Joo-Ran Kim

TL;DR: EIF5A, like its bacterial ortholog EFP, is proposed to stimulate the peptidyl transferase activity of the ribosome and facilitate the reactivity of poor substrates like Pro.

TL;DR: It is shown that a human X-chromosomal neurological disorder characterized by intellectual disability and microcephaly is caused by a missense mutation in eIF2γ (encoded by EIF2S3), the core subunit of the heterotrimeric eIF3 complex, and this findings directly link intellectual disability to impaired translation initiation.

TL;DR: It is proposed that the body of eif5A functionally substitutes for polyamines to promote general protein synthesis and that the hypusine modification on eIF5A is critically important for poor substrates like proline.

TL;DR: The cryoEM structure of the naturally long-lived ribosome complex with eIF5B and Met-tRNAiMet immediately before transition into elongation is determined and uncovers an unexpected, eukaryotic specific and dynamic fidelity checkpoint implemented by eif5B in concert with components of the large ribosomal subunit.