Evidence map›Paper›PMID 21151568›Full record

ArticlePloS one2010

Deletion of CDKAL1 affects mitochondrial ATP generation and first-phase insulin exocytosis.

Mica Ohara-Imaizumi, Masashi Yoshida, Kyota Aoyagi, Taro Saito, Tadashi Okamura, Hitoshi Takenaka, Yoshihiro Akimoto, Yoko Nakamichi, Rieko Takanashi-Yanobu, Chiyono Nishiwaki and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
5.6field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Eperisone Analogs, Rescuers ofACS medicinal chemistry letters · 2025
    Article
  8. Review
  9. Molybdenum Cofactor Deficiency in Humans.Molecules (Basel, Switzerland) · 2022
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. First Step in Catalysis of the RadicalJournal of the American Chemical Society · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

15 authors at 5 institutions in 1 country.

Mica Ohara-ImaizumiDepartment of Biochemistry, Kyorin University School of Medicine, Tokyo, Japan.
Masashi Yoshida
Kyota Aoyagi
Taro Saito
Tadashi Okamura
Hitoshi Takenaka
Yoshihiro Akimoto
Yoko Nakamichi
Rieko Takanashi-Yanobu
Chiyono Nishiwaki
Hayato Kawakami
Norihiro Kato
Shin-ichi Hisanaga
Masafumi Kakei
Shinya Nagamatsu
Kyorin University · JPNational Center for Global Health and Medicine · JPTokyo Metropolitan University · JPJichi Medical University · JPJichi Medical University Saitama Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA variant of the CDKAL1 gene was reported to be associated with type 2 diabetes and reduced insulin release in humans; however, the role of CDKAL1 in β cells is largely unknown. Therefore, to determine the role of CDKAL1 in insulin release from β cells, we studied insulin release profiles in CDKAL1 gene knockout (CDKAL1 KO) mice. PRINCIPAL

findingsTotal internal reflection fluorescence imaging of CDKAL1 KO β cells showed that the number of fusion events during first-phase insulin release was reduced. However, there was no significant difference in the number of fusion events during second-phase release or high K(+)-induced release between WT and KO cells. CDKAL1 deletion resulted in a delayed and slow increase in cytosolic free Ca(2+) concentration during high glucose stimulation. Patch-clamp experiments revealed that the responsiveness of ATP-sensitive K(+) (K(ATP)) channels to glucose was blunted in KO cells. In addition, glucose-induced ATP generation was impaired. Although CDKAL1 is homologous to cyclin-dependent kinase 5 (CDK5) regulatory subunit-associated protein 1, there was no difference in the kinase activity of CDK5 between WT and CDKAL1 KO islets. CONCLUSIONS/SIGNIFICANCE: We provide the first report describing the function of CDKAL1 in β cells. Our results indicate that CDKAL1 controls first-phase insulin exocytosis in β cells by facilitating ATP generation, K(ATP) channel responsiveness and the subsequent activity of Ca(2+) channels through pathways other than CDK5-mediated regulation.

Indexed as

Adenosine TriphosphateAnimalsB-LymphocytesCyclin-Dependent Kinase 5CytosolDiabetes Mellitus, Type 2ExocytosisGenetic VariationGlucoseInsulinMiceMice, KnockoutMitochondriaNerve Tissue ProteinsPatch-Clamp TechniquesPotassiumAdenosine TriphosphateCdk5 protein, mouseCDKAL1 protein, mouseCyclin-Dependent Kinase 5GlucoseInsulinNerve Tissue ProteinsPotassiumtRNA Methyltransferases

Identifiers

PMID21151568
PMCPMC3000340
OpenAlexW2094125028

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.