Evidence map›Paper›PMID 19487689›Full record

ArticleThe Journal of biological chemistry2009

Sorting nexin 33 induces mammalian cell micronucleated phenotype and actin polymerization by interacting with Wiskott-Aldrich syndrome protein.

Juan Zhang, Xiaofei Zhang, Yunqian Guo, Liangliang Xu, Duanqing Pei

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. EnteropathogenicInternational journal of molecular sciences · 2020
    Article
  3. Review
  4. Article
  5. Review
  6. SopB-Mediated Recruitment of SNX18 FacilitatesFrontiers in cellular and infection microbiology · 2017
    Article
  7. Article
  8. Article
  9. Phosphorylation of the Bin, Amphiphysin, and RSV161/167 (BAR) domain of ACAP4 regulates membrane tubulation.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Expression of sorting nexin 18 (SNX18) is dynamically regulated in developing spinal motor neurons.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2011
    Article
  15. Article
  16. Review
  17. 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

5 authors at 3 institutions in 1 country.

Juan ZhangLaboratory of Stem Cell Biology, Department of Biological Sciences and Biotechnology, Institute of Biomedicine, School of Medicine, Tsinghua University, Beijing 100084, China.
Xiaofei Zhang
Yunqian Guo
Liangliang Xu
Duanqing Pei
Chinese Academy of Sciences · CNGuangzhou Institutes of Biomedicine and Health · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sorting nexin 33 (SNX33) is a novel member of the sorting nexin superfamily with three predicted structural domains, SH3-PX-BAR. Very little is known about the cellular function of SNX33. In an effort to analyze its structure/function relationship, we attempted but failed to generate stable cell lines for short hairpin RNA or overexpression SNX33. Transient knockdown of SNX33 induces both HeLa and MCF7 cells to grow multiple long processes, delay the G(1)/M transition, and become more apoptotic, implying that SNX33 may control cell cycle process through influence the cytoskeleton. In vitro cell lineage analysis revealed that cells transfected with SNX33 failed to divide and became micronucleated, suggesting a specific defect in cytokinesis. Further analysis revealed that SNX33 induced the accumulation of actin at the perinuclear space, which might have disabled the cytokinetic machinery. However, SNX33 appears to mediate actin polymerization indirectly, as they do not interact with each other. SNX33 interacts with itself and SNX9. Interestingly, it also interacts with VCA domain of Wiskott-Aldrich syndrome protein (WASp), a protein known to be involved in actin polymerization. Indeed, cells overexpressing WASp failed to divide and form stable colonies as SNX33, consistent with the notion that SNX33 may interfere with cytokinesis. On the other hand, knockdown of WASp alleviates the phenotype induced by SNX33. Taken together, our results suggest that SNX33 plays a role in maintaining cell shape and cell cycle progression through its interaction with WASp.

Indexed as

Gene Expression Regulation, NeoplasticActinsApoptosisBase SequenceCarrier ProteinsCell CycleCell Line, TumorCell ShapeHeLa CellsHumansModels, BiologicalMolecular Sequence DataPhenotypeProtein BindingSorting NexinsVesicular Transport ProteinsActinsCarrier ProteinsSNX33 protein, humanSorting NexinsVesicular Transport ProteinsWiskott-Aldrich Syndrome Protein

Identifiers

PMID19487689
PMCPMC2755889
OpenAlexW2001512246

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.