheng,1 Yanjing Yang,2 Li Zhang,1,* Yudan Cao,1 Weifeng Yao,1 Yuping Tang,1,* and Anwei Ding1
The morphological diversity of insects is important for their survival; in essence, it results from the differential expression of genes during development of the insect body. The silkworm apodal (ap) mutant has degraded thoracic legs making crawling and eating difficult and the female is sterile, which is an ideal subject for studying the molecular mechanisms of morphogenesis. Here, we confirmed that the infertility of ap female moths is a result of the degradation of the bursa copulatrix. Positional cloning of ap locus and expression analyses reveal that the Bombyx mori sister of odd and bowl (Bmsob) gene is a strong candidate for the ap mutant. The expression of Bmsob is down-regulated, while the corresponding Hox genes are up-regulated in the ap mutant compared to the wild type. Analyses with the dual luciferase assay present a declined activity of the Bmsob promoter in the ap mutant. Furthermore, we demonstrate that Bmsob can inhibit Hox gene expression directly and by suppressing the expression of other genes, including the BmDsp gene. The results of this study are an important contribution to our understanding of the diversification of insect body plan.
Molecular mapping and characterization of the silkworm apodal mutant
Peng Chen,1,2,* Xiao-Ling Tong,1,* Ming-Yue Fu,1 Hai Hu,1 Jiang-Bo Song,1 Song-Zhen He,1 Ting-Ting Gai,1 Fang-Yin Dai,a,1,2 and Cheng Lub,1,2
Mice bearing a v-Myc myelocytomatosis viral oncogene homolog (c-Myc) transgene controlled by an Ig-alpha heavy-chain enhancer (iMycCα mice) rarely develop lymphomas but instead have increased rates of memory B-cell turnover and impaired antibody responses to antigen. We found that male progeny of iMycCα mice mated with mice transgenic (Tg) for CD257 (B-cell activating factor, BAFF) developed CD5+ B-cell leukemia resembling human chronic lymphocytic leukemia (CLL), which also displays a male gender bias. Surprisingly, leukemic cells of Myc/Baff Tg mice expressed higher levels of c-Myc than did B cells of iMycCα mice. We found that CLL cells of many patients with progressive disease also expressed high amounts of c-MYC, particularly CLL cells whose survival depends on nurse-like cells (NLC), which express high-levels of BAFF. We find that BAFF could enhance CLL-cell expression of c-MYC via activation the canonical IκB kinase (IKK)/NF-κB pathway. Inhibition of the IKK/NF-κB pathway in mouse or human leukemia cells blocked the capacity of BAFF to induce c-MYC or promote leukemia-cell survival and significantly impaired disease progression in Myc/Baff Tg mice. This study reveals an important relationship between BAFF and c-MYC in CLL which may affect disease development and progression, and suggests that inhibitors of the canonical NF-κB pathway may be effective in treatment of patients with this disease.
nurselike cells, nuclear factor κ-light-chain enhancer of activated B cells, IκB kinase inhibitor, prognostic factors, leukemia-cell survival
B-cell activating factor and v-Myc myelocytomatosis viral oncogene homolog (c-Myc) influence progression of chronic lymphocytic leukemia
Weizhou Zhang,a,1 Arnon P. Kater,b,1 George F. Widhopf, II,c Han-Yu Chuang,c Thomas Enzler,d Danelle F. James,c Maxim Poustovoitov,a Ping-Hui Tseng,e Siegfried Janz,f Carl Hoh,g Harvey Herschman,h,i Michael Karin,a,2 and Thomas J. Kippsc,2
2010 Nov 2;