Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7347320.fastq.gz | Fastqsanger.gz | |||
| SRR7347321.fastq.gz | Fastqsanger.gz |
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Project description:We uncovered an unexpected function of mixed-lineage leukemia (MLL) protein, which is a critical epigenetic factor and whose disruption leads to leukemogenesis, in the functional regulation of miRNAs. We reveal that the MLLC180 subunit alone can colocalize with miRNA-induced silencing complex (miRISC) components in cytoplasm processing bodies (P-bodies), where miRNA-mediated gene silencing takes place. In addition, we show that MLL was specifically required for miRNA-mediated translational repression, but not for miRNA or siRNA-mediated mRNA cleavage. Mechanistically, MLL was necessarily required for recruiting miRNA to the miRISC and P-body core, partly through its binding partner RAN. Furthermore, dysregulation of the miRNA repression function in MLL leukemic cells was essential for high-level expression of MYC, which ensured the survival of MLL leukemic cells. Thus, our investigation discovered that the MLL subunit alone can exert other functions in miRNA-mediated gene silencing apart from the epigenetic function of the whole MLL heterodimer. We also demonstrated as proof-of-principle that functional deregulation of miRNA may play an important role in cancer.
2020-01-01 | GSE115848 | GEO
Project description:To demonstrate RIPSeeker program that is developed for RIP-seq analyses, we generated RIP-seq data corresponding to the protein CCNT1 in HEK293 cell line using standard RIP-seq protocols described in Zhao et al., (2010). We performed two in-house RIP-seq experiments both for CCNT1 in human HEK293 cells. Briefly, we generated tagged CCNT1 using a triple tag system that supports lentiviral stable expression and mammalian affinity purification (MAPLE) Mak et al (2010). The HEK293 cells stably expressing tagged CCNT1 was purified by M2 agarose beads, followed by RNA extraction by Trizol. The library synthesis was carried out according to the RIP-seq protocol described in Zhao et al., (2010) except that one of the two experiments was done with non-strand-specific sequencing.
2012-12-28 | E-GEOD-43170 | biostudies-arrayexpress
Project description:WIN Site inhibitors bind the WIN Site of WDR5 resulting in decreased transcription of WDR5 target genes, many of which encode components of the protein synthesis machinery. In this study, we determined proteome alterations in an MLL-rearranged leukemia cell line treated for either 24 or 72 hours with a WIN Site inhibitor. The data from these studies, along with Ribo-Seq, RNA-Seq, and CRISPR screen experiments, guided us in assembling a collection of compounds that, when combined with WIN Site inhibitor, synergistically inhibit growth of MLL-rearranged leukemia cells.
2023-07-04 | PXD035129 | Pride
Project description:To demonstrate RIPSeeker program that is developed for RIP-seq analyses, we generated RIP-seq data corresponding to the protein CCNT1 in HEK293 cell line using standard RIP-seq protocols described in Zhao et al., (2010).
2012-12-28 | GSE43170 | GEO
Project description:MLL-fusions represent a large group of leukemia drivers, whose diversity originates from the vast molecular heterogeneity of C-terminal fusion partners of MLL protein. While studies of selected MLL-fusions have revealed critical molecular pathways, unifying mechanisms across all MLL-fusions remain poorly understood. We present the first comprehensive survey of protein-protein interactions of seven distantly related MLL-fusion proteins: MLL-AF1p, MLL-AF4, MLL-AF9, MLL-CBP, MLL-EEN, MLL-ENL and MLL-GAS7.
2018-05-25 | PXD009338 | Pride
Project description:The menin tumor suppressor protein (Men1) is deficient in many endocrine tumors and forms an active complex with MLL family histone methyltransferases. This Men1 complex promotes histone H3 lysine 4 trimethylation at target loci including homeobox genes and cyclin-dependent kinase inhibitor genes. The loss of Men1 may be tumorigenic because it leads to decreased histone H3 lysine 4 trimethylation resulting in expressional changes of specific genes. Reversing tumorigenesis induced by a Men1 deficiency might be achieved by inhibition of histone H3 lysine 4 demethylase Rbp2 (Kdm5a). To this end, pancreatic islets from Men1f|f, Rbp2f|f and Men1f|f Rbp2f|f mice were expression profiled to determine what transcriptional changes induced by a Men1 deficiency are reversed by the loss of Rpb2. Pancreatic islets were isolated from Men1flf RIP-Cre mice, Rbp2flf RIP-Cre mice, Men1flf Rbp2flf RIP-Cre mice and two month old matched control mice. Total mRNA was extracted from islets and expression profiled on microarrays.
2011-07-25 | E-GEOD-26978 | biostudies-arrayexpress