Evidence map›Paper›PMID 11739801›Full record

ArticleMolecular biology of the cell2001

Transcriptional activation of cyclin D1 promoter by FAK contributes to cell cycle progression.

J Zhao, R Pestell, J L Guan

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

92 citing papers in PubMed, 199 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Role of synaptotagmin 13 (SYT13) in promoting breast cancer and signaling pathways.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  10. Review
  11. Review
  12. FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

32 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

3 authors at 2 institutions in 1 country.

J ZhaoDepartment of Molecular Medicine, Cornell University College of Veterinary Medicine, Ithaca, NY 14853, USA.
R Pestell
J L Guan
Cornell University · USAlbert Einstein College of Medicine · US

Funding

SIGNAL TRANSDUCTION BY FAK AND ITS ASSOCIATED PROTEINSR01GM052890 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, JUN-LIN · 1995 to 2012
$3.3M
NIGMS NIH HHS GM 52890NIGMS NIH HHS R01 GM052890
6 · The paper itself

Abstract

Integrin-mediated cell adhesion to the extracellular matrix is required for normal cell growth. Cyclin D1 is a key regulator of G1-to-S phase progression of the cell cycle. Our previous studies have demonstrated that integrin signaling through focal adhesion kinase (FAK) plays a role in the regulation of cell cycle progression, which correlates with changes in the expression of cyclin D1 and the cdk inhibitor, p21, induced by FAK. In this report, we first investigated the roles of both cyclin D1 and p21 in the regulation of cell cycle progression by FAK. We found that overexpression of a dominant-negative FAK mutant DeltaC14 suppressed cell cycle progression in p21(-/-) cells as effectively as in the control p21(+/+) cells. Furthermore, we found that overexpression of ectopic cyclin D1 could rescue cell cycle inhibition by DeltaC14. These results suggested that cyclin D1, but not p21, was the primary functional target of FAK signaling pathways in cell cycle regulation. We then investigated the mechanisms underlying the regulation of cyclin D1 expression by FAK signaling. Using Northern blotting and cyclin D1 promoter/luciferase assays, we showed that FAK signaling regulated cyclin D1 expression at the transcriptional level. Using a series of cyclin D1 promoter mutants in luciferase assays as well as electrophoretic mobility shift assays (EMSA), we showed that the EtsB binding site mediated cyclin D1 promoter regulation by FAK. Finally, we showed that FAK regulation of cyclin D1 depends on integrin-mediated cell adhesion and is likely through its activation of the Erk signaling pathway. Together, these studies demonstrate that transcriptional regulation of cyclin D1 by FAK signaling pathways contributes to the regulation of cell cycle progression in cell adhesion.

Indexed as

Cell CycleTranscriptional Activation3T3 CellsAnimalsBlotting, WesternCell AdhesionCyclin D1Cyclin-Dependent Kinase Inhibitor p21CyclinsElectrophoretic Mobility Shift AssayFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesHumansMiceMitogen-Activated Protein KinasesPromoter Regions, GeneticCDKN1A protein, humanCdkn1a protein, mouseCyclin D1Cyclin-Dependent Kinase Inhibitor p21CyclinsFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesMitogen-Activated Protein KinasesProtein-Tyrosine KinasesPTK2 protein, humanPtk2 protein, mouseRNA, Messenger

Identifiers

PMID11739801
PMCPMC60776
OpenAlexW2125967276

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.