Evidence map›Paper›PMID 24921241›Full record

ArticleSmall GTPases2014

A new role for Rab GTPases during early mitotic stages.

Sanchaita Das, Heidi Hehnly, Stephen Doxsey

Abstract read
In one paragraph

Article in Small GTPases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Small RAB GTPases Regulate Multiple Steps of Mitosis.Frontiers in cell and developmental biology · 2016
    Review
  14. 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.

Sanchaita DasProgram in Molecular Medicine; Worcester, MA USA.
Heidi HehnlyProgram in Molecular Medicine; Worcester, MA USA.
Stephen DoxseyProgram in Molecular Medicine; Worcester, MA USA.

Funding

Mother Centriole Appendages Regulate the AMIS Compartment and Cilogenesis.K99GM107355 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HEHNLY, HEIDI · 2013 to 2014
$171k
NIGMS NIH HHS K99 GM107355
6 · The paper itself

Abstract

A recent study revealed new roles for the Rab11 GTPase during mitosis. Rab11 is involved in recycling endosome localization to mitotic spindle poles via dynein-mediated transport. This process is in contrast to Golgi membranes, which disperse in mitosis and do not appear to directly contribute to mitotic functions. Rab11-depletion prevents recycling endosome organization at spindle poles, delays mitotic progression, and disrupts spindle pole protein recruitment, astral microtubule organization, and mitotic spindle orientation. However, Rab11 is not the only endocytic and/or trafficking protein that regulates mitotic progression. Clathrin and two small GTPases (Rab6A', Rab5) play key roles in spindle organization and function. In this commentary, we discuss the roles of all these canonical endocytic and membrane trafficking proteins during mitosis and speculate on possible cross-communication between them and their molecular pathways that ensure faithful progression through mitosis.

Indexed as

MitosisAnimalsClathrinDyneinsEndocytosisEndosomesGolgi ApparatusHumansKinetochoresMicrotubulesrab11 GTP-Binding Proteinsrab5 GTP-Binding Proteinsrab GTP-Binding ProteinsSpindle ApparatusClathrinDyneinsrab11 GTP-Binding Proteinsrab5 GTP-Binding ProteinsRab6 proteinrab GTP-Binding ProteinscentrosomeClathrindyneinendocytosisGolgi apparatusmicrotubulesNuMARab11Rab5Rab6A’secretory systemspindle

Identifiers

PMID24921241
PMCPMC4160335

What OpenQuestion holds

Textmetadata
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.