ArticlePloS one2009
Arrest defective-1 controls tumor cell behavior by acetylating myosin light chain kinase.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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.
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.
Who cites it
36 citing papers in PubMed, 72 citations in OpenAlex.
- NAA10 (N-Alpha-Acetyltransferase 10): A Multifunctional Regulator in Development, Disease, and Cancer.Cells · 2025Review
- Illuminating the impact of N-terminal acetylation: from protein to physiology.Nature communications · 2025Review
- Naa10p promotes cell invasiveness of esophageal cancer by coordinating the c-Myc and PAI1 regulatory axis.Cell death & disease · 2022Article
- Biochemical analysis of novel NAA10 variants suggests distinct pathogenic mechanisms involving impaired protein N-terminal acetylation.Human genetics · 2022Article
- The role of protein acetylation in carcinogenesis and targeted drug discovery.Frontiers in endocrinology · 2022Review
- Hydroxylation of the Acetyltransferase NAA10 Trp38 Is Not an Enzyme-Switch in Human Cells.International journal of molecular sciences · 2021Article
- Naa10p and IKKα interaction regulates EMT in oral squamous cell carcinoma via TGF-β1/Smad pathway.Journal of cellular and molecular medicine · 2021Article
- NAA10 as a New Prognostic Marker for Cancer Progression.International journal of molecular sciences · 2020Review
- Stabilization of ADAM9 by N-α-acetyltransferase 10 protein contributes to promoting progression of androgen-independent prostate cancer.Cell death & disease · 2020Article
- Dual lysine and N-terminal acetyltransferases reveal the complexity underpinning protein acetylation.Molecular systems biology · 2020Article
- Characterization of Lysine Acetyltransferase Activity of Recombinant Human ARD1/NAA10.Molecules (Basel, Switzerland) · 2020Article
- Co-translational, Post-translational, and Non-catalytic Roles of N-Terminal Acetyltransferases.Molecular cell · 2019Review
- FIH permits NAA10 to catalyze the oxygen-dependent lysyl-acetylation of HIF-1α.Redox biology · 2018Article
- N-α-acetyltransferase 10 (NAA10) in development: the role of NAA10.Experimental & molecular medicine · 2018Review
- ARD1/NAA10 in hepatocellular carcinoma: pathways and clinical implications.Experimental & molecular medicine · 2018Review
- Spotlight on protein N-terminal acetylation.Experimental & molecular medicine · 2018Review
- ARD1/NAA10 acetylation in prostate cancer.Experimental & molecular medicine · 2018Review
- ARD1-mediated aurora kinase A acetylation promotes cell proliferation and migration.Oncotarget · 2017Article
- α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling.Molecular medicine reports · 2016Article
- Molecular mechanisms of OLIG2 transcription factor in brain cancer.Oncotarget · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe enhancement of cell motility is a critical event during tumor cell spreading. Since myosin light chain kinase (MLCK) regulates cell behavior, it is regarded as a promising target in terms of preventing tumor invasion and metastasis. Since MLCK was identified to be associated with human arrest defective-1 (hARD1) through yeast two-hybrid screening, we here tested the possibility that hARD1 acts as a regulator of MLCK and by so doing controls tumor cell motility. METHODOLOGY/PRINCIPAL
findingsThe physical interaction between MLCK and hARD1 was confirmed both in vivo and in vitro by immunoprecipitation assay and affinity chromatography. hARD1, which is known to have the activity of protein lysine epsilon-acetylation, bound to and acetylated MLCK activated by Ca(2+) signaling, and by so doing deactivated MLCK, which led to a reduction in the phosphorylation of MLC. Furthermore, hARD1 inhibited tumor cell migration and invasion MLCK-dependently. Our mutation study revealed that hARD1 associated with an IgG motif of MLCK and acetylated the Lys608 residue in this motif. The K608A-mutated MLCK was neither acetylated nor inactivated by hARD1, and its stimulatory effect on cell motility was not inhibited by hARD1. CONCLUSION/SIGNIFICANCE: These results indicate that hARD1 is a bona fide regulator of MLCK, and that hARD1 plays a crucial role in the balance between tumor cell migration and stasis. Thus, hARD1 could be a therapeutic target in the context of preventing tumor invasion and metastasis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.