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Links from GEO DataSets

Items: 20

1.

ERBB2 drives YAP activation and EMT-like processes during cardiac regeneration

(Submitter supplied) RNA-seq comparing WT and caERBB2 over expresising hearts with/out injury
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
16 Samples
Download data: XLSX
Series
Accession:
GSE144391
ID:
200144391
2.

siRNA knockdown of neonatal rat cardiac myocytes and fibroblasts

(Submitter supplied) Primary neonatal rat cardiac myocytes or fibroblasts were isolated and subjected to siRNA mediated Yap knockdown
Organism:
Rattus norvegicus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24782
12 Samples
Download data: XLSX
Series
Accession:
GSE112464
ID:
200112464
3.

RNAseq of regenerating yap mutant zebrafish hearts

(Submitter supplied) A Yap knockout zebrafish line was used to observe how loss of Yap affects cardiac regeneration.
Organism:
Danio rerio
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24776
12 Samples
Download data: XLSX
Series
Accession:
GSE112452
ID:
200112452
4.

Actin cytoskeletal remodeling with protrusion formation is essential for heart regeneration in Hippo-deficient mice

(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:
GPL16331 GPL13692
16 Samples
Download data: BED, BEDGRAPH, GPR
Series
Accession:
GSE138062
ID:
200138062
5.

Cardiac profiling of Yap-bound chromatin in neonatal Salvador mutant mice

(Submitter supplied) In this study, we identified chromatin regions bound by YAP, a major effector of the Hippo tumor suppressor pathway. To disrupt Hippo signaling in the mouse heart, we inactivated the single mammalian Salv ortholog using a Salv conditional null allele and and tamoxifen inducible Myh6-cre/Esr1 allele, Cre activity was induced with 4 consecutive intraperitoneal (i.p.) or subcutaneous injections of tamoxifen from P7-P10.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16331
4 Samples
Download data: BED, BEDGRAPH
Series
Accession:
GSE46529
ID:
200046529
6.

Cardiac gene expression profiling of neonatal Salvador mutant mice

(Submitter supplied) In this study, we identified a number of genes whose expression are regulated by the Hippo tumor suppressor pathway. To disrupt Hippo signaling in the mouse heart, we inactivated the single mammalian Salv ortholog using a Salv conditional null allele and the Nkx2.5 cre allele that directs cardiac cre activity. Total RNA from P8-stage hearts were used for expression profiling.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL13692
12 Samples
Download data: GPR
Series
Accession:
GSE44103
ID:
200044103
7.

Multiscale Analysis of Extracellular Matrix Remodeling in the Failing Heart

(Submitter supplied) Rationale: Cardiac extracellular matrix (ECM) comprises a dynamic molecular network providing structural support to heart tissue function. Understanding the impact of ECM remodeling on cardiac cells during heart failure (HF) is essential to prevent adverse ventricular remodeling and restore organ functionality in affected patients. Objectives: We aimed to (i) identify consistent modifications to cardiac ECM structure and mechanics that contribute to HF and (ii) determine the underlying molecular mechanisms. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21697
12 Samples
Download data: TSV
Series
Accession:
GSE155495
ID:
200155495
8.

The effect of active YAP in neonatal heart of Xinβ knockout mice

(Submitter supplied) Purpose: The goals of this study are 1) to define the transcriptome changes in the heart in the absence of intercalated-disc protein Xinβ, and 2) to define the effect of active Yap overexpression on the cardiac transcriptome in the absence of Xinβ. Methods: Total RNA from heart apex of postnatal day (P) 7.5 Xinβ KO or WT mice were profiled by bulk-RNA sequencing (50bp SE). Total RNA from heart apex of P7.5 Xinβ KO or WT mice injected with AAV9 carrying cardiac troponin T promoter driven active Yap (S127A) or GFP (control) at P1 were profiled by bulk-RNA sequencing (150bp PE). more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
24 Samples
Download data: TXT
Series
Accession:
GSE149647
ID:
200149647
9.

Cardiac-specific YAP activation improve cardiac function and survival in an experimental murine MI model

(Submitter supplied) In this study, we used a cardiac-specific, inducible expression system to activate YAP in adult mouse heart. Activation of YAP in adult heart promoted cardiomyocyte proliferation and did not deleteriously affect heart function. Furthermore, YAP activation after myocardial infarction (MI) preserved heart function and reduced infarct size. Using adeno-associated virus subtype 9 (AAV9) as a delivery vector, we expressed human YAP in the murine myocardium immediately after MI. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
9 Samples
Download data: CEL
Series
Accession:
GSE54612
ID:
200054612
10.

Gene expression changes in beta-blocker treated neonatal hearts

(Submitter supplied) The regeneration potential of the mammalian heart is limited. We found that treatment of beta-blocker robustly enhanced cardiomyocyte proliferation and promoted cardiac regeneration post myocardial infarction. To investigate the gene expression changes, we performed RNA-seq using the hearts treated with beta-blocker for 7 days.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
4 Samples
Download data: TXT
Series
Accession:
GSE186099
ID:
200186099
11.

Overexpression of A kinase interacting protein 1 attenuates myocardial ischemia / reperfusion injury, but does not influence heart failure development

(Submitter supplied) Aims A kinase interacting protein 1 (AKIP1) stimulates physiological growth in cultured cardiomyocytes and attenuates ischemia / reperfusion (I/R) injury in ex vivo perfused hearts. We aimed to determine whether AKIP1 modulates the cardiac response to acute and chronic cardiac stress in vivo. Methods and results Transgenic mice with cardiac-specific overexpression of AKIP1 (AKIP1-TG) were created. AKIP1-TG mice and their wild type (WT) littermates displayed similar cardiac structure and function. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
16 Samples
Download data: TXT
Series
Accession:
GSE83472
ID:
200083472
12.

YAP/TAZ deficiency reprograms macrophage phenotype and improves infarct healing and cardiac function after myocardial infarction

(Submitter supplied) Adverse cardiac remodeling after myocardial infarction (MI) causes structural and functional changes in the heart leading to heart failure. The initial pro-inflammatory response followed by an anti-inflammatory or reparative response post-MI is essential for minimizing the myocardial damage, healing, and scar formation. Bone marrow-derived macrophages (BMDMs) are recruited to the injured myocardium and essential for cardiac repair as they can adopt both pro-inflammatory (M1) or anti-inflammatory/reparative (M2) phenotypes to modulate inflammatory and reparative response, respectively. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
12 Samples
Download data: TXT
Series
Accession:
GSE158889
ID:
200158889
13.

YAP Partially Reprograms Chromatin Accessibility to Directly Induce Adult Cardiogenesis in Vivo

(Submitter supplied) Specialized adult somatic cells, such as cardiomyocytes (CMs), are highly differentiated with poor renewal capacity, an integral reason underlying organ failure in disease and aging. Among the least renewable cells in the human body, CMs renew approximately 1% annually. Consistent with poor CM turnover, heart failure is the leading cause of death. Here, we show that an active version of the Hippo pathway effector YAP, termed YAP5SA, partially reprograms adult mouse CMs to a more fetal and proliferative state. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL19057
12 Samples
Download data: BIGWIG, TXT, WIG
Series
Accession:
GSE123457
ID:
200123457
14.

Yap dependent reprogramming of Lgr5+ stem cells drives intestinal regeneration and cancer

(Submitter supplied) Hippo signalling has been implicated as a key regulator of tissue regeneration. In the intestine, ex vivo organoid cultures model aspects of crypt epithelial regeneration. Therefore in order to uncover the Yap regulated transcriptional programs during crypt regeneration we performed RNA-sequencing of Yap wt and Yap deficient organoids, as well as organoids inducibly expressing Yap.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: TXT
Series
Accession:
GSE66567
ID:
200066567
15.

Interaction of YAP1 with the Myb-MuvB (MMB) complex sustain proliferation in the postnatal heart

(Submitter supplied) YAP, a major downstream effector of the Hippo signaling pathway, is an important regulator of cell proliferation. Previous studies have shown that YAP cooperates with the two transcription factors E2F and MYC to mediate G1 to S transition by regulating early cell cycle gene expression. On the other hand, the ability of YAP to regulate G2/M gene expression is dependent on the Myb-MuvB (MMB) complex, consisting of the evolutionary MuvB core complex of five proteins and the facultative subunit B-MYB, a transcription factor. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
22 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE137132
ID:
200137132
16.

Mst1/2-Yap in lung epithelial progenitor cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing
Platforms:
GPL6246 GPL11154 GPL13112
14 Samples
Download data: CEL, TXT
Series
Accession:
GSE61628
ID:
200061628
17.

RNA-seq analysis of Mst1/2 deleted bronchiolar epithelial cells from adult mouse lungs

(Submitter supplied) Mst1 and Mst2 were conditionally deleted from non-ciliated bronchiolar epithelial cells in the mature lung. Bronchiolar epithelial cells from control and Mst1/2 deleted mice were isolated by cell sorting and used for RNA-seq analysis.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: TXT, XLS
Series
Accession:
GSE61627
ID:
200061627
18.

RNA-seq analysis of bronchosphere cultures of primary human bronchiolar epithelial cells

(Submitter supplied) Primary human bronchial epithelial cells were transduced with control or hYAP(S127A) lentivirus in sphere forming conditions. Bronchospheres were harvested on day 18-20 for RNAseq analysis
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: TXT, XLS
Series
Accession:
GSE61626
ID:
200061626
19.

Microarray of Mst1/2 deleted epithelial cells from E18.5 mouse lungs

(Submitter supplied) ShhCre;Mst1/2flx/flx (Mst1/2 D/D) mice were generated to conditionally delete Mst1 and Mst2 from epithelial progenitors during lung morphogenesis. Lungs from E18.5 control and Mst1/2 D/D mice were mechanically and enzymatically dissociated to generate single cell suspension. Epcam(+) cells were isolated using magnetic microbeads. Microarray analysis of mRNAs isolated from Epcam(+) epithelial cells from E18.5 control and Mst1/2 D/D mice was performed to identify transcriptional changes following deletion of the mammalian Hippo kinases (Mst1 and Mst2) from the embryonic lung.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
8 Samples
Download data: CEL
Series
Accession:
GSE61582
ID:
200061582
20.

Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression

(Submitter supplied) We tested the hypothesis that increasing matrix stiffness on which normal human lung fibroblasts are grown promotes the expression of a fibrogenic cellular transcriptomic program. Keywords: Human lung fibroblast, matrix stiffness, PTGS2, COX-2, Prostaglandin E2
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
15 Samples
Download data: CEL
Series
Accession:
GSE22011
ID:
200022011
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