Project description:Analysis of MOLT-4 cells at various time points up to 6 hours following treatment with mouse anti-CD47 antibody (MABL) and goat anti-mouse IgG (GAM) as the crosslinker of MABL. MABL induces apoptosis in CD47-positive MOLT-4 cells. Cell death signals via CD47 ligation were analyzed by using Affymetrix Human Genome U133A microarray.
Project description:Analysis of MOLT-4 cells at various time points up to 6 hours following treatment with mouse anti-CD47 antibody (MABL) and goat anti-mouse IgG (GAM) as the crosslinker of MABL. MABL induces apoptosis in CD47-positive MOLT-4 cells. Cell death signals via CD47 ligation were analyzed by using Affymetrix Human Genome U133A microarray. MOLT-4 cell line was obtained from the American Type Culture Collection (ATCC) and grown in RPMI1640 medium (SIGMA) with 10% FBS(JBS). It was maintained at 37 degree C and 5% CO2. Cells were washed with PBS(-) followed by treatment with 10 ug/mL MABL (anti-CD47 antibody) for 0, 0.5, 1, 3 and 6 h. Total RNA was isolated and converted to cDNA using a Superscript Double Stranded cDNA synthesis kit (Invitrogen). Fragmented cDNA was hybridized to Affymetrix Human Genome U133A array and gene expression signals were analyzed. Probes showing >2 or <0.5 fold-change for both replicates compared with the control (geometric mean of 0h replicate signals) were selected at any time.
Project description:Cut&Run analysis was performed in MOLT-4 cells to analyze the level of H3K27ac and DNA bindings of SMARCA4 and RUNX1 after DMSO or BRM014 treatment.
Project description:H3K27ac Hi-ChIP analysis was performed in MOLT-4 and DND-41 cells to analyze active chromatin-chromatin interactions after DMSO or ACBI-1 treatment.
Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic tumor, which arises from the malignant transformation of T-cell progenitors. Here we want to understand the influence of Cannabis extracts on T-ALL cells (Molt-4)
Project description:DNA damage induction by either radio- or chemo-therapy has been the most widely used approach in cancer therapy, exploiting the genomic instability of cancer cells. A promising strategy takes advantage of tumour specific abnormalities in DNA damage response. Inhibition of the ATR/Chk1 pathway has been shown to be synthetically lethal in cells with high levels of oncogene-induced replication stress and in p53- or ATM- deficient cells. In the presented study, we aimed to elucidate molecular mechanisms underlying radiosensitization of MOLT-4 cells by VE-821, a higly potent and specific inhibitor of ATR. We combined multiple approaches: cell biology techniques to reveal the inhibitor-induced phenotypes, and quantitative proteomics, phosphoproteomics, and metabolomics to comprehensively describe drug-induced changes in irradiated cells.
Project description:Variations of hepatopancreatic transcript expression related to induced molt cycle were identified in male Cherax quadricarinatus using a cDNA microarray estimated to contain 2180 unique sequences. Molt induction was performed by X-organ sinus gland extirpation or by repeated 20-hydroxyecdysone injections. Manipulated males were sacrificed at premolt or early postmolt and a reference population at intermolt. Their isolated hepatopancreatic mRNA was hybridized onto the microarray and differentially-expressed genes were identified, sequenced, and annotated. Clusters of similarly expressed transcripts, in correlation with the four combinations of induction methods and molt stages were identified, containing both known and novel genes. Biologically interesting clusters were characterized by general shift of expression throughout premolt and early postmolt vs. intermolt, or by different premolt vs. postmolt expression. Several genes were differentially expressed in 20-hydroxyecdysone injected crayfish vs. X-organ sinus gland extirpated ones. Keywords: Physiological state analysis