RNA binding of CBFB and hnRNPK
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA490343 | ENA |
REPOSITORIES: ENA
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Project description:RNA immunoprecipitation assay followed by next generation sequencing (RIPseq) to identify RNAs bound by CBFB and hnRNPK in breast cells.
2019-04-18 | GSE119800 | GEO
Project description:Ewing sarcoma is a highly aggressive tumor characterized by a translocation between members of the FET family of RNA binding proteins and one of several ETS transcription factors, with the most common translocation being EWS-FLI1. EWS-FLI1 leads to changes in gene expression through mechanisms that are not completely understood. We performed RNA sequencing analysis on primary pediatric human mesenchymal progenitor cells (pMPCs) expressing EWS-FLI1 in order to identify novel target genes. This analysis identified lnc277 as a previously uncharacterized long non-coding RNA upregulated by EWS-FLI1 in pMPCs. Inhibiting the expression of lnc277 diminished the ability of Ewing sarcoma cell lines to proliferate and form colonies in soft agar whereas inhibiting lnc277 had no effect on other cell types tested. By analyzing gene expression after shRNA knockdown, we found that both EWS-FLI1 and lnc277 repressed many more genes that they induced and that a significant fraction of EWS-FLI1 repressed targets were also repressed by lnc277. Analysis of primary human Ewing sarcoma RNA sequencing data further supports a role for lnc277 in mediating gene repression. We identified hnRNPK as an RNA binding protein that interacts directly with lnc277. We found a significant overlap in the genes repressed by hnRNPK and those repressed by both EWS-FLI1 and lnc277, suggesting that hnRNPK participates in lnc277 mediated gene repression. Thus, lnc277 is a previously uncharacterized long non-coding RNA downstream of EWS-FLI1 that facilitates the development of Ewing sarcoma via the repression of target genes. Our studies identify a novel mechanism of oncogenesis downstream of a chromosomal translocation and underscore the importance of lncRNA-mediated gene repression as a mechanism of EWS-FLI1 transcriptional regulation. A673 Ewing cells expressing an shRNA targeting hnRNPK or control were subjected to paired end RNA sequencing and compared to shGFP control.
2014-11-01 | E-GEOD-60890 | biostudies-arrayexpress
Project description:The goal is to profile RUNX2 and CBFB binding sites in an osteosarcoma cell line, SAOS2.
2017-02-11 | GSE76937 | GEO
Project description:Dominant RUNX1 inhibition has been proposed as a common pathway for CBF-leukemia. CBFb-SMMHC, a fusion protein in human acute myeloid leukemia (AML), dominantly inhibits RUNX1 largely through its RUNX1 high-affinity binding domain (HABD). We generated knock-in mice expressing CBFb-SMMHC with a HABD deletion, CBFb-SMMHCd179-221. These mice developed leukemia highly efficiently, even though hematopoietic defects associated with Runx1-inhibition were partially rescued. To identify changes in gene expression with the deletion of the HABD, we compared the gene expression profile in leukemia samples from mice expressing CBFb-SMMHCd179-221 with those from mice expressing full length CBFb-SMMHC. Spleen cells were isolated from leukemic knock-in mice with full length CBFb-SMMHC at 2 months after ENU treatment and 2 leukemic CBFb-SMMHCd179-221 expressing chimeric mice at 3 weeks after birth. For each genotype, we performed two independent experiments with 4 Affymetrix GeneChip 430 chips.
2011-03-29 | E-GEOD-21155 | biostudies-arrayexpress
Project description:Dominant RUNX1 inhibition has been proposed as a common pathway for CBF-leukemia. CBFb-SMMHC, a fusion protein in human acute myeloid leukemia (AML), dominantly inhibits RUNX1 largely through its RUNX1 high-affinity binding domain (HABD). We generated knock-in mice expressing CBFb-SMMHC with a HABD deletion, CBFb-SMMHCd179-221. These mice developed leukemia highly efficiently, even though hematopoietic defects associated with Runx1-inhibition were partially rescued. To identify changes in gene expression with the deletion of the HABD, we compared the gene expression profile in leukemia samples from mice expressing CBFb-SMMHCd179-221 with those from mice expressing full length CBFb-SMMHC.
2011-03-29 | GSE21155 | GEO
Project description:Here, we report the first genomic-scale comprehensive characterization of mouse transcripts bound to hnRNPK. hnRNPK binding at the isoform level was evaluated via RNA-sequencing of liver samples obtained from obese and wild-type mouse models. The comparison of hnRNPK co-immunoprecipitated fractions with total RNA fractions in a given mouse model enabled quantitative evaluation of the binding affinity of hnRNPK for thousands of isoforms.
2015-10-01 | GSE65887 | GEO
Project description:To check the subcellular location-specific HNRNPK binding sites on mouse SINEB2 repeat element, we prepared seCLIP (single-end enhanced crosslinking and immunoprecipitation assay) libraries from SINEUP-GFP transfected nuclear and cytoplasmic fractions from HEK293T/17 cells.
2023-03-16 | GSE227250 | GEO
Project description:It is known that CBFB-MYH11, the fusion gene generated by inversion of chromosome 16 in human acute myeloid leukemia, is causative for oncogenic transformation. However, the mechanism by which CBFB-MYH11 initiates leukemogenesis is not clear. Previously published reports showed that CBFB-MYH11 dominantly inhibits RUNX1 and CBFB, and such inhibition has been suggested as the mechanism for leukemogenesis. However, knockin mice expressing Cbfb-MYH11 (Cbfb+/MYH11) showed defects in primitive hematopoiesis not seen in Cbfb null (Cbfb-/-) embryos indicating that Cbfb-MYH11 has repression independent activities as well. To identify gene expression changes associated with this novel activity, we compared the gene expression profile in the blood cells of Cbfb+/MYH11 and Cbfb-/- embryonic day 12.5 (E12.5) embryos with that of their wildtype littermates. Cbfb-MYH11 chimeras were mated to C57/Bl6 females to generate Cbfb+/MYH11 (Cbfb+/MYH11) and Cbfb+/+ (WT) embryos. Cbfb+/- x Cbfb+/- matings were used to generate Cbfb+/+ (Cbfb+/+) and Cbfb-/- (Cbfb-/-) embryos. Blood from 8-10 E12.5 embryos of the same genotype was pooled, and RNA was isolated, labeled, and hybridized to Affymetrix Genechip mouse microarray (430 2.0) chips. 4 chips were used for both the Cbfb+/MYH11 and littermate control samples. 3 chips were used for the Cbfb-/- samples and littermate control samples.
2010-04-12 | E-GEOD-19194 | biostudies-arrayexpress
Project description:Background: SCF-Fbxo4 is suspected to regulate activity of RNA binding protein hnRNPK by non-degradive ubiquitylation. Research strategy: To determine the genomic output of SCF-Fbxo4 - hnRNPK interplay, murine embryonic fibroblasts (MEFs) with different status of hnRNPK/Fbxo4 were subjected to Ribosome profiling. Sequencing was performed on total RNA and RNA protected by ribosomes for each condition.
2022-09-21 | GSE196483 | GEO
Project description:The HIV-1 accessory protein Vif hijacks a cellular Cullin-RING ubiquitin ligase, CRL5, to promote degradation of the APOBEC3 (A3) family of restriction factors. Recently, the cellular transcription cofactor CBFb was shown to form a complex with CRL5-Vif and to be essential for A3 degradation and viral infectivity. We now demonstrate that CBFb is required for assembling a well-ordered CRL5-Vif complex by inhibiting Vif oligomerization and by activating CRL5-Vif via direct interaction. The CRL5-Vif-CBFb holoenzyme forms a welldefined heterohexamer, indicating that Vif simultaneously hijacks CRL5 and CBFb. Heterodimers of CBFb and RUNX transcription factors contribute toward the regulation of genes, including those with immune system functions. We show that binding of Vif to CBFb is mutually exclusive with RUNX heterodimerization and impacts the expression of genes whose regulatory domains are associated with RUNX1. Our results provide a mechanism by which a pathogen with limited coding capacity uses one factor to hijack multiple host pathways. Identification of RUNX1 binding sites in the Jurkat cell line
2013-01-17 | E-GEOD-42575 | biostudies-arrayexpress