國家衛生研究院 NHRI:Item 3990099045/14394
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    题名: Genetic disruption of KLF1 K74 sUMOylation in hematopoietic system promotes healthy longevity in mice
    作者: Shyu, YC;Liao, PC;Huang, TS;Yang, CJ;Lu, MJ;Huang, SM;Lin, XY;Liou, CC;Kao, YH;Lu, CH;Peng, HL;Chen, JR;Cherng, WJ;Yang, NI;Chen, YC;Pan, HC;Jiang, ST;Hsu, CC;Lin, GG;Yuan, SS;Hsu, PWC;Wu, KJ;Lee, TL;Shen, CKJ
    贡献者: Institute of Molecular and Genomic Medicine
    摘要: The quest for rejuvenation and prolonged lifespan through transfusion of young blood has been studied for decades with the hope of unlocking the mystery of the key substance(s) that exists in the circulating blood of juvenile organisms. However, a pivotal mediator has yet been identified. Here, atypical findings are presented that are observed in a knockin mouse model carrying a lysine to arginine substitution at residue 74 of Kruppel-like factor 1 (KLF1/EKLF), the SUMOylation-deficient Klf1(K74R/K74R) mouse, that displayed significant improvement in geriatric disorders and lifespan extension. Klf1(K74R/K74R) mice exhibit a marked delay in age-related physical performance decline and disease progression as evidenced by physiological and pathological examinations. Furthermore, the KLF1(K74R) knockin affects a subset of lymphoid lineage cells; the abundance of tumor infiltrating effector CD8(+) T cells and NKT cells is increased resulting in antitumor immune enhancement in response to tumor cell administration. Significantly, infusion of hematopoietic stem cells (HSCs) from Klf1(K74R/K74R) mice extends the lifespan of the wild-type mice. The Klf1(K74R/K74R) mice appear to be an ideal animal model system for further understanding of the molecular/cellular basis of aging and development of new strategies for antiaging and prevention/treatment of age-related diseases thus extending the healthspan as well as lifespan.
    日期: 2022-09
    關聯: Advanced Science. 2022 Sep;9(25):Article number e2201409.
    Link to: http://dx.doi.org/10.1002/advs.202201409
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2198-3844&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000823624100001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85134055389
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