Project description:MZ1 is a newly designed pan-BET-targeting PROTAC that binds to target proteins (BET proteins such as BRD2, BRD3, and BRD4) and recruits them to the ubiquitin/protease pathway for selective destruction. However, the role of MZ1 in NB models has yet to be determined. The effect of MZ1 on NB cells was investigated using RNA-seq analysis in this work. MZ1 is a newly designed pan-BET-targeting PROTAC that binds to target proteins (BET proteins such as BRD2, BRD3, and BRD4) and recruits them to the ubiquitin/protease pathway for selective destruction. However, the role of MZ1 in NB models has yet to be determined. The effect of MZ1 on NB cells was investigated using RNA-seq analysis in this work.
Project description:Protein expression in Staphylococcus sp. NIOSBK35 isolated from marine environment (mangrove sediments) to different concentrations of arsenic (III)
Project description:To investigate the function of MZ1 in the regulation of gene expression, we treated U87 cells with control (DMSO) or MZ1, respectively. We then performed gene expression profiling analysis using data obtained from RNA-seq of control and MZ1 treatment.
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare RNA-seq results for NB4 cell line in either the absence or presence of MZ1
Project description:Glioblastoma (GBM) is a relatively more common primary central nervous system tumor with a high degree of malignancy, high mortality, and complex surgical complete resection. MZ1 is a von Hippel-Lindau tumor suppressor (VHL)-based pan-BET-targeting PROTAC, which can bind to the target proteins (BET proteins, including BRD2, BRD3, and BRD4) and recruit them to the ubiquitin/ proteasome system for degradation. However, the function of MZ1 has not been assessed in GBM cells so far. In the present study, ChIP-Seq analysis was performed to explore the effect of MZ1 on GBM cells.
Project description:4 lymphoma cell lines (DOHH2, OCILy10, TMD8 and Toledo) have been treated with MZ1. The transcriptome has been sequenced after 6hrs from the treatment
Project description:Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy. B-cell acute myeloid leukemia (B-ALL) predominates in ALL, with current cure rates of ∼80%. However, the long-term survival rate of patients with early relapse or refractory B-ALL is very low. In recent years, Bromodomains and extra-terminal (BET) protein inhibitors have shown considerable prospect in hematological tumors. MZ1 is a novel BET inhibitor that degrades target proteins and inhibits tumor growth through proteolysis-targeting chimeras (PROTAC) technology. This study shows that MZ1 has cytotoxic effects on 697 (TCF3/PBX1) and RS4;11 (MLL-AF4) B-ALL cell lines representing different molecular subtypes of B-ALL. Furthermore, we observed that MZ1 could promote cell apoptosis, induce cells cycle arrest and inhibit B-ALL cell proliferation by depleting BET protein and downregulating the transcription of CCND3. Collectively, our results indicate that MZ1 might be exploited as a novel therapeutic strategy for the treatment of B-ALL.
