Evidence map›Paper›PMID 28046085›Full record

ArticlePloS one2017

Differential HDAC1 and 2 Recruitment by Members of the MIER Family.

Roya Derwish, Gary D Paterno, Laura L Gillespie

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. 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

3 authors at 1 institution in 1 country.

Roya DerwishTerry Fox Cancer Research Laboratories, Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland and Labrador, Canada.
Gary D PaternoTerry Fox Cancer Research Laboratories, Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland and Labrador, Canada.
Laura L GillespieTerry Fox Cancer Research Laboratories, Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland and Labrador, Canada.ORCID http://orcid.org/0000-0002-7368-6184
Memorial University of Newfoundland · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mier family consists of three related genes encoding ELM2-SANT containing proteins. MIER1 has been well characterized and is known to function in transcriptional repression through its ability to recruit HDAC1 and 2. Little is known about MIER2 or MIER3 function and no study characterizing these two proteins has been published. In this report, we investigate MIER2 and MIER3 localization and function. Confocal analysis revealed that, while MIER2 and MIER3 are mainly nuclear proteins, a substantial proportion (32%) of MIER2 is localized in the cytoplasm. Co-immunoprecipitation experiments demonstrated that the MIER proteins do not dimerize; that MIER2, but not MIER3, can recruit HDACs; and that recruitment is cell line-dependent. MIER2 was associated with HDAC1 and HDAC2 in HEK293 cells, but only with HDAC1 in MCF7 and HeLa cells. Little or no MIER3 co-immunoprecipitated with either HDAC1 or 2 in any of the three cell lines tested. By contrast, HDAC1 and 2 were readily detected in MIER1α complexes in all three cell lines. Histone deacetylase assays confirmed that MIER2, but not MIER3 complexes, have associated deacetylase activity, leading to the conclusion that MIER3 does not function in HDAC recruitment in these cell lines. In contrast to what has been reported for other ELM2-SANT associated HDACs, addition of D-myo-inositol-1,4,5,6-tetrakisphosphate led to only a small increase in MIER1α associated deacetylase activity and no effect on that associated with MIER2. Deletion analysis revealed that HDAC recruitment occurs through the ELM2 domain. Finally, using site-directed mutagenesis, we show that, like MIER1, 228W in the ELM2 domain is a critical residue for HDAC recruitment by MIER2.

Indexed as

Amino Acid SequenceCell NucleusDNA-Binding ProteinsHEK293 CellsHeLa CellsHistone Deacetylase 1Histone Deacetylase 2HumansImmunoprecipitationInositol PhosphatesMCF-7 CellsMultiprotein ComplexesNuclear ProteinsProtein BindingProtein DomainsProtein TransportDNA-Binding ProteinsHDAC1 protein, humanHDAC2 protein, humanHistone Deacetylase 1Histone Deacetylase 2inositol-1,4,5,6-tetrakisphosphateInositol PhosphatesMIER1 protein, humanMIER2 protein, humanMIER3 protein, humanMultiprotein ComplexesNuclear ProteinsTranscription Factors

Identifiers

PMID28046085
PMCPMC5207708
OpenAlexW2569347110

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.