Entinostat (MS-275)

目录号:S1053 别名: SNDX-275

Entinostat (MS-275) Chemical Structure

Molecular Weight(MW): 376.41

Entinostat (MS-275)强烈抑制HDAC1HDAC3,无细胞试验中IC50分别为0.51 μM和1.7 μM,抑制作用强于HDACs 4, 6, 8,和10。Phase 3。

规格 价格 库存 购买数量  
RMB 746.45 现货
RMB 564.33 现货
RMB 1233.32 现货
RMB 2234.07 现货
RMB 6301.79 现货
有超大折扣

今日订购,明日送达,全国免运费!

全国免费电话:400-668-6834   |   Email:info@selleck.cn

客户使用Selleck该产品发表文献63篇:

客户使用该产品的14个实验数据:

  • (A) U87 cells were cultured in the presence of DMSO, 1 uM MS-275 alone, 100 ng/ml IFN-λ1 alone, or both for the course of 4 d. Cell numbers were manually determined by hemacytometer counting at the indicated time points. (B, F) Cell proliferation of U87 cells or U87 spheroids in 3D culture with indicated treatment were performed using the WST-1 assay, which measures active cellular metabolism. (C) U87 spheroid formation in 3D culture was photographed at day 14 in culture (representative images are shown; 200x magnification). (D-E) Quantification of the relative sizes and numbers of U87 spheroids in (C). (G) Cell cycle analysis was performed in U87 cells with indicated treatment using propidium iodide staining. Numbers in the histogram show fractions (percent) of sub-G1, N, 2N, and polyploidy from left to right. (H) U87 cells with indicated treatment were stained with Annexin V-FITC and 7-AAD. Numbers indicate the percentage of FITC-positive cells (upper left quadrant). FITC, fluorescein isothiocyanate; 7-AAD, 7-Aminoactinomycin. In all panels, data represent the mean and SEM of at least three experiments.

    PLoS Biol 2014 12, e1001758. Entinostat (MS-275) purchased from Selleck.

    Inhibition of HDAC1-mediated DNMT1 deacetylation promotes DNMT1 proteasomal degradation. (A) Knockout of HAUSP potentiates HDAC inhibitor (HDACi)-induced DNMT1 degradation. Parental or HAUSP KO DLD1 cells were treated or not with 5 μM HDACi MS-275 for 72 hours and cell lysates were blotted with the indicated antibodies. (B) HDAC inhibition induces DNMT1 ubiquitination. HAUSP WT or KO cells were treated with or without HDACi for 24 hours and MG132 for 12 hours before being harvested to make cell lysates. DNMT1 immunoprecipitates were blotted with an antibody against ubiquitin. Because the abundance of DNMT1 in the HAUSP KO cells is lower than in WT cells, more KO cells were used than WT cells to obtain equal amounts of precipitated DNMT1 proteins. (C) DNMT1 is acetylated after HDACi treatment. DNMT1 immunoprecipitates from cells treated with HDACi were blotted with an antibody against acetylated lysine (Ac-K). (D) A DNMT1 acetylation site mutant is resistant to HDACi-induced degradation. HEK 293 cells were transfected with WT DNMT1 or a DNMT1 mutant lacking four known acetylation sites (K173R, K1113R, K115R, and K117R) and treated with MS-275 for 48 hours and with CHX for 24 hours. Cell lysates were blotted with the indicated antibodies. (E) Knockdown of HDAC1 decreases the abundance of DNMT1. RKO cells were treated with the indicated concentration of doxycycline (Dox) for 48 hours to induce expression of an shRNA directed against HDAC1. Western blots were performed with the indicated antibodies. (F) Knockdown of HDAC1 leads to increased acetylation of DNMT1. RKO cells expressing an inducible HDAC1 shRNA were treated with or without Dox (4 mg/ml) for 36 hours and then with MG132 for 12 hours. DNMT1 immunoprecipitates were blotted with an antibody against Ac-K. Cell lysates were also blotted with antibodies against HDAC1 and b-actin.

     

     

    Sci Signal 2010 3, ra80. Entinostat (MS-275) purchased from Selleck.

  • The E3 ligase UHRF1 ubiquitinates DNMT1. (A) HDAC inhibition enhances DNMT1 interaction with UHRF1. HEK 293 cells were transfected with plasmids expressing Myc-DNMT1 and Flag-UHRF1 and treated with or without MS-275 for 24 hours. Myc-DNMT1 immunoprecipitates were blotted with the indicated antibodies. (B and C) HDAC inhibition enhances the interaction of endogenous DNMT1 and UHRF1. Cells were treated with or without MS-275 and UHRF1 (B) or DNMT1 (C) immunoprecipitates were blotted with the indicated antibodies. (D) UHRF1 ubiquitinates DNMT1. HEK 293 cells were transfected with the indicated plasmids. Antibodies against Myc immunoprecipitates were blotted with antibody against HA to detect ubiquitinated DNMT1. Myc-DNMT1D, DNMT1 mutant lacking the HAUSP-interacting domain. UHRF1DRING, UHRF1 with a RING domain deletion. (E) Knockdown of UHRF1 blocks HDACi-induced DNMT1 degradation. HEK 293 cells were transfected with control siRNA or siRNAs against UHRF1 and treated with or without MS-275. Western blotting was performed with the indicated antibodies. (F) Overexpression of UHRF1 leads to degradation of a DNMT1 mutant lacking the HAUSP-interacting domain (DNMT1D). Full-length DNMT1 or DNMT1D was cotransfected into HEK 293 cells with the indicated expression vectors. Cell lysates were blotted with the indicated antibodies. (G) DNMT1, HAUSP, UHRF1, HDAC1, and PCNA associate with Tip60. Flag-tagged Tip60 immunoprecipitates were blotted with the indicated antibodies.

     

     

    Sci Signal 2010 3, ra80. Entinostat (MS-275) purchased from Selleck.

    HAUSP KO cells are more sensitive to HDACi-induced apoptosis.(A) HDAC inhibition induces apoptosis in HAUSP KO cells.HAUSP WT or KO cells were treated with or without MS-275 at the indicated concentration for 72 hours, then fixed and stained with propidium iodide. Flow cytometric analyses were used to profile sub-G1, G1, and G2-M cell populations. Apoptotic cells were quantified after the indicated clones were treated with either 5 or 10 μM MS-275. The means and SDs of three independent experiments were plotted (*P<0.001, t test). (B) HDAC inhibition induces apoptosis in HAUSP KO cells but leads to G2-M arrest in WT cells.Cell cycle profiles of HAUSP WT or KOcells that were treated or not with 5 μM MS-275. (C)HDAC inhibition increases the abundance of apoptotic cell markers. The indicated cells were treated with or without MS-275 for 72 hours.Cell lysates were blotted with antibodies against cleaved caspase 3 and β-actin. (D) Ectopic overexpression of DNMT1 in HAUSP KO cells suppresses apoptosis. HAUSP KO clones or HAUSP KO cells inducibly

    overexpressingDNMT1 were treatedwith 10 μM MS-275. Apoptotic cell populations were quantified by fluorescence-activated cell sorting (FACS) analyses (*P < 0.001, t test). Cell lysates from these cells were blotted with the indicated antibodies. (E) HDAC inhibition arrests the growth of HAUSP KO cells. DLD1, HAUSP KO, and KO cells ectopically expressing HAUSP were treated with the indicated concentration of MS-275 for 4 days. Cell numbers were determined and data from eight replicates were plotted (**P <0.001, t test). (FandG) HDACi inhibits tumor xenograft formation ofHAUSP KOcells.Athymic nudemice (five in each group)were injectedsubcutaneously and bilaterallywith cells of the indicated genotypes. Mice were treated with or without MS-275 at 15mg/kg for 4 weeks. Tumors were harvested and photographed (F). Tumor sizes of the indicated groupsweremeasuredweekly and theaveragevolumes at each timepoint were plotted (G).MANOVA analyses were performed to determine whether there was an overall difference of the tumor sizes, as well as whether there was a difference in development over time of tumor sizes between the two groups (P < 0.0001).
     

     

    Sci Signal 2010 3, ra80. Entinostat (MS-275) purchased from Selleck.

  • Numerous APC (+) oligodendrocytes (middle upper panel) with ellipsoid nuclei labeled with Sytox (left upper panel) were observed in 8 week old Thy-1 mitoCFP control MONs. NF-200 (+) neurofilaments extended along the MON as linear individual fibers (right upper panel). A period of OGD (60 min) caused a significant loss of APC (+) oligodendrocytes, a gain in the appearance of pyknotic nuclei (dense, brighter nuclei, white arrows, OGD panel), and loss of NF-200 (+) axon structures, which were, replaced with axonal head and bulb formation (white asterisks). Pretreatment with SAHA (1uM) or MS-275 (1uM) effectively preserved APC (+) oligodendrocytes, together with numerous linear individual NF-200 (+) axons. Note fewer pyknotic nuclei (white arrows, SAHA and MS-275 panels) after OGD in MONs treated with SAHA or MS-275.

    J Neurosci 2011 31, 3990-9. Entinostat (MS-275) purchased from Selleck.

    Notch1ICD, Notch2ICD, and Notch3ICD were transduced into human aortic SMCs, which were then treated with HDAC inhibitors TSA or MS-275 or with vehicle DMSO (con). The top 2 rows are different exposures of the same blot to detect the epitope tags on the N ICD constructs. Longer (top row) and shorter ( second row) exposures are shown because t he level of N2ICD expression was lower than that of N1ICD and N3ICD. SMC markers were analyzed and were similarly induced by activation of each Notch r eceptor. Both TSA and MS-275 significantly suppressed the induction of SMC proteins by Notch activation.

    J Am Heart Assoc 2012 1, e000901. Entinostat (MS-275) purchased from Selleck.

  • LSD1 and HDAC inhibitors exhibit synergistic growth inhibition. Cells were simultaneously treated with pargyline or HDAC inhibitors for 48 h.

     

     

    Breast Cancer Res Treat 2012 131, 777-789. Entinostat (MS-275) purchased from Selleck.

    Histone acetylation in the spinal cord after HDACI treatment. Histone acetylation in the lumbar spinal cord of mice receiving i.t. SAHA (25 μg) or MS-275 (0.5 μg) for 30 min was analyzed by immunoblot (A, B) and immunofluorescent histochemistry (C) for antigens indicated. Animals receiving i.t. saline were used as control. Images of the H3K9/18ac signals in the left half of the lumbar spinal cord are shown in the first row in C. Immunosignals of indicated antigens in the superficial dorsal horn are presented in the rest rows in C.

    Mol Pain 2010 6, 51. Entinostat (MS-275) purchased from Selleck.

  • B. Confluent quiescent foreskin fibroblasts were treated with HDAC1 inhibitor or vehicle for 24 hours. Type I procollagen protein levels in whole cell lysates were determined by immunoblotting. A representative result of three independent experiments is shown. The band density was evaluated by densitometry. C. Under the same conditions, mRNA levels of the α1(I) collagen (COL1A1) gene were determined using reverse transcription quantitative real-time PCR. The graph represents -fold change in COL1A1 mRNA levels in comparison to unstimulated controls, which were arbitrarily set at 100. The mean and SD from three separate experiments are shown. * p<0.05 versus control cells treated with vehicle.

    PLoS One 2013 8, e74930. Entinostat (MS-275) purchased from Selleck.

    Inhibition of LSD1 activity by HDAC inhibitors. a MDA-MB-231 and MDA-MB-468 cells were exposed to indicated HDAC inhibitors for 24 h.

     

     

    Exp Dermatol 2010 19, 1096-1102. Entinostat (MS-275) purchased from Selleck.

  • HCT116 p53 null cells were treated with different HDACIs (1 μM TSA, 5 μM M344, 1 μM MS-275, 5 mM But, 10 mM VPA) for 24 h, and their expression of GRP78, PERK-eIF2α axis and ATF4, ATF3, CHOP and DR5 proteins.

    Biochem Biophys Res Commun 2014 10.1016/j.bbrc.2014.01.184. Entinostat (MS-275) purchased from Selleck.

    HCT116 p53 null cells were treated with different HDACIs (1 μM TSA, 5 μM M344, 1 μM MS-275, 5 mM But, 10 mM VPA) for 24 h. ATF4, ATF3, CHOP and DR5 proteins were measured by Western blot.

    Biochem Biophys Res Commun 2014 10.1016/j.bbrc.2014.01.184. Entinostat (MS-275) purchased from Selleck.

  •  

    HDAC inhibition increases SMN-luciferase reporter mRNA levels. qRT-PCR was used to measure increases of SMN-luciferase mRNA following treatment with HDAC inhibitors. Fold increase of mRNA was normalized to GAPDH.

    Biochem Bioph Res Co 2010 414, 25-30. Entinostat (MS-275) purchased from Selleck.

    Western blot analysis of Acetyl-H3 and H3. 0-20μM MS-275 was added.

     

     

    2011 Dr. Zhang of Tianjin Medical University. Entinostat (MS-275) purchased from Selleck.

产品安全说明书

HDAC抑制剂选择性比较

生物活性

产品描述 Entinostat (MS-275)强烈抑制HDAC1HDAC3,无细胞试验中IC50分别为0.51 μM和1.7 μM,抑制作用强于HDACs 4, 6, 8,和10。Phase 3。
靶点
HDAC1 [2]
(Cell-free assay)
HDAC3 [2]
(Cell-free assay)
0.51 μM 1.7 μM
体外研究

MS-275通过作用于2′-氨基而抑制HDACs。MS-275作用于 K562细胞,诱导 p21WAF1/CIP1和凝溶胶蛋白的累积。MS-275作用于A2780细胞,可以降低S期细胞,提高G1期细胞。 MS-275通过抑制HAD而抑制人类肿瘤细胞系,包括 A2780, Calu-3, HL-60, K562, St-4, HT-29, KB-3-1, Capan-1, 4-1St和 HCT-15细胞增殖, IC50 为41.5 nM到4.71 μM。[1]MS-275抑制HDACs,作用于HDAC1和 HDAC3时IC50 分别为0.51 μM和1.7 μM。而对其他的HDACs没有抑制效果,如HDAC4, 6, 8和10。[2]MS-275有效抑制人类白血病和淋巴癌细胞,包括U937, HL-60, K562, 和Jurkat。MS-275可以诱导U937细胞p21CIP1/WAF1 调节的生长和变异Marker (CD11b)的表达。MS-275降低cyclin D1和抗凋亡蛋白Mcl-1与XIAP的表达。[3]

Cell Data
Cell Lines Assay Type