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1996年5月7日 · ATP adopted a well-defined but distinct binding mode in K52R ERK2 compared to the binding mode in the wild-type enzyme. The structural and kinetic data show that mutation of K52 created a nonproductive binding mode for ATP and suggest that K52 is essential for orienting ATP for catalysis.

Plasmid GFP-ERK2 K52R from Dr. Philip Stork's lab contains the insert ERK2 K52R and is published in Exp Cell Res. 2003 May 1;285(2):208-20. This plasmid is available through Addgene. Image: Illustrated plasmid map in PNG format

We report that Raf/MEK/ERK activation decreases the DHPS-ERK1/2 interaction while increasing DHPS-eIF5A association in cells. We determined the cryoelectron microscopy (cryo-EM) structure of the DHPS-ERK2 complex at 3.5 Å to show that ERK2 hinders substrate entrance to the DHPS active site, subsequently inhibiting deoxyhypusination in vitro.

1996年5月7日 · ATP adopted a well-defined but distinct binding mode in K52R ERK2 compared to the binding mode in the wild-type enzyme. The structural and kinetic data show that mutation of K52 created a nonproductive binding mode for ATP and suggest that K52 is essential for orienting ATP for catalysis.

We next determined whether kinase activity is necessary for ERK1/2 to mediate cell death by examining the effects of Lys52Arg (K52R) replacement in the active site of ERK2 in LNCaP-ΔRaf-1:ER, HEK293-ΔRaf-1:ER, and U251-ΔRaf-1:ER cells.

2024年12月31日 · The lactylation of aldehyde dehydrogenase 2 (ALDH2) is identified at lysine 52 (K52la), revealing that ALDH2 lactylation exacerbates tubular injury and mitochondrial dysfunction. Conversely, the ALDH2 K52R mutation alleviates these injuries in HK-2 cells and adeno-associated virus-infected kidney tissues in mice.

2009年11月27日 · Indeed, ERK2-K52R selectively restored Raf-induced growth inhibitory signaling in ERK1/2-depleted cells, as manifested by regained cellular ability to undergo growth arrest and to control the cell cycle regulators without affecting c-Myc and morphology.

2009年11月11日 · Indeed, ERK2-K52R selectively restored Raf-induced growth inhibitory signaling in ERK1/2-depleted cells, as manifested by regained cellular ability to undergo growth arrest and to control the cell cycle regulators without affecting c-Myc and morphology.

To examine events necessary for ERK nuclear translocation, wild-type and mutant ERK2 proteins were microinjected into mammalian cells. ERK2, phosphorylated on both tyrosine and threonine, either wild-type or the kinase-deficient mutant K52R, accumulated in the nucleus.