Evidence map›Paper›PMID 10570150›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Defects in inositol 1,4,5-trisphosphate receptor expression, Ca(2+) signaling, and insulin secretion in the anx7(+/-) knockout mouse.

M Srivastava, I Atwater, M Glasman, X Leighton, G Goping, H Caohuy, G Miller, J Pichel, H Westphal, D Mears and 2 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Cavβ3 Regulates CaDiabetes · 2021
    Article
  5. Annexin Animal Models-From Fundamental Principles to Translational Research.International journal of molecular sciences · 2021
    Review
  6. Annexin A7 Regulates Endometrial Receptivity.Frontiers in cell and developmental biology · 2020
    Article
  7. Annexins in Adipose Tissue: Novel Players in Obesity.International journal of molecular sciences · 2019
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Influence of annexin A7 on insulin sensitivity of cellular glucose uptake.Pflugers Archiv : European journal of physiology · 2015
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

12 authors at 1 institution in 1 country.

M SrivastavaDepartment of Anatomy, Institute for Molecular Medicine, Uniformed Services University School of Medicine, Bethesda, MD 20814, USA. msrivastava@usuhs.mil
I Atwater
M Glasman
X Leighton
G Goping
H Caohuy
G Miller
J Pichel
H Westphal
D Mears
E Rojas
H B Pollard
National Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mammalian anx7 gene codes for a Ca(2+)-activated GTPase, which supports Ca(2+)/GTP-dependent secretion events and Ca(2+) channel activities in vitro and in vivo. To test whether anx7 might be involved in Ca(2+) signaling in secreting pancreatic beta cells, we knocked out the anx7 gene in the mouse and tested the insulin-secretory properties of the beta cells. The nullizygous anx7 (-/-) phenotype is lethal at embryonic day 10 because of cerebral hemorrhage. However, the heterozygous anx7 (+/-) mouse, although expressing only low levels of ANX7 protein, is viable and fertile. The anx7 (+/-) phenotype is associated with a substantial defect in insulin secretion, although the insulin content of the islets, is 8- to 10-fold higher in the mutants than in the normal littermate control. We infer from electrophysiological studies that both glucose-stimulated secretion and voltage-dependent Ca(2+) channel functions are normal. However, electrooptical recordings indicate that the (+/-) mutation has caused a change in the ability of inositol 1,4,5-trisphosphate (IP(3))-generating agonists to release intracellular calcium. The principle molecular consequence of lower anx7 expression is a profound reduction in IP(3) receptor expression and function in pancreatic islets. The profound increase in islets, beta cell number, and size may be a means of compensating for less efficient insulin secretion by individual defective pancreatic beta cells. This is a direct demonstration of a connection between glucose-activated insulin secretion and Ca(2+) signaling through IP(3)-sensitive Ca(2+) stores.

Indexed as

Calcium SignalingInositol 1,4,5-TrisphosphateAnimalsAnnexin A7CalciumCalcium ChannelsCell LineCytosolElectrophysiologyGenetic VectorsGlucoseGTP PhosphohydrolasesHyperplasiaHypertrophyImmunohistochemistryInositol 1,4,5-Trisphosphate ReceptorsAnnexin A7CalciumCalcium ChannelsGlucoseGTP PhosphohydrolasesInositol 1,4,5-TrisphosphateInositol 1,4,5-Trisphosphate ReceptorsInsulinReceptors, Cytoplasmic and Nuclear

Identifiers

PMID10570150
PMCPMC24142
OpenAlexW2137257005

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.