| http://purl.uniprot.org/citations/8948588 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/8948588 | http://www.w3.org/2000/01/rdf-schema#comment | "TGF-beta1 is a known inhibitor of branching morphogenesis when added exogenously to mouse embryonic lungs in culture. However, the issue of whether endogenous TGF-beta signaling has a function in the process of lung organogenesis is not completely resolved. We utilized immunoperturbation and antisense oligodeoxynucleotide inhibitory strategies to abrogate TGF-beta type II receptor function in embryonic mouse lungs undergoing branching morphogenesis in serumless explant culture. Antisera directed against a TGF-beta type II receptor N-terminal peptide that perturbs TGF-beta ligand-receptor binding increased branching by 70%. Similarly, antisense TGF-beta type II receptor oligodeoxynucleotides (40 microM) resulted in a 58% increase in branching, compared to scrambled and mismatched sequence controls, while TGF-beta, type II receptor mRNA and its protein expression levels were suppressed by 95 and 84%, respectively. Addition of exogenous TGF-beta1 did not overcome the stimulatory effects either of TGF-beta type II receptor immunoperturbation or of antisense oligodeoxynucleotide treatment on lung branching morphogenesis. Using in situ hybridization and immunohistochemistry, both TGF-beta type II receptor mRNA and protein were localized to the epithelium lining the developing airways, and to the surrounding mesenchyme, indicating that TGF-beta type II receptor is an important regulator of epithelial-mesenchymal interaction. Exogenous TGF-beta1 decreased cyclin A mRNA levels in control embryonic lung explants, while TGF-beta type II receptor antisense oligodeoxynucleotides prevented the downregulation of cyclin A mRNA expression by exogenous TGF-beta1. In addition, PCNA immunostaining of the primitive bronchial epithelium was increased in the presence of TGF-beta type II receptor antisense oligodeoxynucleotides either alone or together with exogenous TGF-beta1, whereas TGF-beta1 alone decreased PCNA staining. Thus, abrogation of TGF-beta type II receptor expression prevented TGF-beta1-induced epithelial cell G1 arrest. These results demonstrate, for the first time, that abrogation of the TGF-beta type II receptor stimulates embryonic lung organogenesis in culture and reverses the negative influence of endogenous TGF-beta signaling upon epithelial cell cycle progression."xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.org/dc/terms/identifier | "doi:10.1006/dbio.1996.0298"xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/author | "Bu D."xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/author | "Lee M."xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/author | "Zhao J."xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/author | "Warburton D."xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/author | "Slavkin H.C."xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/author | "Hall F.L."xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/date | "1996"xsd:gYear |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/name | "Dev Biol"xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/pages | "242-257"xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/title | "Abrogation of transforming growth factor-beta type II receptor stimulates embryonic mouse lung branching morphogenesis in culture."xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://purl.uniprot.org/core/volume | "180"xsd:string |
| http://purl.uniprot.org/citations/8948588 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/8948588 |
| http://purl.uniprot.org/citations/8948588 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/8948588 |
| http://purl.uniprot.org/uniprot/#_Q62312-mappedCitation-8948588 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/8948588 |
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| http://purl.uniprot.org/uniprot/#_Q8BQS9-mappedCitation-8948588 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/8948588 |
| http://purl.uniprot.org/uniprot/#_Q78JJ8-mappedCitation-8948588 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/8948588 |
| http://purl.uniprot.org/uniprot/#_Q91ZR8-mappedCitation-8948588 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/8948588 |
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| http://purl.uniprot.org/uniprot/#_Q8BRS2-mappedCitation-8948588 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/8948588 |
| http://purl.uniprot.org/uniprot/Q8BQS9 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/8948588 |
| http://purl.uniprot.org/uniprot/Q543C0 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/8948588 |