Evidence map›Paper›PMID 21852232›Full record

ArticleThe Journal of biological chemistry2011

Protein kinase A-mediated serine 35 phosphorylation dissociates histone H1.4 from mitotic chromosome.

Chi-Shuen Chu, Pang-Hung Hsu, Pei-Wen Lo, Elisabeth Scheer, Laszlo Tora, Hang-Jen Tsai, Ming-Daw Tsai, Li-Jung Juan

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Review
  3. Maintaining Transcriptional Specificity Through Mitosis.Annual review of genomics and human genetics · 2022
    Review
  4. Article
  5. Review
  6. The missing linkGenes & development · 2021
    Review
  7. Article
  8. Histone H1 Post-Translational Modifications: Update and Future Perspectives.International journal of molecular sciences · 2020
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  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

8 authors at 5 institutions in 2 countries.

Chi-Shuen ChuInstitute of Molecular Medicine, National Taiwan University, Taipei 100, Taiwan; Genomics Research Center, Academia Sinica, Taipei 115, Taiwan.
Pang-Hung HsuGenomics Research Center, Academia Sinica, Taipei 115, Taiwan; Department of Life Science, National Taiwan Ocean University, Keelung, Taiwan 20224; Institute of Bioscience and Biotechnology, National Taiwan Ocean University, Keelung, Taiwan 20224.
Pei-Wen LoGenomics Research Center, Academia Sinica, Taipei 115, Taiwan.
Elisabeth ScheerProgram of Functional Genomics and Cancer, Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS UMR 7104, INSERM U964, Université de Strasbourg, BP 10142-67404 Illkirch Cedex, France.
Laszlo ToraProgram of Functional Genomics and Cancer, Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS UMR 7104, INSERM U964, Université de Strasbourg, BP 10142-67404 Illkirch Cedex, France.
Hang-Jen TsaiGenomics Research Center, Academia Sinica, Taipei 115, Taiwan.
Ming-Daw TsaiGenomics Research Center, Academia Sinica, Taipei 115, Taiwan; Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan.
Li-Jung JuanInstitute of Molecular Medicine, National Taiwan University, Taipei 100, Taiwan; Genomics Research Center, Academia Sinica, Taipei 115, Taiwan. Electronic address: ljjuan@gate.sinica.edu.tw.
Genomics Research Center, Academia Sinica · TWCentre National de la Recherche Scientifique · FRInserm · FRNational Taiwan Ocean University · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Global histone H1 phosphorylation correlates with cell cycle progression. However, the function of site-specific H1 variant phosphorylation remains unclear. Our mass spectrometry analysis revealed a novel N-terminal phosphorylation of the major H1 variant H1.4 at serine 35 (H1.4S35ph), which accumulates at mitosis immediately after H3 phosphorylation at serine 10. Protein kinase A (PKA) was found to be a kinase for H1.4S35. Importantly, Ser-35-phosphorylated H1.4 dissociates from mitotic chromatin. Moreover, H1.4S35A substitution mutant cannot efficiently rescue the mitotic defect following H1.4 depletion, and inhibition of PKA activity increases the mitotic chromatin compaction depending on H1.4. Our results not only indicate that PKA-mediated H1.4S35 phosphorylation dissociates H1.4 from mitotic chromatin but also suggest that this phosphorylation is necessary for specific mitotic functions.

Indexed as

Amino Acid SubstitutionChromatinChromosomes, HumanCyclic AMP-Dependent Protein KinasesHeLa CellsHistonesHumansMitosisMutation, MissensePhosphorylationSerineChromatinCyclic AMP-Dependent Protein KinasesHistonesSerine

Identifiers

PMID21852232
PMCPMC3195632
OpenAlexW2014711736

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.