Evidence map›Paper›PMID 22422508›Full record

ArticleJournal of cellular physiology2012

GRP78/BiP is a novel downstream target of IGF-1 receptor mediated signaling.

Kyle T Pfaffenbach, Michelle Pong, Todd E Morgan, Hongjun Wang, Kate Ott, Beiyun Zhou, Valter D Longo, Amy S Lee

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. GRP78 facilitates M2 macrophage polarization and tumour progression.Cellular and molecular life sciences : CMLS · 2021
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  9. Observational
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  12. Article
  13. Review
  14. Article
  15. Juvenile hormone differentially regulates twoThe Journal of biological chemistry · 2017
    Article
  16. Article
  17. Review
  18. Article
  19. GRP78 and α2-macroglobulin are new promising targets for metastatic castrate-resistant prostate cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2015
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Kyle T PfaffenbachDepartment of Biochemistry and Molecular Biology, University of Southern California, Norris Comprehensive Cancer Center, Keck School of Medicine of USC, Los Angeles, California 90089-9176, USA.
Michelle Pong
Todd E Morgan
Hongjun Wang
Kate Ott
Beiyun Zhou
Valter D Longo
Amy S Lee
University of Southern California · USRogers (United States) · US

Funding

STRESS INDUCTION OF THE GLUCOSE REGULATED PROTEINSR01CA027607 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LEE, AMY S · 1985 to 2021
$11.1M
The Role of the Glucose-regulated Protein GRP78/BiP in Stress Resistance and AginP01AG034906 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LONGO, VALTER D. · 2011 to 2016
$9.3M
VIRAL AND CHEMICAL CARCINOGENESIST32CA009320 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JONES, PETER A · 1985 to 2012
$2.5M
COORDINATED GENE EXPRESSION IN MAMMALIAN CELLSR37CA027607 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LEE, AMY S · 1988 to 1995
–
NCI NIH HHS 5T32 CA009320NCI NIH HHS CA027607NCI NIH HHS R01 CA027607NCI NIH HHS T32 CA009320NIA NIH HHS AG034906NIA NIH HHS P01 AG034906
6 · The paper itself

Abstract

Glucose regulated protein 78/immunoglobulin binding protein (GRP78/BiP) is an endoplasmic reticulum (ER) chaperone protein and master regulator of the unfolded protein response (UPR). The response of GRP78 to overt pharmacologically induced ER stress is well established, whereas the modulation of GRP78 to physiologic changes is less characterized. In this study, we examined the regulation of GRP78 in response to reduced IGF-1 growth factor signaling, a common consequence of calorie restriction (CR). ER chaperone protein expression was quantified in cell lysates prepared from the livers of calorie restricted (CR) and ad libitum fed mice, as well as MEFs grown in normal medium or serum starved. The requirement of IGF-1 signaling on GRP78 expression was studied using MEFs with IGF-1 receptor overexpression (R+) or deletion (R-), and the regulatory mechanism was examined using mTORC1 and PI3K inhibitors, as well as R- cells with knockdown of transcription factor FOXO1 compared to shRNA control. We observed a 40% reduction in GRP78 protein expression in CR mice and in serum-starved MEF cells. R- cells had drastically reduced AKT phosphorylation and exhibited lower levels of ER chaperones, in particular 80% less GRP78. Despite an 80% reduction in GRP78 expression, R- cells were not under chronic ER stress, but were fully capable of activating the UPR. Neither forced expression of FOXO1-AAA nor knockdown of FOXO1 in R- cells affected GRP78 expression. In conclusion, we report that IGF-1 receptor signaling regulates GRP78 expression via the PI3K/AKT/mTORC1 axis independent of the canonical UPR and FOXO1.

Indexed as

AnimalsCaloric RestrictionCells, CulturedEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPForkhead Box Protein O1Forkhead Transcription FactorsGene Expression RegulationGene Knockdown TechniquesHeat-Shock ProteinsHumansMaleMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMultiprotein ComplexesEndoplasmic Reticulum Chaperone BiPForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, mouseHeat-Shock ProteinsHSPA5 protein, humanHspa5 protein, mouseMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProteinsProto-Oncogene Proteins c-aktReceptor, IGF Type 1TOR Serine-Threonine Kinases

Identifiers

PMID22422508
PMCPMC3421054
OpenAlexW2065820380

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.