ArticlePloS one2010
p21-Activated kinases are required for transformation in a cell-based model of neurofibromatosis type 2.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 23 citations in OpenAlex.
- Regulation of Cancer Metastasis by PAK2.International journal of molecular sciences · 2024Review
- NF2-Related Schwannomatosis (NF2): Molecular Insights and Therapeutic Avenues.International journal of molecular sciences · 2024Review
- p21-Activated Kinases in Thyroid Cancer.Endocrinology · 2020Review
- Nonsteroidal sulfamate derivatives as new therapeutic approaches for Neurofibromatosis 2 (NF2).BMC pharmacology & toxicology · 2019Article
- Group I Paks are essential for epithelial- mesenchymal transition in an Apc-driven model of colorectal cancer.Nature communications · 2018Article
- Targeting group I p21-activated kinases to control malignant peripheral nerve sheath tumor growth and metastasis.Oncogene · 2017Article
- Comprehensive pharmacological profiling of neurofibromatosis cell lines.American journal of cancer research · 2017Article
- Inhibiting p21-Activated Kinase Induces Cell Death in Vestibular Schwannoma and Meningioma via Mitotic Catastrophe.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2017Article
- Crizotinib inhibits NF2-associated schwannoma through inhibition of focal adhesion kinase 1.Oncotarget · 2016Article
- Group I Paks as therapeutic targets in NF2-deficient meningioma.Oncotarget · 2015Article
- FRAX597, a small molecule inhibitor of the p21-activated kinases, inhibits tumorigenesis of neurofibromatosis type 2 (NF2)-associated Schwannomas.The Journal of biological chemistry · 2013Article
- Article
- Neurofibromatosis type 2 protein, NF2: an uncoventional cell cycle regulator.Anticancer research · 2013Review
- Vulvar malignancy in neurofibromatosis syndrome.Case reports in obstetrics and gynecology · 2013Article
- Group I p21-activated kinases (PAKs) promote tumor cell proliferation and survival through the AKT1 and Raf-MAPK pathways.Molecular cancer research : MCR · 2012Article
- PAK signaling in cancer.Cellular logistics · 2012Article
- p21-activated kinase 1: PAK'ed with potential.Oncotarget · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNF2 is an autosomal dominant disease characterized by development of bilateral vestibular schwannomas and other benign tumors in central nervous system. Loss of the NF2 gene product, Merlin, leads to aberrant Schwann cell proliferation, motility, and survival, but the mechanisms by which this tumor suppressor functions remain unclear. One well-defined target of Merlin is the group I family of p21-activated kinases, which are allosterically inhibited by Merlin and which, when activated, stimulate cell cycle progression, motility, and increased survival. Here, we examine the effect of Pak inhibition on cells with diminished Merlin function. METHODOLOGY/PRINCIPAL
findingsUsing a specific peptide inhibitor of group I Paks, we show that loss of Pak activity restores normal cell movement in cells lacking Merlin function. In addition, xenografts of such cells form fewer and smaller tumors than do cells without Pak inhibition. However, in tumors, loss of Pak activity does not reduce Erk or Akt activity, two signaling proteins that are thought to mediate Pak function in growth factor pathways. CONCLUSIONS/SIGNIFICANCE: These results suggest that Pak functions in novel signaling pathways in NF2, and may serve as a useful therapeutic target in this disease.
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.