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DESCRIBE <http://purl.uniprot.org/SHA-384/17E9A33053F3A114A68BD38F2BD1F2B6D8F0406C349AC45EFC87C625F8D8497F3419938B4B0739917111D4570056A335>
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http://purl.uniprot.org/SHA-384/17E9A33053F3A114A68BD38F2BD1F2B6D8F0406C349AC45EFC87C625F8D8497F3419938B4B0739917111D4570056A335
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/17E9A33053F3A114A68BD38F2BD1F2B6D8F0406C349AC45EFC87C625F8D8497F3419938B4B0739917111D4570056A335
http://www.w3.org/2000/01/rdf-schema#comment
"These results demonstrate that overexpression of IAP-2 renders the heart more resistant to apoptosis and ischemia/reperfusion injury."
xsd:string
http://purl.uniprot.org/uniprot/#_54CEF0F7DA5C0529491AB141B1308B67CD6A70DF07366DCA21B24D8EB2A446A4980988A10A89415BCF88149890283737
http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.uniprot.org/SHA-384/17E9A33053F3A114A68BD38F2BD1F2B6D8F0406C349AC45EFC87C625F8D8497F3419938B4B0739917111D4570056A335
http://purl.uniprot.org/uniprot/A2CGA5
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/17E9A33053F3A114A68BD38F2BD1F2B6D8F0406C349AC45EFC87C625F8D8497F3419938B4B0739917111D4570056A335
http://purl.uniprot.org/uniprot/#_A2CGA5-mappedCitation-17321613
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/17E9A33053F3A114A68BD38F2BD1F2B6D8F0406C349AC45EFC87C625F8D8497F3419938B4B0739917111D4570056A335