Evidence map›Paper›PMID 27200088›Full record

ReviewFrontiers in genetics2016

Anchoring a Leviathan: How the Nuclear Membrane Tethers the Genome.

Rafal Czapiewski, Michael I Robson, Eric C Schirmer

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.4field-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

42 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. CTCF supports preferentially short lamina-associated domains.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2022
    Article
  12. Article
  13. The LEM-ESCRT toolkit: Repair and maintenance of the nucleus.Frontiers in cell and developmental biology · 2022
    Review
  14. Article
  15. Article
  16. A novel biallelicClinical case reports · 2021
    Article
  17. Article
  18. Article
  19. Review
  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.

Rafal CzapiewskiThe Wellcome Trust Centre for Cell Biology and Institute of Cell Biology, University of Edinburgh Edinburgh, UK.
Michael I RobsonThe Wellcome Trust Centre for Cell Biology and Institute of Cell Biology, University of Edinburgh Edinburgh, UK.
Eric C SchirmerThe Wellcome Trust Centre for Cell Biology and Institute of Cell Biology, University of Edinburgh Edinburgh, UK.
Wellcome Centre for Cell Biology · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

It is well established that the nuclear envelope has many distinct direct connections to chromatin that contribute to genome organization. The functional consequences of genome organization on gene regulation are less clear. Even less understood is how interactions of lamins and nuclear envelope transmembrane proteins (NETs) with chromatin can produce anchoring tethers that can withstand the physical forces of and on the genome. Chromosomes are the largest molecules in the cell, making megadalton protein structures like the nuclear pore complexes and ribosomes seem small by comparison. Thus to withstand strong forces from chromosome dynamics an anchoring tether is likely to be much more complex than a single protein-protein or protein-DNA interaction. Here we will briefly review known NE-genome interactions that likely contribute to spatial genome organization, postulate in the context of experimental data how these anchoring tethers contribute to gene regulation, and posit several hypotheses for the physical nature of these tethers that need to be investigated experimentally. Significantly, disruption of these anchoring tethers and the subsequent consequences for gene regulation could explain how mutations in nuclear envelope proteins cause diseases ranging from muscular dystrophy to lipodystrophy to premature aging progeroid syndromes. The two favored hypotheses for nuclear envelope protein involvement in disease are (1) weakening nuclear and cellular mechanical stability, and (2) disrupting genome organization and gene regulation. Considerable experimental support has been obtained for both. The integration of both mechanical and gene expression defects in the disruption of anchoring tethers could provide a unifying hypothesis consistent with both.

Indexed as

gene positionNE-chromatin interactionNETnuclear envelopeperipheral heterochromatin

Identifiers

PMID27200088
PMCPMC4859327
OpenAlexW2347179113

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.