ArticleGene regulation and systems biology2008
The MAPK signaling cascade is a central hub in the regulation of cell cycle, apoptosis and cytoskeleton remodeling by tripeptidyl-peptidase II.
Article in Gene regulation and systems biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Transcriptome Analysis Identifies Strategies Targeting Immune Response-Related Pathways to Control EnterotoxigenicFrontiers in veterinary science · 2021Article
- Promotive effect of Talin-1 protein on gastric cancer progression through PTK2-PXN-VCL-E-Cadherin-CAPN2-MAPK1 signaling axis.Journal of clinical laboratory analysis · 2020Article
- Transcriptome analysis and identification of significantly differentially expressed genes in Holstein calves subjected to severe thermal stress.International journal of biometeorology · 2017Article
- The protein-interaction network with functional roles in tumorigenesis, neurodegeneration, and aging.Molecular and cellular biochemistry · 2016Review
- Tripeptidyl Peptidase II Mediates Levels of Nuclear Phosphorylated ERK1 and ERK2.Molecular & cellular proteomics : MCP · 2015Article
- Differential gene expression profiling of porcine epithelial cells infected with three enterotoxigenic Escherichia coli strains.BMC genomics · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripeptidyl-peptidase II (TPPII) is a serine peptidase highly expressed in malignant Burkitt's lymphoma cells (BL). We have previously shown that overexpression of TPPII correlates with chromosomal instability, centrosomal and mitotic spindle abnormalities and resistance to apoptosis induced by spindle poisons. Furthermore, TPPII knockdown by RNAi was associated with endoreplication and the accumulation of polynucleated cells that failed to complete cell division, indicating a role of TPPII in the cell cycle. Here we have applied a global approach of gene expression analysis to gain insights on the mechanism by which TPPII regulates this phenotype. mRNA profiling of control and TPPII knockdown BL cells identified one hundred and eighty five differentially expressed genes. Functional categorization of these genes highlighted major physiological functions such as apoptosis, cell cycle progression, cytoskeleton remodeling, proteolysis, and signal transduction. Pathways and protein interactome analysis revealed a significant enrichment in components of MAP kinases signaling. These findings suggest that TPPII influences a wide network of signaling pathways that are regulated by MAPKs and exerts thereby a pleiotropic effect on biological processes associated with cell survival, proliferation and genomic instability.
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