Role of BOK at the intersection of endoplasmic reticulum stress and apoptosis regulation

MARCOS A. CARPIO; MICHAEL MICHAUD; WENPING ZHOU; JILL K. FISHER; LOREN D. WALENSKY; SAMUEL G. KATZ

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

NATL ACAD SCIENCES

Lugar: Washington DC, USA; Año: 2016 vol. 113 p. 494 - 494

0027-8424

he B-cell lymphoma 2 (BCL-2) ovarian killer (BOK) is an intriguing BCL-2 family protein with highest homology to the multidomain executioner proteins BAX and BAK, yet its role in apoptosis regulation has been questionable because of the reported absence of phenotypic findings in Bok KO mice (1). In an independent Bok KO model, we identify a selective apoptotic defect in response to endoplasmic reticulum (ER) stress (2).Differences in mouse model phenotypes can arise from alternate mouse strains, backgrounds, and targeting strategies. Our Bok KO mice were backcrossed to C57BL/6 mice for eight generations, and although they contain a short transcript, notably lacking key functional domains, no BOK protein was detected by Western analyses. Ultimately, such differences in modeling approach may or may not impact the functional insights gleaned, but do necessitate rigorous mechanistic validation of the generated hypotheses.