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DESCRIBE <http://purl.uniprot.org/SHA-384/C480CCF82F06E45BE6A55A2D54AF395E6EE795A3550B98701B67C29764BEABF3339CB8938E3B0FEDE9D751470FBF4E82>
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http://purl.uniprot.org/SHA-384/C480CCF82F06E45BE6A55A2D54AF395E6EE795A3550B98701B67C29764BEABF3339CB8938E3B0FEDE9D751470FBF4E82
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/C480CCF82F06E45BE6A55A2D54AF395E6EE795A3550B98701B67C29764BEABF3339CB8938E3B0FEDE9D751470FBF4E82
http://www.w3.org/2000/01/rdf-schema#comment
"Mst1-induced defective mitophagy evoked cellular oxidative stress energy metabolism and calcium overload. Through excessive mitochondrial fission and aberrant mitophagy Mst1 launched caspase 9-related mitochondrial apoptosis and abrogated F-actin/lamellipodium-dependent cellular migration."
xsd:string
http://purl.uniprot.org/uniprot/#_41852B71823CDF4841B6533D92890C63275DDECC7D0FDC7173A94342DF872F6E631ED3E6F199C8B8BA37671C9D51EF44
http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.uniprot.org/SHA-384/C480CCF82F06E45BE6A55A2D54AF395E6EE795A3550B98701B67C29764BEABF3339CB8938E3B0FEDE9D751470FBF4E82
http://purl.uniprot.org/uniprot/Q13043
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/C480CCF82F06E45BE6A55A2D54AF395E6EE795A3550B98701B67C29764BEABF3339CB8938E3B0FEDE9D751470FBF4E82
http://purl.uniprot.org/uniprot/#_Q13043-mappedCitation-29448246
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/C480CCF82F06E45BE6A55A2D54AF395E6EE795A3550B98701B67C29764BEABF3339CB8938E3B0FEDE9D751470FBF4E82