| http://purl.uniprot.org/citations/24158981 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24158981 | http://www.w3.org/2000/01/rdf-schema#comment | "Kidney injury molecule-1 (KIM-1)/T cell Ig and mucin domain-containing protein-1 (TIM-1) is upregulated more than other proteins after AKI, and it is highly expressed in renal damage of various etiologies. In this capacity, KIM-1/TIM-1 acts as a phosphatidylserine receptor on the surface of injured proximal tubular epithelial cells, mediating phagocytosis of apoptotic cells, and it may also act as a costimulatory molecule for immune cells. Despite recognition of KIM-1 as an important therapeutic target for kidney disease, the regulators of KIM-1 transcription in the kidney remain unknown. Using a bioinformatics approach, we identified upstream regulators of KIM-1 after AKI. In response to tubular injury in rat and human kidneys or oxidant stress in human proximal tubular epithelial cells (HPTECs), KIM-1 expression increased significantly in a manner that corresponded temporally and regionally with increased phosphorylation of checkpoint kinase 1 (Chk1) and STAT3. Both ischemic and oxidant stress resulted in a dramatic increase in reactive oxygen species that phosphorylated and activated Chk1, which subsequently bound to STAT3, phosphorylating it at S727. Furthermore, STAT3 bound to the KIM-1 promoter after ischemic and oxidant stress, and pharmacological or genetic induction of STAT3 in HPTECs increased KIM-1 mRNA and protein levels. Conversely, inhibition of STAT3 using siRNAs or dominant negative mutants reduced KIM-1 expression in a kidney cancer cell line (769-P) that expresses high basal levels of KIM-1. These observations highlight Chk1 and STAT3 as critical upstream regulators of KIM-1 expression after AKI and may suggest novel approaches for therapeutic intervention."xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.org/dc/terms/identifier | "doi:10.1681/asn.2013020161"xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/author | "Park P.J."xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/author | "Frank D.A."xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/author | "Kim T.M."xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/author | "Vaidya V.S."xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/author | "Ajay A.K."xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/author | "Ramirez-Gonzalez V."xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/name | "J Am Soc Nephrol"xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/pages | "105-118"xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/title | "A bioinformatics approach identifies signal transducer and activator of transcription-3 and checkpoint kinase 1 as upstream regulators of kidney injury molecule-1 after kidney injury."xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://purl.uniprot.org/core/volume | "25"xsd:string |
| http://purl.uniprot.org/citations/24158981 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24158981 |
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