Conjugation to a cell-penetrating peptide drives the tumour accumulation of the GLP1R antagonist exendin(9-39).

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第一作者： Estel,Collado Camps

第一单位： Department of Medical Imaging, Radboudumc, P.O. Box 9101, 6500 HB, Nijmegen, The Netherlands.

作者： Estel,Collado Camps ^[1] ; Sanne A M,van Lith ^[2] ; Annemarie,Kip ^[3] ; Cathelijne,Frielink ^[1] ; Lieke,Joosten ^[1] ; Roland,Brock ^[1] ; Martin,Gotthardt ^[1]

作者单位： Department of Medical Imaging, Radboudumc, P.O. Box 9101, 6500 HB, Nijmegen, The Netherlands. ^[1] Department of Biochemistry, Radboud Institute for Molecular Life Sciences, Radboudumc, Nijmegen, The Netherlands. ^[2] Department of Tumour Immunology, Radboud Institute for Molecular Life Sciences, Radboudumc, 278 Tumor Immunology, Radboudumc, P.O. Box 9101, 6500 HB, Nijmegen, The Netherlands. ^[3] Department of Medical Biochemistry, College of Medicine and Medical Sciences, Arabian Gulf University, Manama, Kingdom of Bahrain. ^[4] Department of Medical Imaging, Radboudumc, P.O. Box 9101, 6500 HB, Nijmegen, The Netherlands. martin.gotthardt@radboudumc.nl. ^[5]

关键词 Antagonist Cell-penetrating peptide Cellular internalisation Exendin Tracer

主题词人类(Humans);细胞穿透性肽类(Cell-Penetrating Peptides);组织分布(Tissue Distribution);胰岛素瘤(Insulinoma);胰腺肿瘤(Pancreatic Neoplasms);毒液类(Venoms)

DOI 10.1007/s00259-022-06041-y

PMID 36446951

发布时间 2023-04-25

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