Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA binding of CBFB and hnRNPK

ABSTRACT: RNA immunoprecipitation assay followed by next generation sequencing (RIPseq) to identify RNAs bound by CBFB and hnRNPK in breast cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE119800 | GEO | 2019/04/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA binding of CBFB and hnRNPK

Project description:RNA binding of CBFB and hnRNPK

| PRJNA490343 | ENA

RNA binding of DDX20 in the testis of postnatal 7-day-old C57BL/6 mice.

Project description:RNA immunoprecipitation assay followed by Next-Generation Sequencing (RIPseq) to identify RNAs bound by DDX20 in testis of postnatal 7-day-old C57BL/6 mice.

2023-10-01 | GSE217687 | GEO

Analysis of nucleus and cytoplasm-specific HNRNPK binding on SINEUP RNA by seCLIP

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

Next Generation Sequencing Analysis of control and hnRNPK-/- RKO cells Transcriptomes

Project description:We generated the hnRNPK-/- RKO cells,and collected the cells at 2 days after transfectd with siRNA. Then,we extracted RNAs and performed next generation sequencing. By comparing sequcing data from control and hnRNPK -/- samples, we profiled the alternative splicing events and gene expression regulated by hnRNPK in CRC.

2018-10-26 | GSE85522 | GEO

hnRNPK is involved in mRNA processing of a significant fraction of the transcriptome

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

Cbfb/Runx1-repression independent blockage of differentiation and accumulation of Csf2rb expressing cells by Cbfb-MYH11

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

Accelerated leukemogenesis by truncated CBFb-SMMHC defective in high-affinity binding with RUNX1

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

Cbfb/Runx1-repression independent blockage of differentiation and accumulation of Csf2rb expressing cells by Cbfb-MYH11

2010-03-31 | GSE19194 | GEO

Accelerated leukemogenesis by truncated CBFb-SMMHC defective in high-affinity binding with RUNX1

2011-03-29 | GSE21155 | GEO

RIP-seq for hnRNPK in Min6 cells

Project description:RNA immunoprecipitation followed by RNA-seq (RIP-seq) for hnRNPK was performed in Min6 cells treated with high glucose and palmitate levels for 30hrs. RNA-seq was performed on both immunoprecipitated RNA and total RNA for enrichment analysis.

2019-12-31 | GSE121296 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data