Absence of post-translational aspartyl beta-hydroxylation of epidermal growth factor domains in mice leads to developmental defects and an increased incidence of intestinal neoplasia.

@article{Dinchuk2002AbsenceOP,
  title={Absence of post-translational aspartyl beta-hydroxylation of epidermal growth factor domains in mice leads to developmental defects and an increased incidence of intestinal neoplasia.},
  author={Joseph E. Dinchuk and Richard J. Focht and Jennifer A Kelley and Nancy L Henderson and Nina I Zolotarjova and Richard Wynn and Nicola T Neff and John Link and Reid M Huber and Timothy C. Burn and Mark J. Rupar and Mark R. Cunningham and Bernard H. Selling and Jianhong Ma and Andrew Stern and Gregory F. Hollis and Robert B. Stein and Paul A. Friedman},
  journal={The Journal of biological chemistry},
  year={2002},
  volume={277 15},
  pages={12970-7}
}
The BAH genomic locus encodes three distinct proteins: junctin, humbug, and BAH. All three proteins share common exons, but differ significantly based upon the use of alternative terminal exons. The biological roles of BAH and humbug and their functional relationship to junctin remain unclear. To evaluate the role of BAH in vivo, the catalytic domain of BAH was specifically targeted such that the coding regions of junctin and humbug remained undisturbed. BAH null mice lack measurable BAH… CONTINUE READING
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