PMID- 21252914
OWN - NLM
STAT- MEDLINE
DCOM- 20110822
LR  - 20211020
IS  - 1476-5403 (Electronic)
IS  - 1350-9047 (Print)
IS  - 1350-9047 (Linking)
VI  - 18
IP  - 6
DP  - 2011 Jun
TI  - Autocrine motility factor/phosphoglucose isomerase regulates ER stress and cell 
      death through control of ER calcium release.
PG  - 1057-70
LID - 10.1038/cdd.2010.181 [doi]
AB  - Autocrine motility factor/ phosphoglucose isomerase (AMF/PGI) promotes cell 
      survival by the pAkt survival pathway. Its receptor, gp78/AMFR, is an E3 
      ubiquitin ligase implicated in endoplasmic reticulum (ER)-associated protein 
      degradation. We demonstrate here that AMF/PGI also protects against thapsigargin 
      (TG)- and tunicamycin (TUN)-induced ER stress and apoptosis. AMF/PGI protection 
      against the ER stress response is receptor mediated as it is not observed in 
      gp78/AMFR-knockdown HEK293 cells. However, AMF/PGI protection against the ER 
      stress response by TG and TUN was mediated only partially through PI3K/Akt 
      activation. AMF/PGI reduction of the elevation of cytosolic calcium in response 
      to either TG or inositol 1,4,5-trisphosphate receptor activation with ATP was 
      gp78/AMFR-dependent, independent of mitochondrial depolarization and not 
      associated with changes in ER calcium content. These results implicate regulation 
      of ER calcium release in AMF/PGI protection against ER stress and apoptosis. 
      Indeed, sequestration of cytosolic calcium with BAPTA-AM limited the ER stress 
      response. Importantly, elevation of cytosolic calcium upon treatment with the 
      calcium ionophore ionomycin, while not inducing an ER stress response, did 
      prevent AMF/PGI protection against ER stress. By regulating ER calcium release, 
      AMF/PGI interaction with gp78/AMFR therefore protects against ER stress 
      identifying novel roles for these cancer-associated proteins in promoting tumor 
      cell survival.
FAU - Fu, M
AU  - Fu M
AD  - Department of Cellular and Physiological Sciences, Life Sciences Institute, 
      University of British Columbia, Vancouver, British Columbia, Canada.
FAU - Li, L
AU  - Li L
FAU - Albrecht, T
AU  - Albrecht T
FAU - Johnson, J D
AU  - Johnson JD
FAU - Kojic, L D
AU  - Kojic LD
FAU - Nabi, I R
AU  - Nabi IR
LA  - eng
GR  - CIHR MT-15132/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110121
PL  - England
TA  - Cell Death Differ
JT  - Cell death and differentiation
JID - 9437445
RN  - 0 (Anti-Bacterial Agents)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Receptors, Cytokine)
RN  - 11089-65-9 (Tunicamycin)
RN  - 67526-95-8 (Thapsigargin)
RN  - EC 2.3.2.27 (AMFR protein, human)
RN  - EC 2.3.2.27 (Receptors, Autocrine Motility Factor)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 5.3.1.9 (Glucose-6-Phosphate Isomerase)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Anti-Bacterial Agents/pharmacology
MH  - Apoptosis/drug effects/physiology
MH  - COS Cells
MH  - Calcium/*metabolism
MH  - Calcium Signaling/drug effects/*physiology
MH  - Cell Survival/drug effects/physiology
MH  - Chlorocebus aethiops
MH  - Endoplasmic Reticulum/genetics/*metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Glucose-6-Phosphate Isomerase/genetics/*metabolism
MH  - HEK293 Cells
MH  - Humans
MH  - Neoplasms/genetics/metabolism
MH  - Receptors, Autocrine Motility Factor
MH  - Receptors, Cytokine/genetics/*metabolism
MH  - Thapsigargin/pharmacology
MH  - Tunicamycin/pharmacology
MH  - Ubiquitin-Protein Ligases/genetics/*metabolism
MH  - Unfolded Protein Response/drug effects/*physiology
PMC - PMC3131941
EDAT- 2011/01/22 06:00
MHDA- 2011/08/23 06:00
PMCR- 2012/06/01
CRDT- 2011/01/22 06:00
PHST- 2011/01/22 06:00 [entrez]
PHST- 2011/01/22 06:00 [pubmed]
PHST- 2011/08/23 06:00 [medline]
PHST- 2012/06/01 00:00 [pmc-release]
AID - cdd2010181 [pii]
AID - 10.1038/cdd.2010.181 [doi]
PST - ppublish
SO  - Cell Death Differ. 2011 Jun;18(6):1057-70. doi: 10.1038/cdd.2010.181. Epub 2011 
      Jan 21.