Evidence map›Paper›PMID 20876536›Full record

ArticleThe Journal of biological chemistry2011

Adenylate kinase 2 links mitochondrial energy metabolism to the induction of the unfolded protein response.

Alison Burkart, Xiarong Shi, My Chouinard, Silvia Corvera

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

37 citing papers in PubMed, 68 citations in OpenAlex.

  1. NanoCortex: A Unified Agentic System for Nanopore Sequencing Analysis.bioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

4 authors at 1 institution in 1 country.

Alison BurkartProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
Xiarong Shi
My Chouinard
Silvia Corvera
University of Massachusetts Chan Medical School · US

Funding

Diabetes Genome Anatomy Project (DGAP)R01DK060837 · NIDDK · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 2002 to 2006
$15.9M
PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
Adipose Tissue Angiogenesis and Metabolic DiseaseR01DK089101 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CORVERA, SILVIA · 2011 to 2024
$5.7M
NIDDK NIH HHS DK32520NIDDK NIH HHS DK60837NIDDK NIH HHS P30 DK032520NIDDK NIH HHS R01 DK060837NIDDK NIH HHS R01 DK089101
6 · The paper itself

Abstract

The unfolded protein response (UPR) is a homeostatic signaling mechanism that balances the protein folding capacity of the endoplasmic reticulum (ER) with the secretory protein load of the cell. ER protein folding capacity is dependent on the abundance of chaperones, which is increased in response to UPR signaling, and on a sufficient ATP supply for their activity. An essential branch of the UPR entails the splicing of XBP1 mRNA to form the XBP1 transcription factor. XBP1 has been shown to be required during adipocyte differentiation, enabling mature adipocytes to secrete adiponectin, and during differentiation of B cells into antibody-secreting plasma cells. Here we find that adenylate kinase 2 (AK2), a mitochondrial enzyme that regulates adenine nucleotide interconversion within the intermembrane space, is markedly induced during adipocyte and B cell differentiation. Depletion of AK2 by RNAi impairs adiponectin secretion in 3T3-L1 adipocytes, IgM secretion in BCL1 cells, and the induction of the UPR during differentiation of both cell types. These results reveal a new mechanism by which mitochondria support ER function and suggest that specific mitochondrial defects may give rise to impaired UPR signaling. The requirement for AK2 for UPR induction may explain the pathogenesis of the profound hematopoietic defects of reticular dysgenesis, a disease associated with mutations of the AK2 gene in humans.

Indexed as

3T3-L1 CellsAdenosine TriphosphateAdenylate KinaseAdiponectinAnimalsCell DifferentiationDNA-Binding ProteinsEndoplasmic ReticulumEnergy MetabolismHematopoiesisHumansLeukopeniaMiceMitochondriaMitochondrial ProteinsMutationAdenosine TriphosphateAdenylate Kinaseadenylate kinase 2AdiponectinDNA-Binding ProteinsMitochondrial ProteinsRegulatory Factor X Transcription FactorsRNA, MessengerTranscription FactorsX-Box Binding Protein 1XBP1 protein, humanXbp1 protein, mouse

Identifiers

PMID20876536
PMCPMC3039340
OpenAlexW2080167853

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.