http://purl.uniprot.org/citations/21567403 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/21567403 | http://www.w3.org/2000/01/rdf-schema#comment | "Latexin is the only known carboxypeptidase A inhibitor in mammals and shares structural similarity with cystatin C, suggesting that latexin regulates the abundance of as yet unidentified target proteins. A forward genetic approach revealed that latexin is involved in homeostasis of hematopoietic stem cells (HSCs) in mice; however, little is known about the mechanisms by which latexin negatively affects the numbers of HSCs. In this study, we found that latexin is preferentially expressed in hematopoietic stem/progenitor cells, and is co-localized with the molecules responsible for the interaction of HSCs with a bone marrow niche, such as N-cadherin, Tie2, and Roundabout 4. Latexin-knockout young female mice showed an increase in the numbers of KSL (c-Kit(+)/Sca-1(+)/linegae marker-negative) cells, which may be attributable to enhanced self-renewal because latexin-deficient KSL cells formed more colonies than their wild-type counterparts in methylcellulose culture. Proteomic analysis of Sca-1(+) bone marrow cells demonstrated that latexin ablation reduced the abundance of multiple cellular proteins, including N-cadherin, Tie2, and Roundabout 4. Finally, we found that latexin expression was lost or greatly reduced in approximately 50% of human leukemia/lymphoma cell lines. These results imply that latexin inhibits the self-renewal of HSCs by facilitating the lodgment of HSCs within a bone marrow niche to maintain HSC homeostasis."xsd:string |
http://purl.uniprot.org/citations/21567403 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcp.22834"xsd:string |
http://purl.uniprot.org/citations/21567403 | http://purl.uniprot.org/core/author | "Kikuchi J."xsd:string |
http://purl.uniprot.org/citations/21567403 | http://purl.uniprot.org/core/author | "Wada T."xsd:string |
http://purl.uniprot.org/citations/21567403 | http://purl.uniprot.org/core/author | "Furukawa Y."xsd:string |
http://purl.uniprot.org/citations/21567403 | http://purl.uniprot.org/core/author | "Mitsunaga K."xsd:string |
http://purl.uniprot.org/citations/21567403 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
http://purl.uniprot.org/citations/21567403 | http://purl.uniprot.org/core/name | "J Cell Physiol"xsd:string |
http://purl.uniprot.org/citations/21567403 | http://purl.uniprot.org/core/pages | "1138-1147"xsd:string |
http://purl.uniprot.org/citations/21567403 | http://purl.uniprot.org/core/title | "Latexin regulates the abundance of multiple cellular proteins in hematopoietic stem cells."xsd:string |
http://purl.uniprot.org/citations/21567403 | http://purl.uniprot.org/core/volume | "227"xsd:string |
http://purl.uniprot.org/citations/21567403 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21567403 |
http://purl.uniprot.org/citations/21567403 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/21567403 |
http://purl.uniprot.org/uniprot/#_Q9BS40-mappedCitation-21567403 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21567403 |
http://purl.uniprot.org/uniprot/Q9BS40 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/21567403 |