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Links from GEO DataSets

Items: 20

1.

C/EBPa Regulates Protease/anti-protease Balance and Mediates Bronchiolar Cell Recovery After Injury

(Submitter supplied) In the present study, we hypothesized that C/EBPa (CCAAT/enhancer-binding protein alpha) plays a role in cell regeneration in response to bronchiolar epithelial cell injury. C/EBPa mediated ciliated cell regeneration after naphthalene bronchiolar epithelial cell injury in vivo. Furthermore, we demonstrated that C/EBPa regulates protease/anti-protease balance after lung injury, and intratracheal treatment with anti-protease (BPTI) restored ciliated cell regeneration after naphthalene injury in CebpaD/D mice.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
18 Samples
Download data: CEL
Series
Accession:
GSE29285
ID:
200029285
2.

C/EBPa is required for pulmonary cytoprotection from hyperoxia injury

(Submitter supplied) We have previously demonstrated that deletion of the Cebpa gene in the developing fetal mouse lung caused death soon after birth from the failure of lung maturation. Many of the transcriptional pathways regulating morphogenesis of the fetal lung are induced postnatally and mediate repair of the injured lung. We hypothesized that C/EBPa plays a role in protection of the alveolar epithelium following hyperoxia injury of the mature lung. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
18 Samples
Download data: CEL
Series
Accession:
GSE14917
ID:
200014917
3.

Involvement of Igf1r in Bronchiolar Epithelial Regeneration: Role During Repair Kinetics after Selective Club Cell Ablation

(Submitter supplied) Regeneration of lung epithelium is vital for maintaining airway function and integrity. An imbalance between epithelial damage and repair is at the basis of numerous chronic lung diseases such as asthma, COPD, pulmonary fibrosis and lung cancer. IGF (Insulin-like Growth Factors) signaling has been associated with most of these respiratory pathologies, although their mechanisms of action in this tissue remain poorly understood. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11002
5 Samples
Download data: FPKM_TRACKING
Series
Accession:
GSE88836
ID:
200088836
4.

Fetal liver development

(Submitter supplied) Hepatoblasts emerging at E8.5 from the foregut endoderm proliferate vigorously and differentiate to hepatocytes and biliary epithelial cells. To find genes important for hepatocyte differentiation during development, we compared gene expression profiles of hepatoblasts/immature hepatocytes at E12.5 and E17.5. As Dlk, also known as Pref-1, is expressed in hepatoblasts/immature hepatocytes, we performed a microarray analysis of the Dlk+ cells isolated from livers at E12.5 and E17.5. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7533
1 Sample
Download data: TXT
Series
Accession:
GSE13363
ID:
200013363
5.

Gene expression alteration in chondrocyte by A-CEBP overexpression.

(Submitter supplied) To investigate loss-of-function of the C/EBP family members, we used A-CEBP which exerts a dominant-negative effect against all CEBPs. DOX-inducible overexpression of A-CEBP into mouse chondrocyte cell line ATDC5 increased expressions of early differentiation markers, decreased those of late differentiation markers. In addition, A-CEBP altered many genes related with skeletal development, cartilage, cell cycle, inflammation and apoptosis.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL13912
2 Samples
Download data: TXT
Series
Accession:
GSE60651
ID:
200060651
6.

Tribbles-1 regulates hepatic lipogenesis through post-transcriptional regulation of C/EBPα

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL13112 GPL10333
12 Samples
Download data: BED, TXT
Series
Accession:
GSE70848
ID:
200070848
7.

Tribbles-1 regulates hepatic lipogenesis through post-transcriptional regulation of C/EBPα [array]

(Submitter supplied) Comparison of gene expression in livers of either WT mice or mice with hepatic specific deletion of the gene Tribbles1. Animal groups were both Trib1 cKO mice homozygous for a floxed allele of Trib1. Mice aged 8-10 weeks were treated with adeno associated virus (AAV) encoding Cre recombinase (AAV_Cre) or no gene (AAV_null). The WT group is mice treated with AAV_Null, the liver-specific KO group treated with AAV_Cre. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10333
4 Samples
Download data: TXT
Series
Accession:
GSE70846
ID:
200070846
8.

Tribbles-1 regulates hepatic lipogenesis through post-transcriptional regulation of C/EBPα [ChIP-Seq]

(Submitter supplied) We report ChIP-Seq data for C/EBPa in livers of mice with liver-specific KO (LSKO) of Trib1 as compared to WT controls, or in livers of mice overexpressing C/EBPa via adeno-associated virus (AAV) as compared to controls.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: BED
Series
Accession:
GSE70716
ID:
200070716
9.

A genome-wide expression comparison of productive and unproductive airway epithelial repair

(Submitter supplied) Defective epithelial repair in the setting of chronic lung disease has been suggested to contribute to uncontrolled extracellular matrix (ECM) deposition and development of fibrosis. We sought to directly test this hypothesis through gene expression profiling of total lung RNA isolated from mouse models of selective epithelial cell injury that are associated with either productive or abortive repair. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL9047
32 Samples
Download data: TXT
Series
Accession:
GSE17693
ID:
200017693
10.

Genome-wide analysis of epicardial gene expression in E11.5 mouse hearts

(Submitter supplied) Identification of epicardium-enriched genes in the embryonic heart. The epicardium encapsulates the heart and functions as a source of multipotent progenitor cells and paracrine factors essential for cardiac development and repair. Injury of the adult heart results in re-activation of a developmental gene program in the epicardium, but the transcriptional basis of epicardial gene expression has not been delineated. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
2 Samples
Download data: TXT
Series
Accession:
GSE41959
ID:
200041959
11.

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [scATAC-seq]

(Submitter supplied) Cell plasticity theoretically extends to all possible cell types, but naturally decreases as cells differentiate, whereas injury-repair re-engages the developmental plasticity. Here we show that the lung alveolar type 2 (AT2)-specific transcription factor (TF), CEBPA, restricts AT2 cell plasticity in the mouse lung. AT2 cells undergo transcriptional and epigenetic maturation postnatally. Without CEBPA, both neonatal and mature AT2 cells reduce the AT2 program, but only the former reactivate the SOX9 progenitor program. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: BROADPEAK, BW, RDS
Series
Accession:
GSE264098
ID:
200264098
12.

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24247 GPL19057
42 Samples
Download data: BROADPEAK, BW, NARROWPEAK
Series
Accession:
GSE247272
ID:
200247272
13.

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [ChIP-seq]

(Submitter supplied) Cell plasticity theoretically extends to all possible cell types, but naturally decreases as cells differentiate, whereas injury-repair re-engages the developmental plasticity. Here we show that the lung alveolar type 2 (AT2)-specific transcription factor (TF), CEBPA, restricts AT2 cell plasticity in the mouse lung. AT2 cells undergo transcriptional and epigenetic maturation postnatally. Without CEBPA, both neonatal and mature AT2 cells reduce the AT2 program, but only the former reactivate the SOX9 progenitor program. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
30 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE247271
ID:
200247271
14.

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [1]

(Submitter supplied) Cell plasticity theoretically extends to all possible cell types, but naturally decreases as cells differentiate, whereas injury-repair re-engages the developmental plasticity. Here we show that the lung alveolar type 2 (AT2)-specific transcription factor (TF), CEBPA, restricts AT2 cell plasticity in the mouse lung. AT2 cells undergo transcriptional and epigenetic maturation postnatally. Without CEBPA, both neonatal and mature AT2 cells reduce the AT2 program, but only the former reactivate the SOX9 progenitor program. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: BROADPEAK, CLOUPE, H5, RDS, TBI, TSV
Series
Accession:
GSE247130
ID:
200247130
15.

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL19057 GPL24247
78 Samples
Download data: BED, BEDGRAPH, BROADPEAK, CLOUPE, CSV, H5, NARROWPEAK, TBI, TSV
Series
Accession:
GSE158205
ID:
200158205
16.

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [ChIP-seq]

(Submitter supplied) Differential use of identical DNA sequences leads to distinct tissue lineages and then multiple cell types within a lineage, an epigenetic process central to progenitor and stem cell biology. The associated genomic changes, especially in native tissues, remain insufficiently understood, and are hereby addressed in the mouse lung, where the same lineage transcription factor NKX2-1 promotes the diametrically opposed alveolar type 1 (AT1) versus AT2 cell fate. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
54 Samples
Download data: BEDGRAPH, BROADPEAK, NARROWPEAK
Series
Accession:
GSE158201
ID:
200158201
17.

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [scATAC-Seq]

(Submitter supplied) Differential use of identical DNA sequences leads to distinct tissue lineages and then multiple cell types within a lineage, an epigenetic process central to progenitor and stem cell biology. The associated genomic changes, especially in native tissues, remain insufficiently understood, and are hereby addressed in the mouse lung, where the same lineage transcription factor NKX2-1 promotes the diametrically opposed alveolar type 1 (AT1) versus AT2 cell fate. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
1 Sample
Download data: BED, BEDGRAPH, BROADPEAK, CLOUPE, CSV, H5, TBI, TSV
Series
Accession:
GSE158196
ID:
200158196
18.

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [scRNA-Seq]

(Submitter supplied) Differential use of identical DNA sequences leads to distinct tissue lineages and then multiple cell types within a lineage, an epigenetic process central to progenitor and stem cell biology. The associated genomic changes, especially in native tissues, remain insufficiently understood, and are hereby addressed in the mouse lung, where the same lineage transcription factor NKX2-1 promotes the diametrically opposed alveolar type 1 (AT1) versus AT2 cell fate. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
14 Samples
Download data: CLOUPE, MTX, TSV
Series
Accession:
GSE158192
ID:
200158192
19.

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [ATAC-seq]

(Submitter supplied) Differential use of identical DNA sequences leads to distinct tissue lineages and then multiple cell types within a lineage, an epigenetic process central to progenitor and stem cell biology. The associated genomic changes, especially in native tissues, remain insufficiently understood, and are hereby addressed in the mouse lung, where the same lineage transcription factor NKX2-1 promotes the diametrically opposed alveolar type 1 (AT1) versus AT2 cell fate. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
9 Samples
Download data: BEDGRAPH, BROADPEAK
Series
Accession:
GSE158024
ID:
200158024
20.

Transcriptomic analysis of lung epithelial cells after LPS inhalation

(Submitter supplied) Lung ECs express low levels of MHC-I at their surface. These levels are modestly increase 96h after LPS inhalation. At the transcriptional level, AT1, AT2 and Bronchiolar ECs highly increase the expression of MHC-I coding transcripts that reach level as high as mTECs. The amount of transcripts coding for Tap1, Tap2, Psmb8, Psmb9 and Psmb10 stay low compare to mTECs and seems limiting for an efficient surface expression of MHC-I in these three types of lung ECs.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
34 Samples
Download data: TXT
Series
Accession:
GSE176228
ID:
200176228
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