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MRNA-sequencing for MM.1S cells that were treated with pomalidomide or were expressing shRNA against ARID2 or Aiolos.

ABSTRACT: mRNA-sequencing for MM.1S cells that were treated with pomalidomide or were expressing shRNA against ARID2 or Aiolos.

PROVIDER: PRJNA521983 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8568270_1.fastq.gz	Fastqsanger.gz
	SRR8568270_2.fastq.gz	Fastqsanger.gz
	SRR8568280_1.fastq.gz	Fastqsanger.gz
	SRR8568280_2.fastq.gz	Fastqsanger.gz
	SRR8568271_1.fastq.gz	Fastqsanger.gz

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mRNA-sequencing for MM.1S cells that were treated with pomalidomide or were expressing shRNA against ARID2 or Aiolos.

Project description:To dissect the roles of ARID2 and Aiolos in pomalidomide-induced transcriptional changes, we performed mRNA-sequencing of MM.1S cells expressing shRNA against ARID2 or Aiolos and compared them with MM.1S cells that were treated with pomalidomide for 24, 48, or 72 hours.

2020-07-22 | GSE126463 | GEO

mRNA-sequencing for MM.1S cells that were treated with pomalidomide or were expressing shRNA against ARID2 or Aiolos.

Project description:mRNA-sequencing for MM.1S cells that were treated with pomalidomide or were expressing shRNA against ARID2 or Aiolos.

| PRJNA521983 | ENA

Global proteomics in MM.1S treated with pomalidomide or dipeptides

Project description:Global proteomics of Multiple Myeloma cell line MM.1S treated with pomalidomide or cyclic imide dipeptides for 10 h. The samples were labeled with TMT-16pro.

2022-07-28 | PXD025336 | Pride

Expression profile of MM.1S tumors folloiwing treatment with bortezomib

Project description:MM.1S orthotopic tumors were analyzed fro their gene expression upon tumor outgrowth. In contorl/bortezomib/elesclmol and combo treatments.

2019-03-27 | GSE123637 | GEO

Aiolos regulated genes in A549, lung carcinoma cells

Project description:Analysis of transcriptional profiling change comparing A549 cells expressing control empty vector and A549 cells expressing Aiolos. Results provide insight into molecular mechanisms underlying functional consequence of ectopic expression of Aiolos in solid cancer cells. Two-condition experiment, A549-empty vs. A549-Aiolos cells. Biological replicates: 3 control, 3 transfected, independently grown and harvested. One replicate per array.

2013-09-13 | E-GEOD-50812 | biostudies-arrayexpress

ARID2 promotes clear cell renal cell carcinoma in the absence of functional PBRM1 [ARID2 ChIP-seq]

Project description:Subunits of SWI/SNF chromatin remodeling complexes are frequently mutated in human malignancies. The PBAF complex is composed of multiple subunits, including the putative tumor suppressor proteins PBRM1 (BAF180) and ARID2 (BAF200) that are unique to this SWI/SNF complex. PBRM1 is mutated in various cancers, with a high mutation frequency in clear cell renal cell carcinoma (ccRCC). Here, we integrate RNA-seq, ARID2 and histone mark ChIP-seq, and ATAC-seq data to show that PBAF acts to enhance or repress gene expression depending on the genomic context. At baseline, ARID2 binds to areas of open chromatin at both active enhancers and promoters. Depletion of PBRM1 leads to attenuated and redistributed ARID2 chromatin binding that correlates significantly with gene expression changes. At enhancers, ARID2 binding loss leads to diminishment of the histone mark H3K4me1 and gene downregulation. Alternatively, at a subset of promoters, ARID2 binding loss derepresses gene expression. Interestingly, ARID2, which remains bound to other PBAF subunits after loss of PBRM1, is essential for many of the pro-tumorigenic transcriptional changes observed after loss of PBRM1, whereas other core SWI/SNF components are dispensable. Upon loss of PBRM1, ARID2 positively regulates cancer-related genes and pathways, including the cancer stem cell marker ALDH1A1 and EGF signaling, to stimulate tumor cell growth. Therefore, ARID2 is crucial for maintaining the transformed state of PBRM1-deficient ccRCC cells. In total, this study suggests a novel mechanism of transcriptional control by PBRM1, whereby its loss alters the chromatin distribution of the residual PBAF complex leading to altered transcription that promotes tumorigenesis.

2018-08-14 | GSE102803 | GEO

Expression analysis after co-treatment of GSK126 and pomalidomide

Project description:To determine combination effect of GSK126 and pomalidomide at the RNA levels in EZH2 Y641 mutant DLBCL, We performed gene expression profiling in WSU-DLCL2 cell line after co-treatment of GSK126 and pomalidomide

2020-09-23 | GSE147320 | GEO

ARID2 mitigates hepatic steatosis via promoting the ubiquitination of JAK2

Project description:Non-alcoholic fatty liver disease (NAFLD) has become a growing public health problem. However, the complicated pathogenesis of NAFLD contributes to the deficiency of effective clinical treatment. Here, we elucidated that liver-specific loss of Arid2 induced hepatic steatosis and this progression could be exacerbated by HFD. Mechanistic study revealed that ARID2 repressed JAK2-STAT5-PPARγ signaling pathway by promoting the ubiquitination of JAK2, which was mediated by NEDD4L, a novel E3 ligase for JAK2. ChIP assay revealed that ARID2 recruited CARM1 to increase H3R17me2 level at NEDD4L promoter and activated the transcription of NEDD4L. Moreover, inhibition of Jak2 by Fedratinib in liver-specific Arid2 knockout mice alleviated HFD-induced hepatic steatosis. Downregulation of ARID2 and the reverse correlation between ARID2 and JAK2 were also observed in clinical samples. Therefore, our study has revealed an important role of ARID2 in the development of NAFLD and provides a potential therapeutic strategy for NAFLD.

2022-11-17 | GSE216171 | GEO

Transcription profiling of mouse bone marrow with Aiolos and OBF-1 deletions from 7 week old mice

Project description:The chromatin regulator Aiolos and the transcriptional coactivator OBF-1 have been implicated in regulating aspects of B cell maturation and activation. Mice lacking either of these factors have a largely normal early B cell development. However, when both factors are eliminated simultaneously a block is uncovered at the transition between pre-B and immature B cells, indicating that these proteins exert a critical function in developing B lymphocytes. In mice deficient for Aiolos and OBF-1, the numbers of immature B cells are reduced, small pre-BII cells are increased and a significant impairment in immunoglobulin light chain DNA rearrangement is observed. We identified genes whose expression is deregulated in the pre-B cell compartment of these mice. In particular, we found that components of the pre-BCR, such as the surrogate light chain genes l5l5 and VpreB, fail to be efficiently silenced in double-mutant mice. Strikingly, developmentally regulated nuclear repositioning of the l5l5 gene is impaired in pre-B cells lacking OBF-1 and Aiolos. These studies uncover a novel role for OBF-1 and Aiolos in controlling the transcription and nuclear organization of genes involved in pre-BCR function. OBF-1 or Aiolos or both were deleted and the gene expression profiles for these animals investigated using Affymetrix arrays Experiment Overall Design: Two control wildtype animals, then duplicates for each of the single Aiolos or OBF-1 mutants and further duplicates for the Aiolos/OBF-1 double mutants

2008-11-13 | E-GEOD-12356 | biostudies-arrayexpress

A Variant in Human AIOLOS Impairs Adaptive Immunity by Interfering with IKAROS

Project description:A missense mutation (G158R) in Aiolos, encoded by Ikzf3 gene, resulted in defective generation of B cells in mice. Pre-B cells were profoundly decreased in homozygous mutant mice. Heterozygous mutant mice showed milder B cell developmental defects, and B cells in the secondary lymphoid organs decreased. Genome-wide binding of Aiolos and Ikaros were altered in the thymus of homozygous Ikzf3 G158R mice. Our findings indicate that Aiolos-G158R hinders B cell development by interfering Ikaros' function via formation of heterodimers. A heterozygous missense variant (G159R) in AIOLOS, encoded by IKZF3 gene, resulted in impaired adaptive immunity, which predominantly manifested as profound B cell developmental defect. Genome-wide binding of wild-type AIOLOS and AIOLOS G159R mutant were examined in IKZF3 knock-out human pre-B cell line NALM-6, retrovirally transduced with doxycycline inducible wild-type AIOLOS or AIOLOS G159R. Changes in genome-wide binding and binding motif were observed for AIOLOS G159R mutant.

2021-05-01 | GSE167487 | GEO

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