Evidence map›Paper›PMID 16301993›Full record

ArticleOncogene2006

The G12/13-RhoA signaling pathway contributes to efficient lysophosphatidic acid-stimulated cell migration.

D Bian, C Mahanivong, J Yu, S M Frisch, Z K Pan, R D Ye, S Huang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

65 citing papers in PubMed, 127 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Functions of RhoA in the female reproductive system.Reproductive and developmental medicine · 2025
    Review
  5. Article
  6. GRespiratory research · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. World journal of gastrointestinal oncology · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. GαJournal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  16. Article
  17. Review
  18. Review
  19. Gα-13 induces CThe Journal of biological chemistry · 2019
    Article
  20. Article

5 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 1 country.

D BianDepartment of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.
C Mahanivong
J Yu
S M Frisch
Z K Pan
R D Ye
S Huang
Scripps Research Institute · USUniversity of Illinois Chicago · USUniversity of Toledo · USWest Virginia University · US

Funding

BACTERIA, SIGNALING &LEUKOCYTE TRANSCRIPTION ACTIVATIONR01AI043524 · NIAID · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI PAN, ZHIXING K · 2000 to 2010
$2.6M
The Regulation of UPA and UPAR in Human Carcinoma CellsR01CA093926 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI HUANG, SHUANG · 2002 to 2010
$2.5M
NCI NIH HHS R01 CA93926NIAID NIH HHS R01 AI043524
6 · The paper itself

Abstract

The membrane redistribution and phosphorylation of focal adhesion kinase (FAK) have been reported to be important for cell migration. We previously showed that Lysophosphatidic acid (LPA) induced FAK membrane redistribution and autophosphorylation in ovarian cancer SK-OV3 cells and the signaling pathway consisting of Gi-Ras-MEKK1 mediated LPA-induced FAK membrane redistribution but not FAK autophosphorylation. We also showed that the disruption of the Gi-Ras-MEKK1 pathway led to a significant reduction in LPA-stimulated cell migration. These findings raised the question of whether LPA-induced FAK autophosphorylation was required for LPA-stimulated cell migration and what signaling mechanism was involved in LPA-induced FAK autophosphorylation. In this study, we expressed the membrane anchored wild-type FAK (CD2-FAK) in SK-OV3 cells and found that the expression of CD2-FAK greatly rescued LPA-stimulated cell migration in Gi or Ras-inhibited cells. However, Gi inhibitor pertussis toxin or dominant-negative H-Ras still significantly inhibited LPA-stimulated cell migration in cells expressing the membrane anchored FAK containing a mutation in the autophosphorylation site [CD2-FAK(Y397A)]. These results suggest that FAK autophosphorylation plays a role in LPA-stimulated cell migration. With the aid of p115RhoGEF-RGS, G12 and G13 minigenes to inhibit G12/13, we found that the G12/13 pathway was required for LPA-induced FAK autophosphorylation and efficient cell migration. Moreover, LPA activated RhoA and Rho kinase (ROCK) in a G12/13-dependent manner and their activities were required for LPA-induced FAK autophosphorylation. However, Rho or ROCK inhibitors displayed no effect on LPA-induced FAK membrane redistribution although they abolished LPA-induced cytoskeleton reorganization. Our studies show that the G12/13-RhoA-ROCK signaling pathway mediates LPA-induced FAK autophosphorylation and contributes to LPA-stimulated cell migration.

Indexed as

Signal TransductionCell MembraneCell MovementCytoskeletonFemaleFocal Adhesion Protein-Tyrosine KinasesFocal AdhesionsGenes, rasGTP-Binding Protein alpha Subunits, G12-G13HumansIntracellular Signaling Peptides and ProteinsLysophospholipidsMutationOvarian NeoplasmsPertussis ToxinPhosphorylationFocal Adhesion Protein-Tyrosine KinasesGTP-Binding Protein alpha Subunits, G12-G13Intracellular Signaling Peptides and Proteinslysophosphatidic acidLysophospholipidsPertussis ToxinProtein Serine-Threonine Kinasesras ProteinsrhoA GTP-Binding Proteinrho-Associated Kinases

Identifiers

PMID16301993
OpenAlexW2054429361

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.