Probing the role of the hyper-reactive histidine residue of arginase

Arch Biochem Biophys. 2005 Dec 1;444(1):15-26. doi: 10.1016/j.abb.2005.09.009. Epub 2005 Oct 13.

Abstract

Rat liver arginase (arginase I) is potently inactivated by diethyl pyrocarbonate, with a second-order rate constant of 113M(-1)s(-1) for the inactivation process at pH 7.0, 25 degrees C. Partial protection from inactivation is provided by the product of the reaction, l-ornithine, while nearly complete protection is afforded by the inhibitor pair, l-ornithine and borate. The role of H141 has been probed by mutagenesis, chemical modulation, and X-ray diffraction. The hyper-reactivity of H141 towards diethyl pyrocarbonate can be explained by its proximity to E277. A proton shuttling role for H141 is supported by its conformational mobility observed among the known arginase structures. H141 is proposed to serve as an acid/base catalyst, deprotonating the metal-bridging water molecule to generate the metal-bridging hydroxide nucleophile, and by protonating the amino group of the product to facilitate its departure.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Arginase / antagonists & inhibitors
  • Arginase / chemistry*
  • Borates / chemistry
  • Crystallography, X-Ray
  • Diethyl Pyrocarbonate / chemistry
  • Histidine / chemistry*
  • Kinetics
  • Models, Molecular
  • Mutagenesis, Site-Directed
  • Ornithine / chemistry
  • Protein Conformation
  • Rats

Substances

  • Borates
  • Histidine
  • Ornithine
  • Arginase
  • Diethyl Pyrocarbonate

Associated data

  • PDB/1TA1
  • PDB/1TBH
  • PDB/1TBJ
  • PDB/1TBL
  • PDB/1ZPE
  • PDB/1ZPG