Evidence map›Paper›PMID 15024070›Full record

ArticleMolecular and cellular biology2004

Cellular senescence requires CDK5 repression of Rac1 activity.

Kamilah Alexander, Hai-Su Yang, Philip W Hinds

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. 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
1.8field-weighted citation impact, top 16% 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, 67 citations in OpenAlex.

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  20. Cell senescence culturing methods.Methods in molecular biology (Clifton, N.J.) · 2013
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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.

Kamilah AlexanderDepartment of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Hai-Su Yang
Philip W Hinds
Harvard University · USTufts Medical Center · US

Funding

Role of pRb in Osteogenesis, Cell Cycle Exit and CancerR01AG020208 · NIA · TUFTS MEDICAL CENTER · PI HINDS, PHILIP W. · 2002 to 2011
$3.6M
NIA NIH HHS AG20208NIA NIH HHS R01 AG020208
6 · The paper itself

Abstract

Cellular senescence is a tumor-suppressive process characterized by an irreversible cell cycle exit, a unique morphology, and expression of senescence-associated beta-galactosidase (SA-beta-Gal). We report here a role for CDK5 in induction of senescent cytoskeletal changes. CDK5 activation is upregulated in senescing cells. The increased activity of CDK5 further reduces GTPase Rac1 activity and Pak activation. The repression of the activity of the GTPase Rac1 by CDK5 is required for expression of the senescent phenotype. CDK5 regulation of Rac1 activity is necessary for actin polymerization accompanying senescent morphology in response to expression of pRb, activated Ras, or continuous passage. Inhibition of CDK5 attenuates SA-beta-Gal expression and blocks actin polymerization. These results point to a unique, nonneuronal role for CDK5 in regulation of Rac1 activity in senescence, illuminating the mechanisms underlying induction of senescence and the senescent shape change.

Indexed as

Cellular SenescenceActinsAdenoviridaeCell Line, TumorCyclin-Dependent Kinase 5Cyclin-Dependent KinasesCytoskeletonEnzyme ActivationHumansPurinesrac1 GTP-Binding ProteinRecombinant Fusion ProteinsRetinoblastoma ProteinRoscovitineActinsCDK5 protein, humanCyclin-Dependent Kinase 5Cyclin-Dependent KinasesPurinesrac1 GTP-Binding ProteinRecombinant Fusion ProteinsRetinoblastoma ProteinRoscovitine

Identifiers

PMID15024070
PMCPMC371103
OpenAlexW2151605417

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.