ArticleOncogene2001
Cytoskeletal organization in tropomyosin-mediated reversion of ras-transformation: Evidence for Rho kinase pathway.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 47 citations in OpenAlex.
- The remodelling of actin composition as a hallmark of cancer.Translational oncology · 2021Review
- Epigenetic silencing of TPM2 contributes to colorectal cancer progression upon RhoA activation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Crosstalk of Ras and Rho: activation of RhoA abates Kras-induced liver tumorigenesis in transgenic zebrafish models.Oncogene · 2014Article
- From the Cover: Neutralization of terminal differentiation in gliomagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Protein Expression of STRO-1 Cells in Response to Different Topographic Features.Journal of tissue engineering · 2011Article
- New insights into the regulation of the actin cytoskeleton by tropomyosin.International review of cell and molecular biology · 2010Review
- A mediator of Rho-dependent invasion moonlights as a methionine salvage enzyme.Molecular & cellular proteomics : MCP · 2009Article
- Differential tissue-specific protein markers of vaginal carcinoma.British journal of cancer · 2009Article
- Caldesmon and the regulation of cytoskeletal functions.Advances in experimental medicine and biology · 2008Review
- Identification of squamous cell carcinoma associated proteins by proteomics and loss of beta tropomyosin expression in esophageal cancer.World journal of gastroenterology · 2006Article
- Resensitization of breast cancer cells to anoikis by tropomyosin-1: role of Rho kinase-dependent cytoskeleton and adhesion.Oncogene · 2005Article
- Human diploid fibroblasts are resistant to MEK/ERK-mediated disruption of the actin cytoskeleton and invasiveness stimulated by Ras.Oncogene · 2005Article
- Loss of expression of tropomyosin-1, a novel class II tumor suppressor that induces anoikis, in primary breast tumors.Oncogene · 2003Article
- Functional analysis of the actin-binding protein, tropomyosin 1, in neuroblastoma.British journal of cancer · 2003Article
- Extracellular signal-regulated kinase mediates phosphorylation of tropomyosin-1 to promote cytoskeleton remodeling in response to oxidative stress: impact on membrane blebbing.Molecular biology of the cell · 2003Article
- Overexpression of kinase suppressor of Ras upregulates the high-molecular-weight tropomyosin isoforms in ras-transformed NIH 3T3 fibroblasts.Molecular and cellular biology · 2003Article
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 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tropomyosin (TM) family of cytoskeletal proteins is implicated in stabilizing actin microfilaments. Many TM isoforms, including tropomyosin-1 (TM1), are down-regulated in transformed cells. Previously we demonstrated that TM1 is a suppressor of the malignant transformation, and that TM1 reorganizes microfilaments in the transformed cells. To investigate how TM1 induces microfilament organization in transformed cells, we utilized ras-transformed NIH3T3 (DT) cells, and those transduced to express TM1, and/or TM2. Enhanced expression of TM1 alone, but not TM2, results in re-emergence of microfilaments; TM1, together with TM2 remarkably improves microfilament architecture. TM1 induced cytoskeletal reorganization involves an enhanced expression of caldesmon, but not vinculin, alpha-actinin, or gelsolin. In addition, TM1-induced cytoskeletal reorganization and the revertant phenotype appears to involve re-activation of RhoA controlled pathways in DT cells. RhoA expression, which is suppressed in DT cells, is significantly increased in TM1-expressing cells, without detectable changes in the expression of Rac or Cdc42. Furthermore, expression of a dominant negative Rho kinase, or treatment with Y-27632 disassembled microfilaments in normal NIH3T3 and in TM1 expressing cells. These data suggest that reactivation of Rho kinase directed pathways are critical for TM1-mediated microfilament assemblies.
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.