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http://purl.uniprot.org/SHA-384/F9ADB9A759A77F824985CFC90DC8286554416FF3FD73671876EF9969F62A40A4278F49BF967E3FAA629400905FFA5333http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/F9ADB9A759A77F824985CFC90DC8286554416FF3FD73671876EF9969F62A40A4278F49BF967E3FAA629400905FFA5333http://www.w3.org/2000/01/rdf-schema#comment"Study shows that IRF2 knockdown inhibits growth colony formation of OCI/AML-2 OCI/AML-3 and THP-1 cells. In addition IRF2 knockdown induces apoptosis of acute myeloid leukemia (AML) cells by regulating apoptotic effectors. Further mechanism analysis shows that INPP4B contributes to the effects of IRF2 on apoptosis and growth of AML cells. Thus IRF2 serves as an important regulator in AML by targeting INPP4B."xsd:string
http://purl.uniprot.org/uniprot/#_E8E1937A9C0B6344FCA4B6C385C2441AD085BD7214A1A8AADDBC4457BCFA5EA3D6529B1F526058FA66CAD438E6986C55http://www.w3.org/1999/02/22-rdf-syntax-ns#subjecthttp://purl.uniprot.org/SHA-384/F9ADB9A759A77F824985CFC90DC8286554416FF3FD73671876EF9969F62A40A4278F49BF967E3FAA629400905FFA5333
http://purl.uniprot.org/uniprot/B7Z6T2http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/F9ADB9A759A77F824985CFC90DC8286554416FF3FD73671876EF9969F62A40A4278F49BF967E3FAA629400905FFA5333
http://purl.uniprot.org/uniprot/#_B7Z6T2-mappedCitation-28579269http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/F9ADB9A759A77F824985CFC90DC8286554416FF3FD73671876EF9969F62A40A4278F49BF967E3FAA629400905FFA5333