| http://purl.uniprot.org/citations/20647317 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20647317 | http://www.w3.org/2000/01/rdf-schema#comment | "Melanoma cells are highly resistant to anoikis, a form of apoptosis induced in nonadherent/inappropriate adhesion conditions. Depleting B-RAF or the prosurvival Bcl-2 family protein Mcl-1 renders mutant B-RAF melanoma cells susceptible to anoikis. In this study, we examined the effect of targeting B-RAF on the survival of primary stage melanoma cells cultured in three-dimensional type I collagen gels, which partially mimics the dermal microenvironment. Depletion/inhibition of B-RAF with small interfering RNA or the mutant B-RAF inhibitor, PLX4720, induced apoptosis of mutant B-RAF melanoma cells in three-dimensional collagen. Apoptosis was dependent on two upregulated BH3-only proteins, Bim-EL and Bmf, and was inhibited by ectopic Mcl-1 expression. Akt3 activation has been associated with the survival of melanoma cells. Mutant B-RAF melanoma cells ectopically expressing a constitutively activated form of Akt3 or endogenously expressing mutant Akt3 were protected from apoptosis induced by B-RAF knockdown or PLX4720 treatment. Furthermore, intrinsically resistant metastatic melanoma cells displayed elevated Akt phosphorylation in three-dimensional collagen and were rendered susceptible to PLX4720 by Akt3 knockdown. Importantly, myristylated Akt3 prevented B-RAF targeting-induced upregulation of Bim-EL and Bmf in three-dimensional collagen and partially protected Mcl-1-depleted cells from apoptosis. These findings delineate how mutant B-RAF protects melanoma cells from apoptosis and provide insight into possible resistance mechanisms to B-RAF inhibitors."xsd:string |
| http://purl.uniprot.org/citations/20647317 | http://purl.org/dc/terms/identifier | "doi:10.1158/0008-5472.can-09-4471"xsd:string |
| http://purl.uniprot.org/citations/20647317 | http://purl.uniprot.org/core/author | "Shao Y."xsd:string |
| http://purl.uniprot.org/citations/20647317 | http://purl.uniprot.org/core/author | "Aplin A.E."xsd:string |
| http://purl.uniprot.org/citations/20647317 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20647317 | http://purl.uniprot.org/core/name | "Cancer Res"xsd:string |
| http://purl.uniprot.org/citations/20647317 | http://purl.uniprot.org/core/pages | "6670-6681"xsd:string |
| http://purl.uniprot.org/citations/20647317 | http://purl.uniprot.org/core/title | "Akt3-mediated resistance to apoptosis in B-RAF-targeted melanoma cells."xsd:string |
| http://purl.uniprot.org/citations/20647317 | http://purl.uniprot.org/core/volume | "70"xsd:string |
| http://purl.uniprot.org/citations/20647317 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/20647317 |
| http://purl.uniprot.org/citations/20647317 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/20647317 |
| http://purl.uniprot.org/uniprot/#_P15056-mappedCitation-20647317 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20647317 |
| http://purl.uniprot.org/uniprot/#_Q56A86-mappedCitation-20647317 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20647317 |
| http://purl.uniprot.org/uniprot/#_Q9Y243-mappedCitation-20647317 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20647317 |
| http://purl.uniprot.org/uniprot/P15056 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/20647317 |
| http://purl.uniprot.org/uniprot/Q9Y243 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/20647317 |
| http://purl.uniprot.org/uniprot/Q56A86 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/20647317 |