http://purl.uniprot.org/citations/32747435 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/32747435 | http://www.w3.org/2000/01/rdf-schema#comment | "Homeostasis of intestinal stem cells (ISCs) is maintained by the orchestration of niche factors and intrinsic signaling networks. Here, we have found that deletion of Erk1 and Erk2 (Erk1/2) in intestinal epithelial cells at embryonic stages resulted in an unexpected increase in cell proliferation and migration, expansion of ISCs, and formation of polyp-like structures, leading to postnatal death. Deficiency of epithelial Erk1/2 results in defects in secretory cell differentiation as well as impaired mesenchymal cell proliferation and maturation. Deletion of Erk1/2 strongly activated Wnt signaling through both cell-autonomous and non-autonomous mechanisms. In epithelial cells, Erk1/2 depletion resulted in loss of feedback regulation, leading to Ras/Raf cascade activation that transactivated Akt activity to stimulate the mTor and Wnt/β-catenin pathways. Moreover, Erk1/2 deficiency reduced the levels of Indian hedgehog and the expression of downstream pathway components, including mesenchymal Bmp4 - a Wnt suppressor in intestines. Inhibition of mTor signaling by rapamycin partially rescued Erk1/2 depletion-induced intestinal defects and significantly prolonged the lifespan of mutant mice. These data demonstrate that Erk/Mapk signaling functions as a key modulator of Wnt signaling through coordination of epithelial-mesenchymal interactions during intestinal development."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.org/dc/terms/identifier | "doi:10.1242/dev.185678"xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Chen J."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Fang G."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Fan L."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Hu K."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Li L."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Liu M."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Li D."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Pang X."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Wei G."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Zhang X."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Gao G."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Clevers H."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Gao N."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Zeng Z."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/author | "Fan H.Y."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/name | "Development"xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/pages | "dev185678"xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/title | "Erk and MAPK signaling is essential for intestinal development through Wnt pathway modulation."xsd:string |
http://purl.uniprot.org/citations/32747435 | http://purl.uniprot.org/core/volume | "147"xsd:string |
http://purl.uniprot.org/citations/32747435 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/32747435 |
http://purl.uniprot.org/citations/32747435 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/32747435 |