Cell Biology: ERADicating Survival with BOK

Jerry Edward Chipuk; Mark P. Luna-Vargas

doi:10.1016/j.cub.2016.04.003

Cell Biology: ERADicating Survival with BOK

Jerry Edward Chipuk, Mark P. Luna-Vargas

Research output: Contribution to journal › Short survey › peer-review

4 Scopus citations

Abstract

Mechanistic insights into the function of the pro-apoptotic BCL-2 family member BOK have remained elusive. A recent study shows that healthy cells constitutively degrade BOK via the ER-associated degradation and ubiquitin–proteasome pathways; following proteasome inhibition, BOK is stabilized to initiate a unique pro-apoptotic death program.

Original language	English
Pages (from-to)	R473-R476
Journal	Current Biology
Volume	26
Issue number	11
DOIs	https://doi.org/10.1016/j.cub.2016.04.003
State	Published - 2016

Access to Document

10.1016/j.cub.2016.04.003

Cite this

@article{675b099ea25840a1ac42b49c0ae131fb,

title = "Cell Biology: ERADicating Survival with BOK",

abstract = "Mechanistic insights into the function of the pro-apoptotic BCL-2 family member BOK have remained elusive. A recent study shows that healthy cells constitutively degrade BOK via the ER-associated degradation and ubiquitin–proteasome pathways; following proteasome inhibition, BOK is stabilized to initiate a unique pro-apoptotic death program.",

author = "Chipuk, {Jerry Edward} and Luna-Vargas, {Mark P.}",

note = "Publisher Copyright: {\textcopyright} 2016 Elsevier Ltd",

year = "2016",

doi = "10.1016/j.cub.2016.04.003",

language = "English",

volume = "26",

pages = "R473--R476",

journal = "Current Biology",

issn = "0960-9822",

publisher = "Cell Press",

number = "11",

}

TY - JOUR

T1 - Cell Biology

T2 - ERADicating Survival with BOK

AU - Chipuk, Jerry Edward

AU - Luna-Vargas, Mark P.

PY - 2016

Y1 - 2016

N2 - Mechanistic insights into the function of the pro-apoptotic BCL-2 family member BOK have remained elusive. A recent study shows that healthy cells constitutively degrade BOK via the ER-associated degradation and ubiquitin–proteasome pathways; following proteasome inhibition, BOK is stabilized to initiate a unique pro-apoptotic death program.

AB - Mechanistic insights into the function of the pro-apoptotic BCL-2 family member BOK have remained elusive. A recent study shows that healthy cells constitutively degrade BOK via the ER-associated degradation and ubiquitin–proteasome pathways; following proteasome inhibition, BOK is stabilized to initiate a unique pro-apoptotic death program.

UR - http://www.scopus.com/inward/record.url?scp=84982111753&partnerID=8YFLogxK

U2 - 10.1016/j.cub.2016.04.003

DO - 10.1016/j.cub.2016.04.003

M3 - Short survey

C2 - 27269726

AN - SCOPUS:84982111753

SN - 0960-9822

VL - 26

SP - R473-R476

JO - Current Biology

JF - Current Biology

IS - 11

ER -

Cell Biology: ERADicating Survival with BOK

Abstract

Access to Document

Fingerprint

Cite this