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NUP98-NSD1 its mutated forms interactome

ABSTRACT: Interactome studies of NUP98-NSD1 and its mutated forms in HEK293 cells

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Early Embryonic Cell

SUBMITTER: vittoria matafora

LAB HEAD: Angela Bachi

PROVIDER: PXD026020 | Pride | 2022-02-17

REPOSITORIES: Pride

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			Action	DRS
	ZJ06032020_FG21_1.raw	Raw
	ZJ06032020_FG21_2.raw	Raw
	ZJ30012020_FG1_1.raw	Raw
	ZJ30012020_FG1_2.raw	Raw
	ZJ_26022020_CTL_1.raw	Raw

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1 - 5 of 31

Publications

SMARCA5 interacts with NUP98-NSD1 oncofusion protein and sustains hematopoietic cells transformation.

Jevtic Zivojin Z Matafora Vittoria V Casagrande Francesca F Santoro Fabio F Minucci Saverio S Garre' Massimilliano M Rasouli Milad M Heidenreich Olaf O Musco Giovanna G Schwaller Jürg J Bachi Angela A

Journal of experimental & clinical cancer research : CR 20220124 1

<h4>Background</h4>Acute myeloid leukemia (AML) is characterized by accumulation of aberrantly differentiated hematopoietic myeloid progenitor cells. The karyotyping-silent NUP98-NSD1 fusion is a molecular hallmark of pediatric AML and is associated with the activating FLT3-ITD mutation in > 70% of the cases. NUP98-NSD1 fusion protein promotes myeloid progenitor self-renewal in mice via unknown molecular mechanism requiring both the NUP98 and the NSD1 moieties.<h4>Methods</h4>We used affinity pu ...[more]

PMID: 35073946

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Targeting EZH2 methyltransferase activity in ARID1A mutated cells as a synthetic lethal therapeutic strategy

Project description:ARID1A, an epigentic modifier, is often mutated in ovarian clear cell carcinoma (OCCC). In addition, EZH2 is frequently upregulated in OCCC. Inhibtion of EZH2 with an inhibitor (GSK126) selectively inhibits ARID1A-mutated cells. This study was designed to understand changes in gene expression profiles following EZH2 inhibition or ARID1A restoration. Chromatin remodelers such as ARID1A are frequently mutated in a broad array of cancers. However, targeted cancer therapy based on ARID1A mutation status has not been described. Intriguingly, ARID1A mutated cancers typically lack genomic instability, suggesting significant involvement of epigenetic mechanisms. Here we show that inhibition of the EZH2 methyltransferase acts in a synthetic lethal manner in ARID1A mutated cells. Remarkably, ARID1A mutation status correlated with response to EZH2 inhibitor. Genome-wide profiling revealed antagonistic roles of ARID1A and EZH2 in gene regulation. Further, we identified PIK3IP1 as a direct ARID1A/EZH2 target gene whose upregulation contributes to the observed synthetic lethality in the EZH2 inhibitor treated ARID1A mutated cells. Significantly, EZH2 inhibitor caused the regression of established ARID1A mutated tumors in vivo. Together, this data demonstrate a synthetic lethality between ARID1A mutation and EZH2 inhibition. They indicate that pharmacological inhibition of EZH2 represents a novel treatment strategy for ARID1A mutated cancers.

2015-01-20 | E-GEOD-54979 | biostudies-arrayexpress

Expression profiling in WT vs CDKL5 mutated IPSCs

Project description:Mutations in the human CDKL5 gene have been associated with early onset seizure variant of Rett Syndrome. In order to investigate the potential involvement of CDKL5 in the regulation of gene expression, we compared expression profiles in WT vs CDKL5-mutated IPS clones from two patients (one male and one female) with different mutations using two-colour microarray experiments. For the female patient (CDKL5 mutation p.Gln347X) we compared one clone expressing the mutant CDKL5 allele to another clone from the same patient that expresses the wild-type allele. Maintenance of X chromosome inactivation and the resulting mono-allelic expression of CDKL5 were confirmed by androgen receptor assay and direct sequencing of CDKL5 mRNA. The clone derived from the male patient (CDKL5 mutation p.Thr288Ile) was compared to a clone derived from a normal newborn male. For each mutant/control pair four technical replicates were performed for a total of eight chip hybridizations.

2014-07-02 | E-MTAB-2223 | biostudies-arrayexpress

RNA-sequencing data of TIP60 mutated and control HEK293 cells

Project description:RNA-sequencing data of TIP60 mutated and control HEK293 cells

| PRJNA859779 | ENA

Expression data from intestine of HDAC1 and HDAC2 conditionally mutated mice

Project description:Acetylation and deacetylation of histones and other proteins depend on the opposing activities of histone acetyltransferases and histone deacetylases (HDACs), leading to either positive or negative gene expression changes. The use of HDAC inhibitors (HDACi) has uncovered a role for HDACs in the control of proliferation, apoptosis and inflammation. However, little is known of the roles of specific HDACs in intestinal epithelial cells (IEC). We investigated the consequences of ablating both Hdac1 and Hdac2 in murine IECs gene expression. HDAC1 and HDAC2 conditionally mutated mice were provided by Dr EN Olson (University of Texas Southwestern Medical Center, Dallas, TX) (Montgomery et al., 2007). Floxed HDAC1 and HDAC2 mice were crossed with villin-Cre transgenic mice to insure specific intestinal epithelial cell gene deletion (Madison et al., 2002). Total RNAs from the colon of three control and three HDAC1/2 IEC-specific knockout mice were isolated with the Rneasy kit (Qiagen, Mississauga, ON, Canada).

2013-06-08 | E-GEOD-47745 | biostudies-arrayexpress

Identification of sites of ubiquitination in WT and R->K mutant forms of RAD23A and UBQLN1 by Mass Spectrometry

Project description:To identify sites of ubiquitination in Myc-6His-Tagged forms of RAD23A and UBQLN1 for wild-type and forms with some arginine residues mutated to lysines (see FASTA file for details).

2023-05-09 | PXD036108 | Pride

RNA-sequencing data of TIP60 mutated and control HEK293 cells

Project description:In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to HEK293 cells. To assess the effects of loss of TIP60 on RNA levels, RNA-seq was performed on HEK293 cells, where the TIP60 gene was mutated by CRISPR/Cas9 technology using single guide RNA #1 (g1/C9), single guide RNA #2 (g2/C9), or guide-only controls (g1 or g2). The expression of the guide RNA was induced with doxycycline treatment for 3 days to induce TIP60 gene mutation in the samples also expressing the Cas9 enzyme.

2022-07-22 | GSE208379 | GEO

Expression data from transfected IB3 cells transfected with CFTR mutants

Project description:CFTR plasmid constructs were transfected in CF Bronchial IB3 cell cultures using Lipofectamine 2000™. Global gene mRNA expression profiles at 48 hr after transfection were created with the Affymetrix U133 chip set. We used microarrays to detail the global changes in gene expression occuring as a result of transfecting cells. CFTR mutants and wild type transfected IB3 cells vs. non-transfected IB3 cells

2011-09-30 | E-GEOD-28072 | biostudies-arrayexpress

Expression profiling of murine leukemia stem cell (LSC) lines established ex vivo by coexpression of R882H-mutated DNMT3A and NRAS-G12D post treatment with Dot1l inhibitor (Microarray)

Project description:DNA Methyltransferase 3A (DNMT3A) is frequently mutated in various hematopoietic malignancies; however, the underlying oncogenic mechanisms remain elusive. Here, we report that DNMT3A mutational âhotspotâ at Arg882 (DNMT3A-R882H) cooperates with constitutively activated RAS in transforming murine hematopoietic stem/progenitor cells (HSPCs) ex vivo and inducing acute leukemias in vivo. DNMT3A-R882H potentiates aberrant transactivation of âstemnessâ gene expression programs, notably transcription factors Meis1, Hox-A, Mn1 and Mycn. Mechanistically, R882-mutated DNMT3A directly binds to cis-regulatory elements of these genes and induces focal CpG hypomethylation reminiscent of what was seen in human leukemias bearing DNMT3A R882 mutation. Furthermore, DNMT3A-R882H induced DNA hypomethylation facilitates gene enhancer/promoter activation and recruitment of Dot1l-associated transcription elongation machineries. Inactivation of Dot1l represses DNMT3AR882H-mediated stem cell gene dysregulation and acute leukemogenicity. In this dataset, we provided gene expression profiling data for (1) RH-RAS leukemia stem cells (RH-RAS LSCs), (2) LSCs transformed by MLL-AF9, (3) LSCs transformed by NUP98-JARID1A, and (4) Dot1l inhibitor-treated RH-RAS LSCs. Gene expression data were generated using Mouse Genome 430 2.0 Microarray (Affymetrix) for four independently derived RH-RAS LSC lines (termed as LSC RH-RAS #1, #2, #3 and #4), two RH-RAS LSC lines (LSC RH-RAS #1 and # 3) treated with 1 ÂµM SGC0946 (a Dot1l-specific small-molecule inhibitor) for 4 days, one MLL-AF9-transformed progenitor line and three NUP98-JARID1A transformed progenitor lines.

2016-06-23 | E-GEOD-71439 | biostudies-arrayexpress

Phosphoproteomics analysis of normal and mutated granulocyte colony stimulating factor receptors

Project description:Granulocyte colony stimulating factor receptor (G-CSFR) plays important role in the production of neutrophils from hematopoietic stem cells. Mutated form of the receptor has been directly associated with two distinct malignant phenotype in patients, e.g. acute myeloid leukemia (AML) and chronic neutrophilic leukemia (CNL). However, the signaling mechanism of the mutated G-CSFRs is not well understood. Here, we describe a comprehensive SILAC based quantitative phosphoproteomic analysis of the mutated G-CSFRs compared to the normal receptor using BaF3 cell line based in vitro model system. High pH reversed phase concatenation and Titanium Dioxide Spin Tip column were utilized to increase the dynamic range and detection of the phosphoproteome of G-CSFRs. The dataset was further analyzed using several computational and bioinformatics tools. Overall, this dataset is a first of any phosphoproteomics analysis of granulocyte colony stimulating factor receptors in the normal and disease associated mutations. We anticipate that our dataset will have a strong potential to decipher the phospho-signaling differences between the normal and malignant G-CSFR biology with therapeutic implications.

2019-02-14 | PXD009311 | Pride

Transcription profiling of cultured fibroblastic cell lines from Rett syndrome patients

Project description:Transcription profiling of cultured fibroblastic cell lines from Rett syndrome patients. Rett syndrome (symbolized RTT) is caused by mutations in the gene MECP2 located on the X chromosome. We compared cell lines mutated clones versus non mutated.

2009-12-19 | E-MEXP-1956 | biostudies-arrayexpress

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