Evidence map›Paper›PMID 36768434›Full record

ArticleInternational journal of molecular sciences2023

Tip60/KAT5 Histone Acetyltransferase Is Required for Maintenance and Neurogenesis of Embryonic Neural Stem Cells.

Kaoru Tominaga, Eiji Sakashita, Katsumi Kasashima, Kenji Kuroiwa, Yasumitsu Nagao, Naoki Iwamori, Hitoshi Endo

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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. Kat5 cKO mouse replicates biological domain signatures associated with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Acetyltransferase in cardiovascular disease and aging.The journal of cardiovascular aging · 2024
    Article
  12. 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

7 authors.

Kaoru TominagaDivision of Structural Biochemistry, Department of Biochemistry, Jichi Medical University, Tochigi 321-0498, Japan.ORCID 0000-0001-8799-528X
Eiji SakashitaDivision of Functional Biochemistry, Department of Biochemistry, Jichi Medical University, Tochigi 321-0498, Japan.
Katsumi KasashimaDivision of Functional Biochemistry, Department of Biochemistry, Jichi Medical University, Tochigi 321-0498, Japan.
Kenji KuroiwaDivision of Functional Biochemistry, Department of Biochemistry, Jichi Medical University, Tochigi 321-0498, Japan.
Yasumitsu NagaoCenter for Experimental Medicine, Jichi Medical University, Tochigi 321-0498, Japan.
Naoki IwamoriDepartment of Agriculture, Kyushu University, Fukuoka 819-0395, Japan.
Hitoshi EndoDivision of Functional Biochemistry, Department of Biochemistry, Jichi Medical University, Tochigi 321-0498, Japan.

Funding

Japan Society for the Promotion of Science 17K08497Japan Society for the Promotion of Science 20K07576Japan Society for the Promotion of Science 21K06760
6 · The paper itself

Abstract

Epigenetic regulation via epigenetic factors in collaboration with tissue-specific transcription factors is curtail for establishing functional organ systems during development. Brain development is tightly regulated by epigenetic factors, which are coordinately activated or inactivated during processes, and their dysregulation is linked to brain abnormalities and intellectual disability. However, the precise mechanism of epigenetic regulation in brain development and neurogenesis remains largely unknown. Here, we show that Tip60/KAT5 deletion in neural stem/progenitor cells (NSCs) in mice results in multiple abnormalities of brain development. Tip60-deficient embryonic brain led to microcephaly, and proliferating cells in the developing brain were reduced by Tip60 deficiency. In addition, neural differentiation and neuronal migration were severely affected in Tip60-deficient brains. Following neurogenesis in developing brains, gliogenesis started from the earlier stage of development in Tip60-deficient brains, indicating that Tip60 is involved in switching from neurogenesis to gliogenesis during brain development. It was also confirmed in vitro that poor neurosphere formation, proliferation defects, neural differentiation defects, and accelerated astrocytic differentiation in mutant NSCs are derived from Tip60-deficient embryonic brains. This study uncovers the critical role of Tip60 in brain development and NSC maintenance and function in vivo and in vitro.

Indexed as

Histone AcetyltransferasesNeural Stem CellsAnimalsCell DifferentiationEmbryonic Stem CellsEpigenesis, GeneticMiceNeurogenesisHistone Acetyltransferasesacetyltransferaseepigeneticsgliogenesisneural stem cellneurogenesisTip60/KAT5

Identifiers

PMID36768434
PMCPMC9916716

What Socratic 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 Socratic graph.