RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/24029230http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24029230http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24029230http://www.w3.org/2000/01/rdf-schema#comment"Monosomy 7 and interstitial deletion of 7q (-7/7q-) are well-recognized nonrandom chromosomal abnormalities frequently found among patients with myelodysplastic syndromes (MDSs) and myeloid leukemias. We previously identified candidate myeloid tumor suppressor genes (SAMD9, SAMD9-like = SAMD9L, and Miki) in the 7q21.3 subband. We established SAMD9L-deficient mice and found that SAMD9L(+/-) mice as well as SAMD9L(-/-) mice develop myeloid diseases resembling human diseases associated with -7/7q-. SAMD9L-deficient hematopoietic stem cells showed enhanced colony formation potential and in vivo reconstitution ability. SAMD9L localizes in early endosomes. SAMD9L-deficient cells showed delays in homotypic endosome fusion, resulting in persistence of ligand-bound cytokine receptors. These findings suggest that haploinsufficiency of SAMD9L and/or SAMD9 gene(s) contributes to myeloid transformation."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.org/dc/terms/identifier"doi:10.1016/j.ccr.2013.08.011"xsd:string
http://purl.uniprot.org/citations/24029230http://purl.org/dc/terms/identifier"doi:10.1016/j.ccr.2013.08.011"xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Kanai A."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Kanai A."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Matsui H."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Matsui H."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Nakamura T."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Nakamura T."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Ozaki Y."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Ozaki Y."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Suda T."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Suda T."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Wolff L."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Wolff L."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Inaba T."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Inaba T."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Takubo K."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Takubo K."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Asou H."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Asou H."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Honda H."xsd:string
http://purl.uniprot.org/citations/24029230http://purl.uniprot.org/core/author"Honda H."xsd:string