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David J Reiner1

  • 1Department of Translational Medical Sciences, College of Medicine, Texas A&M Health Science Center, Texas A&M University, Houston, TX 77030, USA; Institute of Biosciences and Technology, Texas A&M Health Science Center, Texas A&M University, Houston, TX 77030, USA.

PubMed
概括

在C. elegans中mTORC1组件Raptor的突变通过减少蛋白质合成,而不是增加自增强了对缺氧的抵抗力. 这突出了mTORC1作为潜在的治疗点与缺氧相关的条件.

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