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Expression data of human pulmonary arterial smooth muscle cells (PASMCs) treated with BMP-4

ABSTRACT: Smad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing. We used expression microarrays to compare the Smad1/5 binding sites identified by ChIP-seq to BMP-induced gene expressions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28847 | GEO | 2011/07/16

SECONDARY ACCESSION(S): PRJNA143113

REPOSITORIES: GEO

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Expression data of human pulmonary arterial smooth muscle cells (PASMCs) treated with BMP-4

Project description:Smad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing. We used expression microarrays to compare the Smad1/5 binding sites identified by ChIP-seq to BMP-induced gene expressions. PASMCs were treated with 50 ng/ml BMP-4 for 0, 2, or 24 hrs. RNA was extracted and hybridized on Affymetrix microarrays.

2011-07-15 | E-GEOD-28847 | biostudies-arrayexpress

SMAD1/5 binding regions of human pulmonary arterial smooth muscle cells (PASMCs) treated with BMP

2011-07-16 | GSE28848 | GEO

Expression data of human umbilical vein endothelial cells (HUVECs) treated with BMP-6 and BMP-9

Project description:Smad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing. We used expression microarrays to compare the Smad1/5 binding sites identified by ChIP-seq to BMP-induced gene expressions. HUVECs were treated with BMP for RNA extraction and hybridization on Affymetrix microarrays.

2011-07-15 | E-GEOD-27631 | biostudies-arrayexpress

Expression data of human umbilical vein endothelial cells (HUVECs) treated with BMP-6 and BMP-9

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BMP signaling in mouse embryonic stem cells (ESCs) in the naÃ¯ve and primed pluripotent states [ChIP-Seq]

Project description:Carrying out both RNA-seq and Smad1/5 genome-wide chromatin immunoprecipitation and sequencing (ChIP-seq) analyses of mESCs in the naÃ¯ve or primed states, we revisit the roles of BMP signaling in mESCs. Smad1/5 binding sites in 2 cell types; mESCs and ES-derived EpiSC (ESD-EpiSCs).

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SMAD1/5 binding regions of human umbilical vein endothelial cells (HUVECs) treated with BMP.

Project description:Smad1/5 binding regions were identified by ChIP-seq. HUVECs were treated with BMP for 1.5 h and anti-SMAD1/5 ChIP-seq analyses were performed using Illumina genome analyzer.

2011-07-15 | E-GEOD-27634 | biostudies-arrayexpress

Smad1 and its target gene Wif1 coordinate BMP and Wnt signaling activities to regulate lung development

Project description:Bone morphogenetic protein 4 (BMP4) is essential for lung development. To define its intracellular signaling mechanisms by which BMP4 regulates lung development, BMP-specific Smad1 or Smad5 was selectively knocked out in fetal mouse lung epithelial cells. Abrogation of lung epithelial-specific Smad1, but not Smad5, resulted in retardation of lung branching morphogenesis and reduced sacculation, accompanied by altered distal lung epithelial cell proliferation and differentiation, and consequently severe neonatal respiratory failure. By combining cDNA microarray with ChIP-chip analyses, Wnt inhibitory factor-1 (Wif1) was identified as a novel target gene of Smad1 in the developing mouse lung epithelial cells. Loss of Smad1 transcriptional activation of Wif1 expression was associated with reduced Wif1 expression and increased Wnt/beta-catenin signaling activity in lung epithelia, resulting in specific fetal lung abnormalities. Therefore, a novel regulatory loop of BMP4-Smad1-Wif1-Wnt/beta-catenin in coordinating BMP and Wnt pathways to control fetal lung development is suggested. mRNA profiling: Total RNA was isolated from left lobe lungs of three pair of E18.5 wild type and Smad1 lung epithelium-specific conditional knockout mice

2011-01-07 | E-GEOD-26502 | biostudies-arrayexpress

Lineage regulators direct BMP and Wnt pathways to cell-specific programs during differentiation and regeneration

Project description:This SuperSeries is composed of the following subset Series: GSE29193: Genome-wide location analysis of BMP (SMAD1) in mouse erythroid progenitors co-occupted with lineage specific regulators (GATA1, GATA2) GSE29194: Genome-wide location analysis of WNT (Tcf7l2) and BMP (SMAD1) in human hematopoeitic progenitors co-occupied with lineage specific regulators (GATA1, GATA2) GSE29195: Genome-wide location analysis of WNT (Tcf7l2) and BMP (SMAD1) in human hematopoeitic cell lines co-occupied with lineage specific regulators (GATA1, GATA2, CEBPA) Refer to individual Series

2011-10-06 | E-GEOD-29196 | biostudies-arrayexpress

Smad1 and its target gene Wif1 coordinate BMP and Wnt signaling activities to regulate lung development

2011-01-07 | GSE26502 | GEO

Operation of the atypical canonical BMP signaling pathway during human odontogenesis

Project description:BMP (bone morphogenetic protein) signaling plays essential roles in the regulation of early tooth development. It is well acknowledged that with binding of extracellular BMP ligands to the type I and type II transmembrane serine/threonine kinase receptor complexes when triggering of the BMP canonical signaling pathway, receptor activated Smad1/5/8 in cytoplasm bind to Smad4, the central mediator of the canonical BMP signaling pathway, to form transfer complexes for entering the nucleus and regulating target gene expression. However, our recent studies reveal the functional operation of a novel BMP mediated signaling pathway named as the atypical BMP canonical signaling pathway in mouse developing tooth, which is Smad1/5/8 dependent but Smad4 independent. In the current study, we investigated whether this atypical BMP canonical signaling is conserved in human odontogenesis. We showed that pSmad1/5/8 is required for expression of MSX1, a well-defined BMP signaling target gene, in human dental mesenchyme, but the typical BMP canonical signaling is indeed not operating in the early human developing tooth, as assessed by the absence of pSMAD1/5/8-SMAD4 complexes in the dental mesenchyme and expression of MSX1 and translocation of pSMAD1/5/8 induced by BMP4 protein is SMAD4-independent in dental mesenchymal cells. Moreover, RNA-Seq data sets comparing the transcriptome profiles of human dental mesenchymal cells with and without SMAD4 knockdown by siRNA displays unchanged expression profiles of pSMAD1/5/8 downstream target genes, further affirming the functional operation of the atypical canonical BMP signaling pathway in a manner of SMAD1/5/8-dependent but SMAD4-independent in the dental mesenchyme during early odontogenesis.

2021-09-30 | GSE179474 | GEO

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