Evidence map›Paper›PMID 27697863›Full record

ArticleMolecular and cellular biology2016

Endoplasmic Reticulum Stress Enhances Mitochondrial Metabolic Activity in Mammalian Adrenals and Gonads.

Manoj Prasad, Anna N Walker, Jasmeet Kaur, James L Thomas, Shirley A Powell, Amit V Pandey, Randy M Whittal, William E Burak, Guy Petruzzelli, Himangshu S Bose

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

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  5. Mitochondrial function in development and disease.Disease models & mechanisms · 2021
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  15. Article
  16. Endocrinology, diabetes & metabolism case reports · 2017
    Article
  17. ACTH Action on StAR Biology.Frontiers in neuroscience · 2016
    Review
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

10 authors at 4 institutions in 3 countries.

Manoj PrasadLaboratory of Biochemistry and Cell Biology, Biomedical Sciences, Mercer University School of Medicine, Savannah, Georgia, USA.
Anna N WalkerDepartment of Pathology, Mercer University School of Medicine, Macon, Georgia, USA.
Jasmeet KaurLaboratory of Biochemistry and Cell Biology, Biomedical Sciences, Mercer University School of Medicine, Savannah, Georgia, USA.
James L ThomasDivision of Basic Medical Sciences, Mercer University School of Medicine, Macon, Georgia, USA.
Shirley A PowellDivision of Basic Medical Sciences, Mercer University School of Medicine, Macon, Georgia, USA.
Amit V PandeyPediatric Endocrinology Diabetology & Metabolism, University Children's Hospital Bern, Bern, Switzerland.
Randy M WhittalDepartment of Chemistry, University of Alberta, Edmonton, Alberta, Canada.
William E BurakMemorial University Medical Center, Anderson Cancer Institute, Savannah, Georgia, USA.
Guy PetruzzelliMemorial University Medical Center, Anderson Cancer Institute, Savannah, Georgia, USA.
Himangshu S BoseLaboratory of Biochemistry and Cell Biology, Biomedical Sciences, Mercer University School of Medicine, Savannah, Georgia, USA bose_hs@mercer.edu.
Mercer University · USMemorial Health University Medical Center · USUniversity Children’s Hospital Bern · CHUniversity of Alberta · CA

Funding

Mechanism of action of steroidogenic acute regulatory protein (StAR)R01HD057876 · NICHD · MERCER UNIVERSITY MACON · PI BOSE, HIMANGSHU S · 2009 to 2013
$1.5M
NICHD NIH HHS R01 HD057876
6 · The paper itself

Abstract

The acute response to stress consists of a series of physiological programs to promote survival by generating glucocorticoids and activating stress response genes that increase the synthesis of many chaperone proteins specific to individual organelles. In the endoplasmic reticulum (ER), short-term stress triggers activation of the unfolded protein response (UPR) module that either leads to neutralization of the initial stress or adaptation to it; chronic stress favors cell death. UPR induces expression of the transcription factor, C/EBP homology protein (CHOP), and its deletion protects against the lethal consequences of prolonged UPR. Here, we show that stress-induced CHOP expression coincides with increased metabolic activity. During stress, the ER and mitochondria come close to each other, resulting in the formation of a complex consisting of the mitochondrial translocase, translocase of outer mitochondrial membrane 22 (Tom22), steroidogenic acute regulatory protein (StAR), and 3β-hydroxysteroid dehydrogenase type 2 (3βHSD2) via its intermembrane space (IMS)-exposed charged unstructured loop region. Stress increased the circulation of phosphates, which elevated pregnenolone synthesis by 2-fold by increasing the stability of 3βHSD2 and its association with the mitochondrion-associated ER membrane (MAM) and mitochondrial proteins. In summary, cytoplasmic CHOP plays a central role in coordinating the interaction of MAM proteins with the outer mitochondrial membrane translocase, Tom22, to activate metabolic activity in the IMS by enhanced phosphate circulation.

Indexed as

Endoplasmic Reticulum StressStress, Physiological3-Hydroxysteroid DehydrogenasesAdrenal GlandsAnimalsCytoplasmGonadsMaleMammalsMiceMitochondriaMitochondrial Membrane Transport ProteinsPhosphatesPhosphoproteinsSteroidogenic Acute Regulatory ProteinTranscription Factor CHOP3-Hydroxysteroid DehydrogenasesDdit3 protein, mouseMitochondrial Membrane Transport ProteinsPhosphatesPhosphoproteinsSteroidogenic Acute Regulatory ProteinTom22 protein, mouseTranscription Factor CHOP

Identifiers

PMID27697863
PMCPMC5126293
OpenAlexW2529623160

What OpenQuestion holds

Textmetadata
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.