Evidence map›Paper›PMID 12482975›Full record

ArticleMolecular and cellular biology2003

Novel p27(kip1) C-terminal scatter domain mediates Rac-dependent cell migration independent of cell cycle arrest functions.

Sandra S McAllister, Michelle Becker-Hapak, Giuseppe Pintucci, Michele Pagano, Steven F Dowdy

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

91 citing papers in PubMed, 208 citations in OpenAlex.

  1. p27Cells · 2025
    Article
  2. Review
  3. p27International journal of molecular sciences · 2022
    Article
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  5. Article
  6. Review
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  8. p27Cells · 2021
    Review
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31 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

5 authors at 2 institutions in 1 country.

Sandra S McAllisterHoward Hughes Medical Institute, University of California San Diego School of Medicine, La Jolla 92093-0686, USA.
Michelle Becker-Hapak
Giuseppe Pintucci
Michele Pagano
Steven F Dowdy
Howard Hughes Medical Institute · USNew York University · US

Funding

REGULATION OF THE GI PHASE BY THE UBIQUITIN PATHWAYR01GM057587 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PAGANO, MICHELE · 1998 to 2018
$7.8M
F-Box Proteins: Deregulated Cell Cycle Control and Proteolysis in CancerR01CA076584 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PAGANO, MICHELE · 1998 to 2021
$4.5M
Transduction of Tumor Suppressor Proteins into GliomasR01CA096098 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI DOWDY, STEVEN F · 2001 to 2005
$1.2M
NCI NIH HHS R01 CA076584NCI NIH HHS R01 CA096098NCI NIH HHS R01-CA76584NIGMS NIH HHS R01 GM057587NIGMS NIH HHS R01-GM57587
6 · The paper itself

Abstract

Hepatocyte growth factor (HGF) signaling via its receptor, the proto-oncogene Met, alters cell proliferation and motility and has been associated with tumor metastasis. HGF treatment of HepG2 human hepatocellular carcinoma cells induces cell migration concomitant with increased levels of the p27(kip1) cyclin-cdk inhibitor. HGF signaling resulted in nuclear export of endogenous p27 to the cytoplasm, via Ser-10 phosphorylation, where it colocalized with F-actin. Introduction of transducible p27 protein (TATp27) was sufficient for actin cytoskeletal rearrangement and migration of HepG2 cells. TATp27 mutational analysis identified a novel p27 C-terminal domain required for cell migration, distinct from the N-terminal cyclin-cyclin-dependent kinase (cdk) binding domain. Loss or disruption of the p27 C-terminal domain abolished both actin rearrangement and cell migration. The cell-scattering activity of p27 occurred independently of its cell cycle arrest functions and required cytoplasmic localization of p27 via Ser-10 phosphorylation. Furthermore, Rac GTPase was necessary for p27-dependent migration but alone was insufficient for HepG2 cell migration. These results predicted a migration defect in p27-deficient cells. Indeed, p27-deficient primary fibroblasts failed to migrate, and reconstitution with TATp27 rescued the motility defect. These observations define a novel role for p27 in cell motility that is independent of its function in cell cycle inhibition.

Indexed as

CDC2-CDC28 KinasesRepressor ProteinsSaccharomyces cerevisiae ProteinsActinsAmino Acid SequenceCarcinoma, HepatocellularCell CycleCell Cycle ProteinsCell MovementCells, CulturedCyclin ACyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent Kinase Inhibitor ProteinsCyclin-Dependent KinasesCytoplasmActinsCDC2-CDC28 KinasesCDK2 protein, humanCell Cycle ProteinsCyclin ACyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent Kinase Inhibitor ProteinsCyclin-Dependent KinasesFAR1 protein, S cerevisiaeFungal ProteinsHepatocyte Growth FactorMAS1 protein, humanProtein Serine-Threonine KinasesProto-Oncogene Masrac GTP-Binding ProteinsRecombinant ProteinsRepressor ProteinsSaccharomyces cerevisiae ProteinsTumor Suppressor Proteins

Identifiers

PMID12482975
PMCPMC140659
OpenAlexW2139829576

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.