Ann Y Park, Michael Leney-Greene, Matthew Lynberg, Justin Q Gabrielski, Xijin Xu, Benjamin Schwarz, Lixin Zheng, Arasu Balasubramaniyam, Hyoungjun Ham, Brittany Chao, Yu Zhang, Helen F Matthews, Jing Cui, Yikun Yao, Satoshi Kubo, Jean Michel Chanchu, Aaron R Morawski, Sarah A Cook, Ping Jiang, Juan C Ravell, Yan H Cheng, Alex George, Aiman Faruqi, Alison M Pagalilauan, Jenna R E Bergerson, Sundar Ganesan, Samuel D Chauvin, Jahnavi Aluri, Joy Edwards-Hicks, Eric Bohrnsen, Caroline Tippett, Habib Omar, Leilei Xu, Geoffrey W Butcher, John Pascall, Elif Karakoc-Aydiner, Ayca Kiykim, Holden Maecker, İlhan Tezcan, Saliha Esenboga, Raul Jimenez Heredia, Deniz Akata, Saban Tekin, Altan Kara, Zarife Kuloglu, Emel Unal, Tanıl Kendirli, Figen Dogu, Esra Karabiber, T Prescott Atkinson, Claude Cochet, Odile Filhol, Catherine M Bosio, Mark M Davis, Richard P Lifton, Erika L Pearce, Oliver Daumke, Caner Aytekin, Gülseren Evirgen Şahin, Aysel Ünlüsoy Aksu, Gulbu Uzel, V Koneti Rao, Sinan Sari, Buket Dalgıç, Kaan Boztug, Deniz Cagdas, Sule Haskologlu, Aydan Ikinciogullari, David Schwefel, Silvia Vilarinho, Safa Baris, Ahmet Ozen, Helen C Su, Michael J Lenardo
Preserving cells in a functional, non-senescent state is a major goal for extending human healthspans. Model organisms reveal that longevity and senescence are genetically controlled, but how genes control longevity in different mammalian tissues is unknown. Here, we report a new human genetic disease that causes cell senescence, liver and immune dysfunction, and early mortality that results from deficiency of GIMAP5, an evolutionarily conserved GTPase selectively expressed in lymphocytes and endothelial cells...
February 2024: Nature Immunology