Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-61582
PROVIDER: PRJNA261705 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1583180.fastq.gz | Fastqsanger.gz | |||
| SRR1583181.fastq.gz | Fastqsanger.gz | |||
| SRR1583182.fastq.gz | Fastqsanger.gz | |||
| SRR1583177.fastq.gz | Fastqsanger.gz | |||
| SRR1583178.fastq.gz | Fastqsanger.gz |
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Project description: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. The mammalian Hippo kinases, Mst1 and Mst2, were conditionally deleted in epithelial progenitors of the developing lung using ShhCre. Epcam(+) epithelial cells were isolated from the lungs of E18.5 control and Mst1/2 deleted mice. mRNA isolated from Epcam(+) epithelial cells was analyzed by microarray.
2015-01-01 | E-GEOD-61582 | biostudies-arrayexpress
Project description: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. Scgb1a1-rtTA/tetO-Cre/Mst1;2-flx/flx (Mst1/2 D/D) mice were generated to conditionally delete Mst1 and Mst2 from non-ciliated, secretory bronchiolar epithelial cells. Adult mice were maintained on doxycycline food for 16 days to induce deletion of Mst1/2. Lin-/CD326+/CD24-intermediate cells were isolated by fluorescence cell sorting to enrich for the targeted airway epithelial cells. mRNA isolated from Lin-/CD326+/CD24-intermediate cells from control and Mst1/2 D/D mice was pooled and analyzed by RNA-seq to identify transcriptional changes following deletion of Mst1 and Mst2 from mature lung bronchiolar epithelial cells.
2015-01-01 | E-GEOD-61627 | biostudies-arrayexpress
Project description: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.
2015-01-01 | GSE61582 | GEO
Project description: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.
2015-01-01 | GSE61627 | GEO
Project description:Defective Hippo/YAP signaling in the liver results in tissue overgrowth and development of hepatocellular carcinoma (HCC). Here, we uncover mechanisms of YAP-mediated hepatocyte reprogramming and HCC pathogenesis. We show that YAP functions as a rheostat maintaining metabolic specialization, differentiation and quiescence within the hepatocyte compartment. Importantly, treatment with siRNA-lipid nanoparticles (siRNA-LNPs) targeting YAP restores hepatocyte differentiation and causes pronounced tumor regression in a genetically engineered mouse HCC model (mice with liver-specific Mst1/Mst2 double knockout). Furthermore, YAP targets are enriched in an aggressive human HCC subtype characterized by a proliferative signature and absence of CTNNB1 mutations. Thus, our work reveals Hippo signaling as a key regulator of positional identity of hepatocytes, supports targeting YAP using siRNA-LNPs as a paradigm of differentiation-based therapy, and identifies an HCC subtype potentially responsive to this approach. Mice with liver-specific Mst1/Mst2 double-knockout (Adeno-Cre injected Mst1-/-; Mst2Flox/Flox mice) were monitored for the formation of HCC by ultrasound imaging. Animals were then randomized to be treated by intravenous injection of either siYap-LNPs or siLuciferase-LNPs for a period of 9 days.
2015-03-07 | E-GEOD-65665 | biostudies-arrayexpress
Project description:The Hippo/YAP pathway plays a critical role in early embryonic kidney development, but its functions in the adult kidney are less well understood. Our previous work has demonstrated that tubular YAP activation induced by double knockout of the upstream Hippo kinases Mst1 and Mst2 (Mst1/2 dKO) promotes tubular injury and renal inflammation under basal conditions. However, the importance of tubular YAP activation remains to be established in injured kidneys in which many other injurious pathways are simultaneously activated. Several secreted factors were found to be increased by YAP in tubular cells, but how the transcriptional network is altered by YAP is largely unknown. Here, we show that tubular YAP was already activated at 6 h after unilateral ureteral obstruction (UUO). Tubular YAP deficiency greatly attenuated tubular cell over-proliferation, tubular injury and renal inflammation induced by UUO or cisplatin. RNA-Seq, ChIP and luciferase assay revealed that YAP promoted the transcription of the transcription factor KLF5 whereas no interaction between YAP and KLF5 was observed. Consistently, the elevated expression of KLF5 and its target genes in Mst1/2 dKO or UUO kidneys was blocked by ablation of Yap in tubular cells. Inhibition of KLF5 prevented tubular cell over-proliferation, tubular injury and renal inflammation in Mst1/2 dKO kidneys. Therefore, our results demonstrate that tubular YAP is a key player in kidney injury. YAP and KLF5 form a transcriptional cascade, in which tubular YAP activation induced by kidney injury promotes KLF5 transcription. Activation of this cascade induces tubular cell over-proliferation, tubular injury and renal inflammation
2024-05-01 | GSE235443 | GEO
Project description:The purpose of this study is to identify the roles of epithelial Yap in lung bronchial morphogenesis. We conditionlly knocked out Yap in lung epithelial cells using the SPC-Cre allele, and sequenced mRNA from E14.5 total lung.
2019-07-31 | GSE126980 | GEO
Project description:mRNA profiles of 4 week-old contol and Mst1/2 dKO and Mst1/2; Yap tKO Initial segments of Epididymis were generated by deep sequencing, in triplicate, using Illumina HiSeq platform.
2020-04-29 | GSE138519 | GEO
Project description:Cancer stem like cells (CSLCs) acquire enhanced immune checkpoint responses to evade immune cell killing and promote tumor progression. Here we show that signal regulatory protein gamma (SIRPG) determines a small population of lung adenocarcinoma (LUAD) cancer cells for both CSLCs properties and immune evasion. SIRPGhigh population displays CSLCs properties and transmits the immune escape signal through sustaining CD47 expression to both SIRPGhigh and SIRPGlow/- tumor cells. SIRPG bridges MST1 and PP2A to facilitate MST1 dephosphorylation, resulting in Hippo/YAP activation leading to cytokine release by CSLCs, which stimulates CD47 expression in LUAD cells and consequently inhibits tumor cell phagocytosis. SIRPG promotes tumor growth and metastasis in vivo through YAP signaling. Notably, SIRPG targeting with genetic SIRPG knockdown or a SIRPG neutralization antibody inhibits CSLC phenotypes and elicits phagocytosis that suppresses tumor growth in vivo. SIRPG is upregulated in human LUAD and its overexpression predicts poor survival outcome. Thus, SIRPGhigh cells serve as CSLCs and tumor immune checkpoint initiating cells propagating the immune escape signal to the whole cancer cell populations. Our study identifies Hippo/YAP signaling as the first mechanism by which SIRPG is engaged and reveals that targeting SIRPG represents an immune and CSLC targeting strategy for lung cancer therapy.
2022-01-02 | GSE192790 | GEO
Project description:Hippo signaling is highly associated with activity in the stem cell compartment of many epithelial tissues. In this study, we examined if Hippo signaling inhibition (by inducing Yap expression) could convert differentiated cells into a progenitor like phenotype. Organoid cells derived from mouse livers under various conditions, wild-type, Yap ON (Plus Dox), and Yap ON then OFF (Minus Dox) was examined. Comparison between freshly isolated hepatocytes; Uninduced_YPF-#.cel against Organoids grown in wild-type conditions (WT), Yap On (in vivo) off (in vitro) - YapOrganoidDoxMinus , and Yap On continuously - YapOrganoidDoxPlus. Organoids grown in culture or YFP+ sorted liver cells after the indicated time of Yap expression were collected. These were amplified using Nugene technology and hybridized to Affymetrix MoGene1.0 st arrays.
2014-06-06 | E-GEOD-55558 | biostudies-arrayexpress