Evidence map›Paper›PMID 18482983›Full record

ArticleThe Journal of biological chemistry2008

Potential molecular mechanism for c-Src kinase-mediated regulation of intestinal cell migration.

Sijo Mathew, Sudeep P George, Yaohong Wang, Mohammad Rizwan Siddiqui, Kamalakkannan Srinivasan, Langzhu Tan, Seema Khurana

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Maresin-2 promotes mucosal repair and has therapeutic potential when encapsulated in thermostable nanoparticles.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  2. Observational
  3. Article
  4. Article
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  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Enterocyte loss of polarity and gut wound healing rely upon the F-actin-severing function of villin.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  12. Review
  13. Article
  14. A TRIF-independent branch of TLR3 signaling.Journal of immunology (Baltimore, Md. : 1950) · 2012
    Article
  15. Article
  16. Review
  17. Article
  18. ILK mediates the effects of strain on intestinal epithelial wound closure.American journal of physiology. Cell physiology · 2011
    Article
  19. Article
  20. Genetic variability in EGFR, Src and HER2 and risk of colorectal adenoma and cancer.International journal of molecular epidemiology and genetics · 2011
    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

7 authors at 1 institution in 1 country.

Sijo MathewDepartment of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.
Sudeep P George
Yaohong Wang
Mohammad Rizwan Siddiqui
Kamalakkannan Srinivasan
Langzhu Tan
Seema Khurana
University of Tennessee Health Science Center · US

Funding

ROLE OF VILLIN IN EPITHELIAL CELL SIGNAL TRANSDUCTIONR01DK054755 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KHURANA, SEEMA · 2000 to 2009
$3.1M
Regulation of epithelial cell motility by villin.R01DK065006 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KHURANA, SEEMA · 2004 to 2008
$1.6M
NIDDK NIH HHS DK-54755NIDDK NIH HHS DK-65006
6 · The paper itself

Abstract

The ubiquitously expressed Src tyrosine kinases (c-Src, c-Yes, and c-Fyn) regulate intestinal cell growth and differentiation. Src activity is also elevated in the majority of malignant and premalignant tumors of the colon. The development of fibroblasts with the three ubiquitously expressed kinases deleted (SYF cells) has identified the role of Src proteins in the regulation of actin dynamics associated with increased cell migration and invasion. Despite this, unexpectedly nothing is known about the role of the individual Src kinases on intestinal cell cytoskeleton and/or cell migration. We have previously reported that villin, an epithelial cell-specific actin-modifying protein that regulates actin reorganization, cell morphology, cell migration, cell invasion, and apoptosis, is tyrosine-phosphorylated. In this report using the SYF cells reconstituted individually with c-Src, c-Yes, c-Fyn, and wild type or phosphorylation site mutants of villin, we demonstrate for the first time the absolute requirement for c-Src in villin-induced regulation of cell migration. The other major finding of our study is that contrary to previous reports, the nonreceptor tyrosine kinase, Jak3 (Janus kinase 3), does not regulate phosphorylation of villin or villin-induced cell migration and is, in fact, not expressed in intestinal epithelial cells. Further, we identify SHP-2 and PTP-PEST (protein-tyrosine phosphatase proline-, glutamate-, serine-, and threonine-rich sequence) as negative regulators of c-Src kinase and demonstrate a new function for these phosphatases in intestinal cell migration. Together, these data suggest that in colorectal carcinogenesis, elevation of c-Src or down-regulation of SHP-2 and/or PTP-PEST may promote cancer metastases and invasion by regulating villin-induced cell migration and cell invasion.

Indexed as

Caco-2 CellsCell Line, TumorCell MovementCSK Tyrosine-Protein KinaseCytoskeletal ProteinsEzrinHeLa CellsHumansJanus Kinase 3Neoplasm InvasivenessPhosphorylationProtein-Tyrosine Kinasessrc-Family KinasesCSK protein, humanCSK Tyrosine-Protein KinaseCytoskeletal ProteinsEzrinJAK3 protein, humanJanus Kinase 3Protein-Tyrosine Kinasessrc-Family Kinases

Identifiers

PMID18482983
PMCPMC2504885
OpenAlexW2054764666

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.