Nature Communications (May 2022)

AIMP2-DX2 provides therapeutic interface to control KRAS-driven tumorigenesis

  • Dae Gyu Kim,
  • Yongseok Choi,
  • Yuno Lee,
  • Semi Lim,
  • Jiwon Kong,
  • JaeHa Song,
  • Younah Roh,
  • Dipesh S. Harmalkar,
  • Kwanshik Lee,
  • Ja-il Goo,
  • Hye Young Cho,
  • Ameeq Ul Mushtaq,
  • Jihye Lee,
  • Song Hwa Park,
  • Doyeun Kim,
  • Byung Soh Min,
  • Kang Young Lee,
  • Young Ho Jeon,
  • Sunkyung Lee,
  • Kyeong Lee,
  • Sunghoon Kim

DOI
https://doi.org/10.1038/s41467-022-30149-2
Journal volume & issue
Vol. 13, no. 1
pp. 1 – 17

Abstract

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Direct targeting of oncogenic KRAS activity is a challenge. Here the authors report that a splice variant of AIMP2, AIMP2-DX2, enhances KRAS stability by blocking ubiquitin-mediated degradation of KRAS via the E3 ligase, Smurf2, and identify a chemical that can hinder AIMP2-DX2 from interacting with KRAS.