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Links from GEO DataSets

Items: 20

1.

p53 governs an alveolar type 1 differentiation program in lung cancer suppression [in_vivo_RNA_seq]

(Submitter supplied) Lung cancer is the leading cause of cancer deaths worldwide. TP53 tumor suppressor gene mutations occur in 50% of lung adenocarcinomas (LUADs) and are linked to poor prognosis, but how p53 suppresses LUAD development remains enigmatic. We show here that p53 suppresses LUAD by governing cell state, by promoting alveolar type 1 (AT1) differentiation. Using mice expressing oncogenic Kras and null, wild-type, or hypermorphic p53 alleles in alveolar type 2 (AT2) cells, we observed graded effects of p53 on LUAD initiation and progression. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
11 Samples
Download data: XLSX
Series
Accession:
GSE231679
ID:
200231679
2.

p53 governs an alveolar type 1 differentiation program in lung cancer suppression

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL21103 GPL19057 GPL24247
45 Samples
Download data: H5, TSV
Series
Accession:
GSE231681
ID:
200231681
3.

p53 governs an alveolar type 1 differentiation program in lung cancer suppression [in_vitro_RNA_seq]

(Submitter supplied) Lung cancer is the leading cause of cancer deaths worldwide. TP53 tumor suppressor gene mutations occur in 50% of lung adenocarcinomas (LUADs) and are linked to poor prognosis, but how p53 suppresses LUAD development remains enigmatic. We show here that p53 suppresses LUAD by governing cell state, by promoting alveolar type 1 (AT1) differentiation. Using mice expressing oncogenic Kras and null, wild-type, or hypermorphic p53 alleles in alveolar type 2 (AT2) cells, we observed graded effects of p53 on LUAD initiation and progression. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
6 Samples
Download data: XLSX
Series
Accession:
GSE231678
ID:
200231678
4.

p53 governs an alveolar type 1 differentiation program in lung cancer suppression [in_vivo_ATAC_seq2]

(Submitter supplied) Lung cancer is the leading cause of cancer deaths worldwide. TP53 tumor suppressor gene mutations occur in 50% of lung adenocarcinomas (LUADs) and are linked to poor prognosis, but how p53 suppresses LUAD development remains enigmatic. We show here that p53 suppresses LUAD by governing cell state, by promoting alveolar type 1 (AT1) differentiation. Using mice expressing oncogenic Kras and null, wild-type, or hypermorphic p53 alleles in alveolar type 2 (AT2) cells, we observed graded effects of p53 on LUAD initiation and progression. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
8 Samples
Download data: H5
Series
Accession:
GSE231677
ID:
200231677
5.

p53 governs an alveolar type 1 differentiation program in lung cancer suppression [in_vivo_ATAC_seq1]

(Submitter supplied) Lung cancer is the leading cause of cancer deaths worldwide. TP53 tumor suppressor gene mutations occur in 50% of lung adenocarcinomas (LUADs) and are linked to poor prognosis, but how p53 suppresses LUAD development remains enigmatic. We show here that p53 suppresses LUAD by governing cell state, by promoting alveolar type 1 (AT1) differentiation. Using mice expressing oncogenic Kras and null, wild-type, or hypermorphic p53 alleles in alveolar type 2 (AT2) cells, we observed graded effects of p53 on LUAD initiation and progression. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
4 Samples
Download data: H5
Series
Accession:
GSE231676
ID:
200231676
6.

p53 governs an alveolar type 1 differentiation program in lung cancer suppression [scRNA-Seq]

(Submitter supplied) Lung cancer is the leading cause of cancer deaths worldwide. TP53 tumor suppressor gene mutations occur in 50% of lung adenocarcinomas (LUADs) and are linked to poor prognosis, but how p53 suppresses LUAD development remains enigmatic. We show here that p53 suppresses LUAD by governing cell state, by promoting alveolar type 1 (AT1) differentiation. Using mice expressing oncogenic Kras and null, wild-type, or hypermorphic p53 alleles in alveolar type 2 (AT2) cells, we observed graded effects of p53 on LUAD initiation and progression. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: H5
Series
Accession:
GSE231675
ID:
200231675
7.

p53 governs an alveolar type 1 differentiation program in lung cancer suppression [10x single cell multiomics RNA-Seq]

(Submitter supplied) Lung cancer is the leading cause of cancer deaths worldwide. TP53 tumor suppressor gene mutations occur in 50% of lung adenocarcinomas (LUADs) and are linked to poor prognosis, but how p53 suppresses LUAD development remains enigmatic. We show here that p53 suppresses LUAD by governing cell state, by promoting alveolar type 1 (AT1) differentiation. Using mice expressing oncogenic Kras and null, wild-type, or hypermorphic p53 alleles in alveolar type 2 (AT2) cells, we observed graded effects of p53 on LUAD initiation and progression. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: H5
Series
Accession:
GSE231674
ID:
200231674
8.

p53 governs an alveolar type 1 differentiation program in lung cancer suppression [10x_multiome_ATAC]

(Submitter supplied) Lung cancer is the leading cause of cancer deaths worldwide. TP53 tumor suppressor gene mutations occur in 50% of lung adenocarcinomas (LUADs) and are linked to poor prognosis, but how p53 suppresses LUAD development remains enigmatic. We show here that p53 suppresses LUAD by governing cell state, by promoting alveolar type 1 (AT1) differentiation. Using mice expressing oncogenic Kras and null, wild-type, or hypermorphic p53 alleles in alveolar type 2 (AT2) cells, we observed graded effects of p53 on LUAD initiation and progression. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: TSV
Series
Accession:
GSE231671
ID:
200231671
9.

Single-cell transcriptional profiling of wildtype Rosa26(YFP) (Y) and Kras(G12D) p53(-/-) Rosa26-YFP (KPY) lung AT2 epithelial cells, AT2 organoids, and co-cultured mesenchymal cells with temporal resolution

(Submitter supplied) The aim of this study was to examine the transcriptional dynamics of AT2 progenitor cells and their surrounding mesenchyme in lung adenocarcinoma across model systems, using temporal and single-cell resolution.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
39 Samples
Download data: H5
Series
Accession:
GSE253461
ID:
200253461
10.

Expression data from adult ATII and E18 Bipotent progenitor cells in the mouse lung

(Submitter supplied) Alveoli are thin-walled sacs that serve as the gas exchange units of the lung. They are affected in devastating lung diseases including COPD, Idiopathic Pulmonary Fibrosis, and the major form (adenocarcinoma) of lung cancer, the leading cause of cancer deaths. The alveolar epithelium is composed of two morphologically distinct cell types: alveolar type (AT) 1 cells, exquisitely thin cells across which oxygen diffuses to reach the blood, and AT2 cells, specialized surfactant-secreting cells. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS5004
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE49346
ID:
200049346
11.
Full record GDS5004

Adult alveolar type 2 and embryonic bipotent progenitor lung cells

Analysis of adult alveolar type (AT) 2 and E18 bipotent progenitor (BP) lung cells. During development, AT1 and AT2 cells arise from a BP; after birth, new AT1 cells derive from rare, long-lived, self-renewing mature AT2 cells. Results provide insight into the molecular basis of AT2 self-renewal.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 age, 2 cell type sets
Platform:
GPL1261
Series:
GSE49346
6 Samples
Download data: CEL, CHP
12.

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
13.

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
14.

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
15.

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
16.

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
17.

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
18.

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
19.

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
20.

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
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