ArticleOncogene2009
Proteasome-mediated degradation of Tob is pivotal for triggering UV-induced apoptosis.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 14 citations in OpenAlex.
- TOB is an effector of the hippocampus-mediated acute stress response.Translational psychiatry · 2022Article
- Reevaluation of ATR signaling in primary resting chronic lymphocytic leukemia cells: evidence for pro-survival or pro-apoptotic function.Oncotarget · 2017Article
- Transducer of ERBB2.1 (TOB1) as a Tumor Suppressor: A Mechanistic Perspective.International journal of molecular sciences · 2015Review
- Tob2 inhibits peroxisome proliferator-activated receptor γ2 expression by sequestering Smads and C/EBPα during adipocyte differentiation.Molecular and cellular biology · 2012Article
- Inhibition of DNA damage-induced apoptosis through Cdc7-mediated stabilization of Tob.The Journal of biological chemistry · 2012Article
- MG132 inhibition of proteasome blocks apoptosis induced by severe DNA damage.Cell cycle (Georgetown, Tex.) · 2011Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eukaryotic cells respond to genotoxic stress by inducing cell growth arrest or apoptosis. Although the p53 tumor suppressor largely contributes to the response by regulating antiproliferative or pro-apoptotic genes, some genotoxic stresses including ultraviolet (UV) light induce apoptosis even in the absence of p53. The molecular mechanisms by which cells respond to UV in the p53-independent manner remain to be established. Here, we show that UV-induced stress promotes proteasome-dependent degradation of Tob, triggering an apoptotic signal. We found that Tob with either short deletion or a tag sequence at the C terminus was resistant to UV-induced degradation. Introduction of the degradation-resistant Tob impaired UV-induced apoptosis. Reciprocally, suppression of Tob by small interfering RNA (siRNA) resulted in frequent induction of apoptosis irrespective of the presence of functional p53 even at UV doses that do not promote Tob degradation. Finally, tob-deficient (tob(-/-)) mice and primary embryonic fibroblasts (MEFs) from tob(-/-) mice exhibit increased sensitivity to UV irradiation. Thus, proteasomal clearance of Tob provides a novel p53-independent pathway for UV-induced apoptosis.
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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.