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http://purl.uniprot.org/citations/27729611http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27729611http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27729611http://www.w3.org/2000/01/rdf-schema#comment"PICT-1 was originally identified as a tumor suppressor. Here, we found that PICT-1 overexpression triggered pro-death autophagy without nucleolar disruption or p53 accumulation in U251 and MCF7 cells. Truncated PICT-1 fragments 181-346 and 1-346, which partly or totally lack nucleolar localization, showed weaker autophagy-inducing effects than full-length PICT-1 and a well-defined nucleolar mutant (181-479). Furthermore, PICT-1 partly localizes to the nucleolar fibrillar center (FC) and directly binds to ribosomal DNA (rDNA) gene loci, where it interacts with upstream binding factor (UBF). Overexpression of PICT-1 or the 181-479 mutant, but not the 1-346 or 181-346 mutants, markedly inhibited the phosphorylation of UBF and the recruitment of rRNA polymerase I (Pol I) to the rDNA promoter in response to serum stimulation, thereby suppressing rRNA transcription, suggesting that rRNA transcription inhibition might be an important contributor to PICT-1-induced autophagy. This is supported by the finding that CX-5461, a specific Pol I inhibitor, also induced autophagy. In addition, both CX-5461 and PICT-1, but not the 1-346 or 181-346 mutants, significantly suppressed the activation of the Akt/mTOR/p70S6K signaling pathway. Our data show that PICT-1 triggers pro-death autophagy through inhibition of rRNA transcription and the inactivation of AKT/mTOR/p70S6K pathway, independent of nucleolar disruption and p53 activation."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.org/dc/terms/identifier"doi:10.18632/oncotarget.12288"xsd:string
http://purl.uniprot.org/citations/27729611http://purl.org/dc/terms/identifier"doi:10.18632/oncotarget.12288"xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Chen H."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Chen H."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Huang L."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Huang L."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Hu B."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Hu B."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Zhou L."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Zhou L."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Zhang F."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Zhang F."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Wang Z."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Wang Z."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Wang L."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Wang L."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Tsai H."xsd:string
http://purl.uniprot.org/citations/27729611http://purl.uniprot.org/core/author"Tsai H."xsd:string