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作 者:Lisa Gregor Sophia Stock Sebastian Kobold
机构地区:[1]Division of Clinical Pharmacology,Department of Medicine IV,University Hospital,Ludwig Maximilian University(LMU)of Munich,Lindwurmstrasse 2a,80337 Munich,Germany [2]Department of MedicineⅢ,University Hospital,Ludwig Maximilian University(LMU)of Munich,Marchioninistrasse 15,81377 Munich,Germany [3]German Cancer Consortium(DKTK),Partner Site Munich,Pettenkoferstrasse 8a,80336 Munich,Germany [4]Einheit für Klinische Pharmakologie(EKLiP),Helmholtz Zentrum München,German Research Center for Environmental Health(HMGU),Ingolstädter Landstrasse 1,85764 Neuherberg,Germany
出 处:《Signal Transduction and Targeted Therapy》2022年第8期2655-2657,共3页信号转导与靶向治疗(英文)
基 金:supported by the Else Kröner-Fresenius Clinician Scientist Program Cancer Immunotherapy,the Munich Clinician Scientist Program(MCSP);the DKTK School of Oncology.This work was supported by the Marie Sklodowska-Curie Program Training Network for Optimizing Adoptive T Cell Therapy of Cancer funded by the H2020 Program of the European Union(Grant 955575,to S.K.);the Hector Foundation(to S.K.);the International Doctoral Program i-Target:Immunotargeting of Cancer funded by the Elite Network of Bavaria(to S.K.);Melanoma Research Alliance Grants 409510(to S.K.);the Else Kröner-Fresenius-Stiftung(2021_EKFK_01,to S.K.);the German Cancer Aid(to S.K.);the Ernst-Jung-Stiftung(to S.K.);the LMU Munich’s Institutional Strategy LMUexcellent within the framework of the German Excellence Initiative(to S.K.);the Bundesministerium für Bildung und Forschung(to S.K.);the Go-Bio Initiative(to S.K.);the m4 award of the Bavarian Ministry for Economical Affairs(to S.K.);the European Research Council Grant 756017,ARMOR-T(to S.K.);the German Research Foundation(DFG)(to S.K.);the SFB-TRR 338/12021-452881907(to S.K.);the Fritz-Bender Foundation(to S.K.);the Deutsche José-Carreras Leukämie-Stiftung(to S.K.).
摘 要:A recent research article published in Science by Ritter et al.reported that endosomal sorting complexes required for transport(ESCRT)proteins mediate repair of lesions in the cell membrane caused by the pore-forming toxin perforin at sites of cytotoxic T cell engagement.1 Subsequent entry of granzymes and initiation of apoptosis of cancer cells is thus limited,leading to reduced sensitivity against T cell‑mediated cytotoxicity.1 Along these lines,this could constitute a new critical resistance mechanism for T cellbased treatment approaches.
关 键 词:al. CYTOTOXICITY DEATH
分 类 号:R329.2[医药卫生—人体解剖和组织胚胎学]
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