Evidence map›Paper›PMID 19261807›Full record

ArticleMolecular biology of the cell2009

Faciogenital dysplasia protein (FGD1) regulates export of cargo proteins from the golgi complex via Cdc42 activation.

Mikhail V Egorov, Mariagrazia Capestrano, Olesya A Vorontsova, Alessio Di Pentima, Anastasia V Egorova, Stefania Mariggiò, M Inmaculada Ayala, Stefano Tetè, Jerome L Gorski, Alberto Luini and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The role of the Golgi apparatus in disease (Review).International journal of molecular medicine · 2021
    Review
  5. Article
  6. Targeting Rac and Cdc42 GEFs in Metastatic Cancer.Frontiers in cell and developmental biology · 2020
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. [Regulatory effect of faciogenital dysplasia 6 gene on hepatic stem cell differentiation].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Human diseases associated with form and function of the Golgi complex.International journal of molecular sciences · 2013
    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

12 authors at 4 institutions in 3 countries.

Mikhail V EgorovDepartment of Cell Biology and Oncology, Consorzio Mario Negri Sud, 66030 Santa Maria Imbaro (Chieti), Italy.
Mariagrazia Capestrano
Olesya A Vorontsova
Alessio Di Pentima
Anastasia V Egorova
Stefania Mariggiò
M Inmaculada Ayala
Stefano Tetè
Jerome L Gorski
Alberto Luini
Roberto Buccione
Roman S Polishchuk
Mario Negri Sud Foundation · ITIvanovo Research Institute of Motherhood and Childhood named after VN Gorodkov · RUUniversity of Chieti-Pescara · ITUniversity of Missouri · US

Funding

Telethon GGP05044
6 · The paper itself

Abstract

Mutations in the FGD1 gene are responsible for the X-linked disorder known as faciogenital dysplasia (FGDY). FGD1 encodes a guanine nucleotide exchange factor that specifically activates the GTPase Cdc42. In turn, Cdc42 is an important regulator of membrane trafficking, although little is known about FGD1 involvement in this process. During development, FGD1 is highly expressed during bone growth and mineralization, and therefore a lack of the functional protein leads to a severe phenotype. Whether the secretion of proteins, which is a process essential for bone formation, is altered by mutations in FGD1 is of great interest. We initially show here that FGD1 is preferentially associated with the trans-Golgi network (TGN), suggesting its involvement in export of proteins from the Golgi. Indeed, expression of a dominant-negative FGD1 mutant and RNA interference of FGD1 both resulted in a reduction in post-Golgi transport of various cargoes (including bone-specific proteins in osteoblasts). Live-cell imaging reveals that formation of post-Golgi transport intermediates directed to the cell surface is inhibited in FGD1-deficient cells, apparently due to an impairment of TGN membrane extension along microtubules. These effects depend on FGD1 regulation of Cdc42 activation and its association with the Golgi membranes, and they may contribute to FGDY pathogenesis.

Indexed as

Animalscdc42 GTP-Binding ProteinCell LineEnzyme ActivationGene SilencingGolgi ApparatusGuanine Nucleotide Exchange FactorsGuanosine DiphosphateHumansIntracellular MembranesMiceMolecular MimicryMutant ProteinsOsteoblastsProtein BindingProteinscdc42 GTP-Binding ProteinFGD1 protein, humanFgd1 protein, mouseGuanine Nucleotide Exchange FactorsGuanosine DiphosphateMutant ProteinsProteins

Identifiers

PMID19261807
PMCPMC2675621
OpenAlexW2171157569

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.