http://purl.uniprot.org/citations/11684708 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/11684708 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/11684708 | http://www.w3.org/2000/01/rdf-schema#comment | "Keratin 8 and 18 (K8/18) are the major components of intermediate filament (IF) proteins of simple or single-layered epithelia. Recent data show that normal and malignant epithelial cells deficient in K8/18 are nearly 100 times more sensitive to tumor necrosis factor (TNF)-induced cell death. We have now identified human TNF receptor type 1 (TNFR1)-associated death domain protein (TRADD) to be the K18-interacting protein. Among IF proteins tested in two-hybrid systems, TRADD specifically bound K18 and K14, type I (acidic) keratins. The COOH-terminal region of TRADD interacted with the coil Ia of the rod domain of K18. Endogenous TRADD coimmunoprecipitated with K18, and colocalized with K8/18 filaments in human mammary epithelial cells. Overexpression of the NH2 terminus (amino acids 1-270) of K18 containing the TRADD-binding domain as well as overexpression of K8/18 in SW13 cells, which are devoid of keratins, rendered the cells more resistant to killing by TNF. We also showed that overexpressed NH2 termini of K18 and K8/18 were associated with endogenous TRADD in SW13 cells, resulting in the inhibition of caspase-8 activation. These results indicate that K18 may sequester TRADD to attenuate interactions between TRADD and activated TNFR1 and moderate TNF-induced apoptosis in simple epithelial cells."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.org/dc/terms/identifier | "doi:10.1083/jcb.200103078"xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.org/dc/terms/identifier | "doi:10.1083/jcb.200103078"xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Nishizawa M."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Nishizawa M."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Kiyono T."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Kiyono T."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Takahashi T."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Takahashi T."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Inagaki M."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Inagaki M."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Izawa I."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Izawa I."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Momoi T."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Momoi T."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Fujita E."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Fujita E."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Inada H."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/author | "Inada H."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/name | "J. Cell Biol."xsd:string |
http://purl.uniprot.org/citations/11684708 | http://purl.uniprot.org/core/name | "J. Cell Biol."xsd:string |