Vistusertib (AZD2014)

Biochem Biophys Res Commun 2014 443(2), 406-12. Vistusertib (AZD2014) purchased from Selleck.

Biochem Biophys Res Commun 2014 443(2), 406-12. Vistusertib (AZD2014) purchased from Selleck.

Biochem Biophys Res Commun 2014 443(2), 406-12. Vistusertib (AZD2014) purchased from Selleck.

HT-29 cells were treated with vehicle or AZD-2014 (50 nM) for 72 h, cell cycle distribution was analyzed by FACS.

Biochem Biophys Res Commun 2014 443, 406-12. Vistusertib (AZD2014) purchased from Selleck.

HT-29 cells were treated with vehicle ("Ctrl") or different concentrations of AZD-2014 for 72 h.

Biochem Biophys Res Commun 2014 443, 406-12. Vistusertib (AZD2014) purchased from Selleck.

Murine macrophages were treated with AZD2014 (10 nm) or rapamycin (10 ng/ml) for the time periods indicated. B, immunoblot analysis of whole cell lysate performed using an antibody detecting total ERK and phospho-ERK (Thr202/Tyr204). C, detection of MKP-1. Immunoblot analysis of whole cell lysate performed using an antibody against MKP-1 and β-actin.

J Biol Chem 2013 288(47), 33966-77. Vistusertib (AZD2014) purchased from Selleck.

Autophagy in NCI-H460 (C, D) and NCI-H460/R (E, F) cells was assessed by fluorescence microscopy. Cells were stained with acridine orange to detect the presence of acidic autophagosomes (acridin orange shifts its fluorescence emission from green to red when found in acidic compartments). Nuclei were counterstained with Hoechst 33342 (blue). Number of autophagosomes increased in NCI-H460 cells (D) after 18 h of 250 nM ADZ2014 treatment, in comparison with untreated cells (C). NCI-H460/R cells treated with 100 nM AZD2014 for 18 h also showed increased number of autophagosomes in the cytoplasm (F) when compared to untreated cells (E).

2013 Dr. Milica Pesic from Institute for Biological Research. Vistusertib (AZD2014) purchased from Selleck.

The effects of SelleckChem inhibitors on sea urchin embryo development evaluated 24 h after fertilization. All compounds were added to embryos suspension 20 min after fertilization. The relative presence of late gastrula, swimming blastula, undeveloped embryos and dead embryos was compared next to untreated control embryos (A). Fertilized egg, swimming blastula and late gastrula are illustrated (B). The embryonic development was relatively synchronized in untreated control samples after 24 h (A, E). GSK690693 treatment sustained the development of embryos. Swimming blastulas kept normal motility regardless the deformities in their shape. Tipifarnib treatment induced significant toxicity due to occurrence of dead fragmented embryos. Some abnormal blastulas kept the motility. AZD2014 treatment sustained the development of embryos. Some developed gastrulas and blastulas were less motile in comparison with control (A, C). WZ811 was the least toxic compound. Significant number of gastrulas and blastulas was developed. However, their motility was considerably suppressed (A, D). In contrast to SelleckChem inhibitors, classic anticancer agent – cisplatin was extremely toxic to sea urchin embryos (A). Cisplatin killed many embryos, while a small amount of survived embryos was stopped at early phases of development: immediately after fertilization or after first and second division (A, F).

2013 Dr. Milica Pesic from Institute for Biological Research. Vistusertib (AZD2014) purchased from Selleck.

Accumulation of autophagosomes in the cytoplasm after 72 h treatment with WORT, CQ, AZD2014 or TMX or their combination with DOX, was visualized after anti-LC3 antibody labeling.

Histochem Cell Biol, 2017, 148(5):529-544. Vistusertib (AZD2014) purchased from Selleck.

Cell Oncol, 2018, doi:10.1007/s13402-018-0380-x. Vistusertib (AZD2014) purchased from Selleck.

Accumulation of cytoplasmic autophagosomes after 24 h treatment in 8505C and Rho- cells, visualized by anti-LC3 antibody labeling. Nuclei were counterstained with Hoechst 33,342. Scale bar = 100 μm. A representative experiment of two independent experiments (n = 2) is presented. The quantification and statistical analysis of anti-LC3 fluorescence intensities are presented in histograms. $p ≤ 0.05, $$p ≤ 0.01 and $$$p ≤ 0.001: statistically significant differences between single or combined treatments and untreated samples. *p ≤ 0.05: statistically significant difference between AZD2014 and combined treatment. #p ≤ 0.05 and ##p ≤ 0.01: statistically significant differences between PTX and combined treatments

Cell Oncol, 2018, doi: 10.1007/s13402-018-0380-x. Vistusertib (AZD2014) purchased from Selleck.

AZD-2014 potentiates resminostat's cytotoxicity against human HCC cells. Established HCC cell lines (HepG2, SMMC-7721 and Hep3B), primary HCC cells (two lines, "HCC-1/-2") or the HL-7702 hepatocytes were treated with resminostat (at applied concentrations) or plus AZD-2014 ("AZD", 10 nM), cells were further cultured and subjected to MTT assay (A, E and F), trypan blue staining assay (B) and proliferation assays (C and D); p-mTOR (Ser-2448) and regular mTOR expression was tested by Western blots (A, upper panel). Data represented the means of three independent experiments ± SD (Same for all figures). For each assay, n = 5 (Same for all figures). "CTRL" indicated untreated control group (Same for all figures). "Veh" indicated vehicle (0.1% DMSO) (AeD). "Rsm" indicated resminostat (E). # indicated statistically significant differences as compared to "CTRL" group. * indicated statistically significant differences as compared to "resminostat" only group.

Biochem Biophys Res Commun, 2016, 477(4):556-62. Vistusertib (AZD2014) purchased from Selleck.

Tumor growth inhibition studies were performed in SCID mice. Mice bearing 300 mm3 tumors were randomly divided into two groups and were treated with 5 mg/kg AZD-2014 (PO, QD x 14; n = 10, the dose was based on results from pre-experiments) or vehicle (saline, PO, QD x 14; n = 10). After AZD-2014 administration, tumor tissues were isolated and lysed, activation of Akt and mTORC1/2 was tested by Western blot.

Biochem Biophys Res Commun, 2014, 443(2): 406-12. Vistusertib (AZD2014) purchased from Selleck.