PMID- 9038234
OWN - NLM
STAT- MEDLINE
DCOM- 19970415
LR  - 20220331
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 272
IP  - 9
DP  - 1997 Feb 28
TI  - Mouse lymphoma cells destined to undergo apoptosis in response to thapsigargin 
      treatment fail to generate a calcium-mediated grp78/grp94 stress response.
PG  - 6087-92
AB  - grp78/grp94 induction is critical for maintaining the viability of epithelial 
      cells and fibroblasts following treatment with thapsigargin (TG), an inhibitor of 
      Ca2+ uptake into the endoplasmic reticulum. In contrast to these cell types, 
      WEHI7.2 mouse lymphoma cells undergo apoptosis when treated with TG, prompting us 
      to examine the grp78/grp94 stress response in WEHI7.2 cells. TG treatment failed 
      to induce grp78/grp94 transcription in WEHI7.2 cells, measured by Northern 
      hybridization and nuclear run-on assays, even if the cells were protected from 
      apoptosis by overexpressing bcl-2. However, grp78/grp94 transcription was induced 
      by the glycosylation inhibitor tunicamycin, suggesting that there are at least 
      two grp78/grp94 signaling pathways, one in response to TG-induced endoplasmic 
      reticulum Ca2+ pool depletion, which is inoperable in WEHI7.2 cells, and one in 
      response to glycosylation inhibition, which is operable in WEHI7.2 cells. Studies 
      of additional lymphoid lines, as well as several nonlymphoid lines, suggested a 
      correlation between grp78/grp94 induction and resistance to apoptosis following 
      TG treatment. In conclusion, the vulnerability of TG-treated WEHI7.2 cells to 
      apoptosis may be due to failure to signal a grp78/grp94 stress response.
FAU - McCormick, T S
AU  - McCormick TS
AD  - Department of Medicine, Case Western Reserve University School of Medicine and 
      the Ireland Cancer Center, University Hospitals of Cleveland, Cleveland, Ohio 
      44106, USA.
FAU - McColl, K S
AU  - McColl KS
FAU - Distelhorst, C W
AU  - Distelhorst CW
LA  - eng
GR  - R01 CA42755/CA/NCI NIH HHS/United States
GR  - T32 CA59366/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Carrier Proteins)
RN  - 0 (Endoplasmic Reticulum Chaperone BiP)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (HSP70 Heat-Shock Proteins)
RN  - 0 (Heat-Shock Proteins)
RN  - 0 (Hspa5 protein, mouse)
RN  - 0 (Membrane Proteins)
RN  - 0 (Molecular Chaperones)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (RNA, Messenger)
RN  - 0 (glucose-regulated proteins)
RN  - 11089-65-9 (Tunicamycin)
RN  - 67526-95-8 (Thapsigargin)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Calcium/*metabolism
MH  - Carrier Proteins/*metabolism
MH  - Electrophoresis, Polyacrylamide Gel
MH  - Endoplasmic Reticulum Chaperone BiP
MH  - Enzyme Inhibitors/*pharmacology
MH  - HSP70 Heat-Shock Proteins/*metabolism
MH  - Heat-Shock Proteins/*metabolism
MH  - Lymphoma/*pathology
MH  - Membrane Proteins/*metabolism
MH  - Mice
MH  - Molecular Chaperones/*metabolism
MH  - Nerve Tissue Proteins/*metabolism
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - RNA, Messenger
MH  - Thapsigargin/*pharmacology
MH  - Tunicamycin/pharmacology
EDAT- 1997/02/28 00:00
MHDA- 1997/02/28 00:01
CRDT- 1997/02/28 00:00
PHST- 1997/02/28 00:00 [pubmed]
PHST- 1997/02/28 00:01 [medline]
PHST- 1997/02/28 00:00 [entrez]
AID - S0021-9258(18)41315-4 [pii]
AID - 10.1074/jbc.272.9.6087 [doi]
PST - ppublish
SO  - J Biol Chem. 1997 Feb 28;272(9):6087-92. doi: 10.1074/jbc.272.9.6087.