Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome of LBR-null mouse kidneys

ABSTRACT: Transcriptome of LBR-null mouse kidneys

PROVIDER: PRJNA715765 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14015970_1.fastq.gz	Fastqsanger.gz
	SRR14015970_2.fastq.gz	Fastqsanger.gz
	SRR14015971_1.fastq.gz	Fastqsanger.gz
	SRR14015971_2.fastq.gz	Fastqsanger.gz
	SRR14015972_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 14

Similar Datasets

Transcriptome of LBR-null mouse kidneys

Project description:We tested overall gene expression change upon chromatin architecture disruption. RNA-seq was performed using nuclear architecture-disrupted mice carrying a loss-of-function mutation in LBR (Lbric-J/ic-J; LBR-null mice). LBR is an INM protein that tethers heterochromatin to the nuclear envelope whose level is decreased in various aging contexts.

2021-06-01 | GSE169240 | GEO

Gene expression of p53 null vs. p53 wild-type mouse kidneys at embryonic day 15.5

Project description:Gene expression microarray analysis was performed on E15.5 p53+/+ and p53-/- litter-matched kidneys. We have previously shown that p53 is expressed in both UB and MM lineages in the kidney, and that p53-null embryos on C57B6L background exhibit a range of congenital abnormalities of the kidney and urinary tract such as duplicated ureters, reduced nephron numbers, and compromised nephron progenitor renewal and differentiation. Here our goal was to reveal the p53 transcriptome in mouse embryonic kidneys at E15.5.

2013-09-05 | GSE49878 | GEO

Mouse Gsr-null liver transcriptome

Project description:Mouse Gsr-null liver transcriptome

| PRJNA512022 | ENA

Transcriptome changes in Slc7a5-null mouse embryos

Project description:Transcriptome changes in Slc7a5-null mouse embryos

| PRJEB24323 | ENA

Mouse Gsr-null liver transcriptome

Project description:Genetic disruption of Gsr in mouse elicits only subtle changes in the liver transcriptome. Transcriptome analysis of Gsr-null livers was performed to further our understanding of pathways that may compensate for loss of Gsr, one of the two NADPH-dependent cytosolic disulfide reductases.

2019-05-01 | GSE124444 | GEO

S6K1 Phosphoproteome in Tsc1-null mouse kidney iMCD3 cells

Project description:Loss of Tsc1 in the kidneys gives rise to rapid polycystogenesis and kidney failure due to the hyperactivation of mTOR complex I (mTORC1). One of the major downstream targets of mTORC1 is S6K1, which is responsible for driving many of the effector functions of mTOR. Strikingly, the loss of S6k1 in the context of hyperactivated mTOR is sufficient to reverse the generation of polycystic kidneys. In an effort to uncover novel direct S6k1 substrates involved in the generation of cystic kidneys, we generated Tsc1-null and Tsc1/S6k1-double null murine inner medullary collecting duct (iMCD3) cell lines using CRISPR/Cas9. Using these two cell lines, we conducted a phosphoproteome screen to search for novel candidates. Using a combination of antibody-motif enrichment and metal affinity enrichment, we provide a comprehensive phosphoproteome profile between these two genotypes.

2020-08-11 | PXD014832 | Pride

Gene expression comparison of E14.5 Foxd1 null and wild type kidneys

Project description:Forkhead transcription factors are essential for diverse processes in early embryonic development and organogenesis. Foxd1 is required during kidney development and its inactivation results in failure of nephron progenitor cell differentiation. Foxd1 is expressed in interstitial cells adjacent to nephron progenitor cells, suggesting an essential role for the progenitor cell niche in nephrogenesis. To better understand how cortical interstitial cells in general, and FOXD1 in particular, influence the progenitor cell niche, we examined the differentiation states of two progenitor cell subtypes in Foxd1-/- tissue. We found that while nephron progenitor cells are retained in a primitive CITED1-expressing compartment, cortical interstitial cells prematurely differentiate. To identify pathways regulated by FOXD1, we used microarray analysis and screened for target genes by comparison of Foxd1 null and wild type tissues. We chose the E14.5 timepoint because at this stage nephron differentiation is present in wild type kidneys but absent from Foxd1 null kidneys. We examined genes that were upregulated or downregulated in the Foxd1 null compared to wild type.

2013-11-14 | GSE52354 | GEO

12-month-old ATM-null mouse cerebellar transcriptome

Project description:12-month-old ATM-null mouse cerebellar transcriptome

| PRJNA1010812 | ENA

Ezh2 WT, Het, and Null Mouse Organoid Transcriptome

Project description:Ezh2 WT, Het, and Null Mouse Organoid Transcriptome

| PRJNA764195 | ENA

Gene expression comparison of E14.5 Foxd1 null and wild type kidneys

2013-11-14 | E-GEOD-52354 | biostudies-arrayexpress