Evidence map›Paper›PMID 18704644›Full record

ArticleMolecular and cellular biochemistry2009

Knockdown endogenous CypA with siRNA in U2OS cells results in disruption of F-actin structure and alters tumor phenotype.

Colonya C Calhoun, Ying-Chun Lu, Jun Song, Robert Chiu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Colonya C CalhounDental Research Institute, UCLA School of Dentistry, Los Angeles, CA 90095, USA.
Ying-Chun Lu
Jun Song
Robert Chiu
University of California, Los Angeles · US

Funding

UCLA FUNDAMENTAL CLINICAL RESEARCH TRAINING PROGRAMT32DE007296 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WONG, DAVID T · 1996 to 2011
$5.8M
Cellular Regulations by RB-Associated ProteinsR01CA066746 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHIU, ROBERT · 1995 to 2005
$1.2M
NCI NIH HHS CA066746NIDCR NIH HHS T32 DE07296
6 · The paper itself

Abstract

Cyclophilin A (CypA) was originally identified as a cytosolic protein possessing peptidyl-prolyl isomerase activity. CypA has been shown to play a pivotal role in the immune response, but little is known about other molecular mechanisms of CypA-mediated biologic events. In our present study, we demonstrate that knockdown CypA expression using RNAi in U2OS cells resulted in disruption of the F-actin structure, as well as decreased anchorage-independent growth, proliferation, and migration. Wild-type U2OS cells treated with cyclosporine A (CsA), a peptidyl-prolyl isomerase inhibitor, displayed the same phenotype as knockdown CypA cells, suggesting that the isomerase activity of CypA is required to maintain a normal phenotype. In vitro and in vivo binding assays revealed that CypA binds to N-WASP, which functions in the nucleation of actin via the Arp2/3 complex. Pulse-chase labeling study indicated an enhanced degradation of N-WASP in cell lacking CypA, suggesting that CypA is required for stabilizing N-WASP to form a N-WASP/Arp2/3 complex for the nucleation/initiation of F-actin polymerization.

Indexed as

Cyclophilin AGene Knockdown TechniquesNeoplasmsRNA, Small InterferingActinsAnimalsCell Line, TumorCell MovementGene SilencingHumansWiskott-Aldrich Syndrome Protein, NeuronalActinsCyclophilin ARNA, Small InterferingWiskott-Aldrich Syndrome Protein, Neuronal

Identifiers

PMID18704644
OpenAlexW2043905366

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.