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Links from GEO DataSets

Items: 20

1.

Genome-wide analysis of PDX1 target genes in human pancreatic progenitors [expression profiling]

(Submitter supplied) Objective: Homozygous loss-of-function mutations in the gene coding for the homeobox transcription factor (TF) PDX1 leads to pancreatic agenesis, whereas heterozygous mutations can cause Maturity-Onset Diabetes of the Young 4 (MODY4). Although the function of Pdx1 is well studied in pre-clinical models during insulin-producing β-cell development and homeostasis, it remains elusive how this TF controls human pancreas development by regulating a downstream transcriptional program. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
4 Samples
Download data: CEL
Series
Accession:
GSE106813
ID:
200106813
2.

Point mutations in the PDX1 transactivation domain impair human β-cell development and function

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL20301 GPL16686 GPL18460
66 Samples
Download data: CEL
Series
Accession:
GSE125770
ID:
200125770
3.

Point mutations in the PDX1 transactivation domain impair human β-cell development and function (RNA-Seq)

(Submitter supplied) Missense mutations in coding region of PDX1 predispose to type-2 diabetes mellitus as well as cause MODY through largely unexplored mechanisms. Here, we screened a large cohort of subjects with increased risk for diabetes and identified two subjects with impaired glucose tolerance carrying heterozygous missense mutations in the PDX1 coding region leading to single amino acid exchanges (P33T, C18R) in its transactivation domain. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
57 Samples
Download data: TXT
Series
Accession:
GSE125769
ID:
200125769
4.

Point mutations in the PDX1 transactivation domain impair human β-cell development and function (ChIP-Seq)

(Submitter supplied) Missense mutations in coding region of PDX1 predispose to type-2 diabetes mellitus as well as cause MODY through largely unexplored mechanisms. Here, we screened a large cohort of subjects with increased risk for diabetes and identified two subjects with impaired glucose tolerance carrying heterozygous missense mutations in the PDX1 coding region leading to single amino acid exchanges (P33T, C18R) in its transactivation domain. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18460
5 Samples
Download data: BED
Series
Accession:
GSE125768
ID:
200125768
5.

Point mutations in the PDX1 transactivation domain impair human β-cell development and function (mRNA microarray)

(Submitter supplied) Missense mutations in coding region of PDX1 predispose to type-2 diabetes mellitus as well as cause MODY through largely unexplored mechanisms. Here, we screened a large cohort of subjects with increased risk for diabetes and identified two subjects with impaired glucose tolerance carrying heterozygous missense mutations in the PDX1 coding region leading to single amino acid exchanges (P33T, C18R) in its transactivation domain. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
4 Samples
Download data: CEL
Series
Accession:
GSE125590
ID:
200125590
6.

Genome-wide analysis of PDX1 target genes in human pancreatic progenitors

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16686 GPL18460
12 Samples
Download data: CEL
Series
Accession:
GSE106950
ID:
200106950
7.

Genome-wide analysis of PDX1 target genes in human pancreatic progenitors [ChIP-seq]

(Submitter supplied) We performed ChIP-seq of PDX1 and H3K27ac on XM001 cells at PP stage
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18460
8 Samples
Download data: BED
Series
Accession:
GSE106949
ID:
200106949
8.

Extensive NEUROG3 occupancy in the human pancreatic endocrine gene regulatory network

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
14 Samples
Download data: BW
Series
Accession:
GSE179264
ID:
200179264
9.

Genes differentially expressed between NEUROG3-Venus positive and negative hiPSC line differentiated to pancreatic endocrine progenitors [RNA-Seq]

(Submitter supplied) Despite this critical role in islet cell development, the precise function and downstream genetic programs regulated directedly by NEUROG3 remain elusive. We therefore mapped genome-wide NEUROG3 occupancy in human induced pluripotent stem cell (iPSC)-derived endocrine progenitors and determined NEUROG3 dependency of associated genes to uncover direct targets. To this aim, we generated a novel hiPSC line (NEUROG3-HA-P2A-Venus), where NEUROG3 is HA-tagged and fused to a self-cleaving fluorescent VENUS reporter. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: XLSX
10.

Genome wide profiling of NEUROG3 occupancy in human pancreatic endocrine progenitors [CUT&RUN]

(Submitter supplied) Despite this critical role in islet cell development, the precise function and downstream genetic programs regulated directedly by NEUROG3 remain elusive. We therefore mapped genome-wide NEUROG3 occupancy in human induced pluripotent stem cell (iPSC)-derived endocrine progenitors and determined NEUROG3 dependency of associated genes to uncover direct targets. To this aim, we generated a novel hiPSC line (NEUROG3-HA-P2A-Venus), where NEUROG3 is HA-tagged and fused to a self-cleaving fluorescent VENUS reporter. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
6 Samples
Download data: BW
Series
Accession:
GSE171963
ID:
200171963
11.

LIM-Domain-Binding 1 maintains the terminally-differentiated state of pancreatic β-cells

(Submitter supplied) Utilize high-throughput transcriptomic and cistromic analysis to determine the functional requirement for LDB1 and ISL1 in mature murine pancreatic β-cells while simultaneously assessing their functional interdependence at the chromatin level.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
21 Samples
Download data: BED, BW, XLSX
Series
Accession:
GSE84759
ID:
200084759
12.

Modelling HNF1B-associated monogenic diabetes using human iPSCs reveals an early stage impairment of the pancreatic developmental program

(Submitter supplied) Heterozygous mutations in HNF1B in humans result in a multi-system disorder, including pancreatic hypoplasia and diabetes mellitus. The underlying mechanisms that contribute to disease pathogenesis remain largely unknown, partially accounted by the fact that mouse models with heterozygous deletions in Hnf1b do not develop diabetes, in contrast to the phenotypes observed in MODY patients. Here we used a well-controlled human induced pluripotent stem cell pancreatic differentiation model to elucidate the molecular mechanisms underlying HNF1B-associated diabetes and pancreatic hypoplasia. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL20301
47 Samples
Download data: TAR, XLSX
Series
Accession:
GSE168071
ID:
200168071
13.

Dysregulation of a Pdx1/Ovol2/Zeb2 axis in dedifferentiated beta-cells triggers the induction of genes associated with epithelial-mesenchymal transition in diabetes

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
14 Samples
Download data: MTX, TSV
Series
Accession:
GSE171254
ID:
200171254
14.

Single-cell RNA-seq in pancreatic islets of Tg7 mice

(Submitter supplied) Objective: beta-cell dedifferentiation has been revealed as a pathological mechanism underlying pancreatic dysfunction in diabetes. However, exactly how such dedifferentiation process affects beta-cell gene expression and islet microenvironment remains incompletely understood Method: We performed single-cell RNA-Sequencing (RNA-seq) in islets obtained from beta-cell-specific miR-7a2 overexpressing mice (Tg7), a murine model of beta-cell dedifferentiation and diabetes. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE171252
ID:
200171252
15.

Bulk RNA-seq in pancreatic islets of Tg7 mice

(Submitter supplied) Objective: beta-cell dedifferentiation has been revealed as a pathological mechanism underlying pancreatic dysfunction in diabetes. However, exactly how such dedifferentiation process affects beta-cell gene expression and islet microenvironment remains incompletely understood Method: We performed bulk in islets obtained from beta-cell-specific miR-7a2 overexpressing mice (Tg7), a murine model of beta-cell dedifferentiation and diabetes. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: CSV
Series
Accession:
GSE171251
ID:
200171251
16.

Global transcriptomic analysis of human pancreatic islets reveals novel genes influencing glucose metabolism

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL6244 GPL11154
178 Samples
Download data: CEL
Series
Accession:
GSE50398
ID:
200050398
17.

Global transcriptomic analysis of human pancreatic islets reveals novel genes influencing glucose metabolism [expression array]

(Submitter supplied) Here we harnessed the potential of expression arrays in 89 human pancreatic islet donors (different levels of blood glucose (HbA1c)) to identify genes regulated in this relevant tissue for type 2 diabetes (T2D).
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
89 Samples
Download data: CEL
Series
Accession:
GSE50397
ID:
200050397
18.

Global transcriptomic analysis of human pancreatic islets reveals novel genes influencing glucose metabolism [RNA-seq]

(Submitter supplied) Here we harnessed the potential of RNA sequencing in 89 human pancreatic islet donors to identify genes and exons regulated in this relevant tissue for T2D.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
89 Samples
Download data: GFF, GTF, TXT
19.

Identification of a small molecule that facilitates the differentiation of human iPSCs/ESCs into pancreatic endocrine cells

(Submitter supplied) Pancreatic beta cell generation from induced pluripotent stem cells (iPSCs) offers an alternative donor tissue source; however, the efficiency of induction of INSULIN (INS)+ cells from human iPSCs (hiPSCs) is low. We aimed to establish an efficient differentiation protocol for generating INS+ cells from hiPSCs by identifying novel inducers. We screened small molecules that increased the induction rate of INS+ cells from hiPSC-derived PDX1+ pancreatic progenitor cells by using high-throughput screening (HTS) system. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: TSV
Series
Accession:
GSE89973
ID:
200089973
20.

ATAC-seq on human pancreatic islets

(Submitter supplied) We have studied the impact of T2D on open chromatin in human pancreatic islets. We used assay for transposase-accessible chromatin using sequencing (ATAC-seq) to profile open chromatin in islets from T2D and non-diabetic donors. We identified ATAC-seq peaks representing open chromatin regions in islets of non-diabetic and diabetic donors. The majority of ATAC-seq peaks mapped near transcription start sites. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
15 Samples
Download data: BEDGRAPH
Series
Accession:
GSE129383
ID:
200129383
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