| http://purl.uniprot.org/citations/21846906 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21846906 | http://www.w3.org/2000/01/rdf-schema#comment | "The function of the tumor suppressor promyelocytic leukemia (PML) protein is disrupted in promyelocytic leukemia. PML has been reported to function as a negative regulator of mTOR (mammalian target of rapamycin) and nuclear Akt under some conditions. mTOR and Akt pathways regulate a diverse array of pathways, including those that control insulin signaling, energy metabolism, growth, cellular survival, and lifespan. Although the PML-mTOR/Akt link suggests that PML may have metabolic functions in the whole organism, very little is known about the metabolic functions of PML. Here we report that PML(-/-) mice did not show any significant metabolic defects. There was no impairment in the mTOR/Akt or AMPK signaling in white adipose tissue, liver, or muscle. However, despite having normal food intake and activity levels, PML(-/-) mice gained body weight faster and had more fat mass, particularly subcutaneous fat mass, in the diet-induced obesity model. Using in vitro adipogenesis models, we discovered that PML is a suppressor of adipogenesis. PML expression decreased during adipogenesis and was undetectable in fully differentiated adipocytes. Loss of PML increased expression of the adipogenic transcription factors CCAAT/enhancer binding protein-α and peroxisome proliferator-activated receptor-γ. We found that the Sirt1-NCor-SMRT corepressor complex, which represses pparg transcription, does not bind to the pparg promoter efficiently upon PML depletion. On the basis of these findings, we propose that PML is a negative regulator of the adipogenic transcription factors and that, in times of energy excess, PML may limit fat accumulation by suppressing the differentiation of preadipocytes into adipocytes."xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpendo.00092.2011"xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/author | "Kang H."xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/author | "Liu M."xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/author | "Lee K.H."xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/author | "Yang S."xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/author | "Park S.J."xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/author | "Chung J.H."xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/author | "Kim M.K."xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/author | "Um J.H."xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/name | "Am J Physiol Endocrinol Metab"xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/pages | "E1130-42"xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/title | "Promyelocytic leukemia inhibits adipogenesis, and loss of promyelocytic leukemia results in fat accumulation in mice."xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://purl.uniprot.org/core/volume | "301"xsd:string |
| http://purl.uniprot.org/citations/21846906 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21846906 |
| http://purl.uniprot.org/citations/21846906 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/21846906 |
| http://purl.uniprot.org/uniprot/#_A0A068EW80-mappedCitation-21846906 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21846906 |
| http://purl.uniprot.org/uniprot/#_D3YXR5-mappedCitation-21846906 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21846906 |
| http://purl.uniprot.org/uniprot/#_F6XUT1-mappedCitation-21846906 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21846906 |
| http://purl.uniprot.org/uniprot/#_D3Z2V0-mappedCitation-21846906 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21846906 |
| http://purl.uniprot.org/uniprot/#_D3Z3A6-mappedCitation-21846906 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21846906 |
| http://purl.uniprot.org/uniprot/#_D6RII9-mappedCitation-21846906 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21846906 |
| http://purl.uniprot.org/uniprot/#_F7BTZ2-mappedCitation-21846906 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21846906 |