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JCRB Cell Bank
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Pasteur Institute
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Hayashibara Biochemical Laboratories
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Image Search Results
Journal: International Journal of Molecular and Cellular Medicine
Article Title: Sesamin Acts as Anti-leukemic Compound Interacting with Novel Phosphoprotein Targets and Inducing Apoptosis in Leukemic Cells
doi: 10.22088/IJMCM.BUMS.11.1.1
Figure Lengend Snippet: Cytotoxic effects of sesamin on (a) MOLT-4 and (b) NB4 cell line after 24 hour and 48 hour treatments compare with PBMC cells after 48 hour treatment. The results showed the percentage of cell inhibition measured by MTT assay. IC 50 at 48 hours for MOLT-4 and NB4 were reported as 104.84 and 121.00 µg/mL, respectively. Data were expressed as the mean±SD of independently three experiments. The differences between sesamin treated and untreated were examined for the statistical significance: *, p < 0.05; **, p < 0.01; ***, p < 0.001
Article Snippet:
Techniques: Inhibition, MTT Assay
Journal: International Journal of Molecular and Cellular Medicine
Article Title: Sesamin Acts as Anti-leukemic Compound Interacting with Novel Phosphoprotein Targets and Inducing Apoptosis in Leukemic Cells
doi: 10.22088/IJMCM.BUMS.11.1.1
Figure Lengend Snippet: The relative normalized expression of apoptotic genes in (a) MOLT-4 and (b) NB4 after sesamin treatment at IC 50 values of 100 and 120 µg/mL, respectively, for 48 hours. The experiment was determined by Real-time PCR. Data were expressed as the mean±SEM of three independent experiments. The differences between sesamin treated and untreated were examined for the statistical significance: *, p < 0.05; **, p < 0.01
Article Snippet:
Techniques: Expressing, Real-time Polymerase Chain Reaction
Journal: International Journal of Molecular and Cellular Medicine
Article Title: Sesamin Acts as Anti-leukemic Compound Interacting with Novel Phosphoprotein Targets and Inducing Apoptosis in Leukemic Cells
doi: 10.22088/IJMCM.BUMS.11.1.1
Figure Lengend Snippet: Venn diagram shows a set of 14 phosphoproteins present only in sesamin treated MOLT-4 (blue) and a different set of 14 phosphoproteins present only in sesamin treated NB4 (yellow)
Article Snippet:
Techniques:
Journal: International Journal of Molecular and Cellular Medicine
Article Title: Sesamin Acts as Anti-leukemic Compound Interacting with Novel Phosphoprotein Targets and Inducing Apoptosis in Leukemic Cells
doi: 10.22088/IJMCM.BUMS.11.1.1
Figure Lengend Snippet: Heatmap of phosphoproteins with significant difference in expression of (A) MOLT-4 and (B) NB4 treated with sesamin in various times compare with the control. The color indicates the expression level from low (green) to high (red). The blue arrow indicates the selected phosphoproteins
Article Snippet:
Techniques: Expressing
Journal: International Journal of Molecular and Cellular Medicine
Article Title: Sesamin Acts as Anti-leukemic Compound Interacting with Novel Phosphoprotein Targets and Inducing Apoptosis in Leukemic Cells
doi: 10.22088/IJMCM.BUMS.11.1.1
Figure Lengend Snippet: The schematic diagram shows the interactions between sesamin, caspase-3 (CASP3), caspase-7 (CASP7), caspase-8 (CASP8), caspase-9 (CASP9), BCL-2, and selected phosphoprotein; PARP4 and IPPK, in MOLT-4 and NB4 leukemic cell lines using STITCH database. The round shape represents protein. The oval shape represents chemical. Red circle indicates selective proteins. Red dashed circle indicates selective chemicals
Article Snippet:
Techniques:
Journal: Biomaterials Research
Article Title: Synthesizing efficacious genistein in conjugation with superparamagnetic Fe 3 O 4 decorated with bio-compatible carboxymethylated chitosan against acute leukemia lymphoma
doi: 10.1186/s40824-020-00187-2
Figure Lengend Snippet: The impact of 48 h treatment with different dose of Genistein on Apoptosis of JURKET cell line obtained by Flow Cytometry (The Flow Cytometry charts supply in )
Article Snippet: MOLT-4, MOLT17 and
Techniques: Flow Cytometry
Journal: Cell Death & Disease
Article Title: Minimizing DNA trapping while maintaining activity inhibition via selective PARP1 degrader
doi: 10.1038/s41419-024-07277-2
Figure Lengend Snippet: A – C T47D ( A ), MDA-MB-231 ( B ), and MOLT4 cells ( C ) were pre-treated with Rucaparib or 180055 (1 μM) for 24 h and then challenged with H 2 O 2 (2 mM) for 1 h. NAD + levels were then determined; values represent mean ± SEM ( n = 3 biological independent samples). Statistical significance was calculated with one-way ANOVA comparing the H 2 O 2 -treated DMSO group to the Rucaparib and 180055 groups. *** p < 0.001, **** p < 0.0001. D – F immunoblot analysis of PARylation levels in T47D ( D ), MDA-MB-231 ( E ), and MOLT4 cells ( F ) treated with either Rucaparib or 180055. Cells were pre-treated with a PARG inhibitor (PDD 00017273, 2 μM) for 1 h and then treated with Rucaparib or 180055 (1 μM) for 1 h. Cells were then challenged with H 2 O 2 (2 mM) for 5 min, and whole cell lysates were analyzed using immunoblot assays with the indicated antibodies.
Article Snippet: Xenograft tumors were established by injecting 8 × 10 6
Techniques: Western Blot
Journal: Cell Death & Disease
Article Title: Minimizing DNA trapping while maintaining activity inhibition via selective PARP1 degrader
doi: 10.1038/s41419-024-07277-2
Figure Lengend Snippet: A , B , DNA trapping of PARP1 in T47D ( A ) and MOLT4 cells ( B ) treated with Rucaparib, 180055 or 180055-NC. Cells were pre-treated with Rucaparib, 180055 or 180055-NC (1 μM) for 24 h followed by a 2-h treatment with DMSO (Mock) or MMS (0.01%). Chromatin-bound proteins were extracted and analyzed using the indicated antibodies. C , D PARP1 bands in T47D ( C ) and MOLT4 cells ( D ) were quantified with ImageJ. The result is representative of three biologically independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001. G DNA damage induced by Rucaparib, 180055 or 180055-NC in T47D cells. Cells were treated with Rucaparib, 180055 or 180055-NC (10 μM) for 48 h, and DNA damage was detected by immunofluorescence staining of γH2AX. The result is representative of two biologically independent experiments. Scale bar, 50 μm. H , I Cell cycle analysis of T47D cells ( H ) and MOLT4 cells ( I ) after Rucaparib or 180055 treatment. T47D cells and MOLT4 cells were treated with Rucaparib or 180055 (10 μM) for 48 h and then were analyzed by flow cytometry. The left and right peaks indicate G1 and G2/M populations. E , F Quantification of data from ( H and I ).
Article Snippet: Xenograft tumors were established by injecting 8 × 10 6
Techniques: Immunofluorescence, Staining, Cell Cycle Assay, Flow Cytometry
Journal: Cell Death & Disease
Article Title: Minimizing DNA trapping while maintaining activity inhibition via selective PARP1 degrader
doi: 10.1038/s41419-024-07277-2
Figure Lengend Snippet: A , B Cardiomyocytes ( A ), and MOLT4 cells ( B ) were subjected to treatment with Rucaparib or 180055 for 144 h. Cell viability was evaluated using the CTG luminescent cell viability assay. C Representative image of tumors from DMSO, 180055 or Rucaparib-treated group of mice ( n = 5 per group). D Tumor growth curves of three groups of mice ( n = 5 per group, mean ± SD). E Lysis of MOLT4 xenograft tumor cells was performed, followed by Western blot analysis to assess the expression levels of PARP1. F Average body weight changes the percentage of the mice in each group during 16 days of treatment ( n = 5 per group, mean ± SD). The average weight of mice was normalized as the average weight of mice in the Ctrl group on the first day of administration as the standard. G – L Detection of Red Blood Cell Count (RBC), Hemoglobin (HGB), Platelet Count (PLT), Neutrophil (NEUT), Lymphocyte (LYMPH) percentage, and glutamic-pyruvic transaminase (GPT) content ( n = 5 per group, mean ± SD). The data of 180055 or Rucaparib group and the Ctrl group were analyzed by t -test. * p < 0.05, ** p < 0. 01, *** p < 0.001, **** p < 0.0001.
Article Snippet: Xenograft tumors were established by injecting 8 × 10 6
Techniques: Cell Viability Assay, Lysis, Western Blot, Expressing, Cell Counting