ArticleThe EMBO journal2011
Antagonistic TSC22D1 variants control BRAF(E600)-induced senescence.
Article in The EMBO journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 27 citations in OpenAlex.
- Epstein-Barr Virus Promotes Gastric Cancer Progression by Modulating m6A-Dependent YTHDF1-TSC22D1 Axis.Microorganisms · 2025Article
- TSC22D1 is a newly identified inhibitor of insulin secretion in pancreatic beta cells.The FEBS journal · 2025Article
- Article
- The dynamic effect of genetic variation on the in vivo ER stress transcriptional response in different tissues.G3 (Bethesda, Md.) · 2022Article
- Identification of Binding Proteins for TSC22D1 Family Proteins Using Mass Spectrometry.International journal of molecular sciences · 2021Article
- Embryonic Barcoding of Equipotent Mammary Progenitors Functionally Identifies Breast Cancer Drivers.Cell stem cell · 2020Article
- Specificity of Phosphorylation Responses to Mitogen Activated Protein (MAP) Kinase Pathway Inhibitors in Melanoma Cells.Molecular & cellular proteomics : MCP · 2018Article
- A Phosphoproteomic Comparison of B-RAFV600E and MKK1/2 Inhibitors in Melanoma Cells.Molecular & cellular proteomics : MCP · 2015Article
- Phosphoproteome dynamics in onset and maintenance of oncogene-induced senescence.Molecular & cellular proteomics : MCP · 2014Article
- Hepatic transforming growth factor-β 1 stimulated clone-22 D1 controls systemic cholesterol metabolism.Molecular metabolism · 2014Article
- A prognostic signature of G(2) checkpoint function in melanoma cell lines.Cell cycle (Georgetown, Tex.) · 2013Article
- TSC22D4 is a molecular output of hepatic wasting metabolism.EMBO molecular medicine · 2013Article
- Nuclear receptor binding protein 1 regulates intestinal progenitor cell homeostasis and tumour formation.The EMBO journal · 2012Article
- Narrowing the knowledge gaps for melanoma.Upsala journal of medical sciences · 2012Review
- Transforming growth factor-β-stimulated clone-22 is a negative-feedback regulator of Ras / Raf signaling: Implications for tumorigenesis.Cancer science · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncogene-induced cellular senescence (OIS) is an increasingly recognized tumour suppressor mechanism that confines the outgrowth of neoplastic cells in vivo. It relies on a complex signalling network, but only few components have been identified so far. Gene-expression profiling revealed a >100-fold increase in the levels of the transcription factor and putative tumour suppressor gene TGFβ-stimulated clone 22 (TSC22D1) in BRAF(E600)-induced senescence, in both human fibroblasts and melanocytes. Only the short TSC22D1 transcript was upregulated, whereas the abundance of the large protein variant was suppressed by proteasomal degradation. The TSC22D1 protein variants, in complex with their dimerization partner TSC22 homologue gene 1 (THG1), exerted opposing functions, as selective depletion of the short form, or conversely, overexpression of the large variant, resulted in abrogation of OIS. This was accompanied by the suppression of several inflammatory factors and p15(INK4B), with TSC22D1 acting as a critical effector of C/EBPβ. Our results demonstrate that the differential regulation of antagonistic TSC22D1 variants is required for the establishment of OIS and suggest distinct contributions of TSC22 family members to the progression of BRAF(E600)-driven neoplasia.
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.