Evidence map›Paper›PMID 24156551›Full record

ArticleBMC biochemistry2013

KCTD20, a relative of BTBD10, is a positive regulator of Akt.

Mikiro Nawa, Masaaki Matsuoka

Open access · hybridAbstract read
In one paragraph

Article in BMC biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–field-weighted citation impact, top 90% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The emerging role of the KCTD proteins in cancer.Cell communication and signaling : CCS · 2021
    Review
  9. Silencing of UCA1 Protects Against MPPNeurochemical research · 2021
    Article
  10. Article
  11. Article
  12. 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

2 authors at 1 institution in 1 country.

Mikiro Nawa
Masaaki MatsuokaDepartment of Pharmacology, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo 160-8042, Japan. sakimatu@tokyo-med.ac.jp.
Tokyo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBTBD10 binds to Akt and protein phosphatase 2A (PP2A) and inhibits the PP2A-mediated dephosphorylation of Akt, thereby keeping Akt activated. Previous studies have suggested that BTBD10 plays an important role in preventing motor neuronal death and accelerating the growth of pancreatic beta cells. Because levels of BTBD10 expression are much lower in many non-nervous tissues than nervous tissues, there may be a relative of BTBD10 that has BTBD10-like function in non-neuronal cells.

resultsA 419-amino-acid BTBD10-like protein, named KCTD20 (potassium channel tetramerization protein domain containing 20), was to found to bind to all Akt isoforms and PP2A. Overexpression of KCTD20 increased Akt phosphorylation at Thr308, as BTBD10 did, which suggests that KCTD20 as well as BTBD10 positively regulates the function of Akt. KCTD20 was ubiquitously expressed in non-nervous as well as nervous tissues.

conclusionsKCTD20 is a positive regulator of Akt and may play an important role in regulating the death and growth of some non-nervous and nervous cells.

Indexed as

Amino Acid SequenceAmyotrophic Lateral SclerosisAnimalsCatalytic DomainCell LineChlorocebus aethiopsCOS CellsHumansIntracellular Signaling Peptides and ProteinsMiceMolecular Sequence DataMotor NeuronsNuclear ProteinsPhosphorylationProtein BindingProtein Phosphatase 2BTBD10 protein, humanIntracellular Signaling Peptides and ProteinsNuclear ProteinsProtein Phosphatase 2Proto-Oncogene Proteins c-akt

Identifiers

PMID24156551
PMCPMC3827329
OpenAlexW2103416446

What OpenQuestion holds

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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.