ArticleJournal of molecular biology2007
Jab1 mediates protein degradation of the Rad9-Rad1-Hus1 checkpoint complex.
Article in Journal of molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- The emerging roles of Jab1/CSN5 in cancer.Medical oncology (Northwood, London, England) · 2016Pooled it
- HUS1 as a Potential Therapeutic Target in Urothelial Cancer.Journal of clinical medicine · 2022Article
- Corrected and Republished from: The COP9 Signalosome Interacts with and Regulates Interferon Regulatory Factor 5 Protein Stability.Molecular and cellular biology · 2018Article
- Neuritin 1 expression in human normal tissues and its association with various human cancers.International journal of clinical and experimental pathology · 2018Article
- Neuritin Inhibits Notch Signaling through Interacted with Neuralized to Promote the Neurite Growth.Frontiers in molecular neuroscience · 2017Article
- The Role of the COP9 Signalosome and Neddylation in DNA Damage Signaling and Repair.Biomolecules · 2015Review
- Loss of jab1 in osteochondral progenitor cells severely impairs embryonic limb development in mice.Journal of cellular physiology · 2014Article
- Emerging roles of Jab1/CSN5 in DNA damage response, DNA repair, and cancer.Cancer biology & therapy · 2014Review
- Dynamic regulation of the COP9 signalosome in response to DNA damage.Molecular and cellular biology · 2014Article
- Different expression of miRNAs targeting helicases in rice in response to low and high dose rate γ-ray treatments.Plant signaling & behavior · 2013Article
- Differential miRNA expression profiles in proliferating or differentiated keratinocytes in response to gamma irradiation.BMC genomics · 2013Article
- The COP9 signalosome interacts with and regulates interferon regulatory factor 5 protein stability.Molecular and cellular biology · 2013Article
- The transcriptional co-regulator Jab1 is crucial for chondrocyte differentiation in vivo.Journal of cell science · 2013Article
- Low penetrance alleles as risk modifiers in familial and sporadic breast cancer.Familial cancer · 2012Article
- JAB1/CSN5: a new player in cell cycle control and cancer.Cell division · 2010Article
- The COP9 signalosome negatively regulates proteasome proteolytic function and is essential to transcription.The international journal of biochemistry & cell biology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The Rad1-Rad9-Hus1 (9-1-1) complex serves a dual role as a DNA-damage sensor in checkpoint signaling and as a mediator in the DNA repair pathway. However, the intercellular mechanisms that regulate the 9-1-1 complex are poorly understood. Jab1, the fifth component of the COP9 signalosome complex, has a central role in the degradation of multiple proteins and is emerging as an important regulator in cancer development. Here, we tested the hypothesis that Jab1 controls the protein stability of the 9-1-1 complex via the proteosome pathway. We provide evidence that Jab1 physically associates with the 9-1-1 complex, and show that this association is mediated through direct interaction between Jab1 and Rad1, one of the subunits of the 9-1-1 complex. Importantly, Jab1 causes translocation of the 9-1-1 complex from the nucleus to the cytoplasm, mediating rapid degradation of the 9-1-1 complex via the 26 S proteasome. Furthermore, Jab1 significantly suppresses checkpoint signaling activation, DNA synthesis recovery from blockage and cell viability after replication stresses such as UV exposure, gamma radiation and treatment with hydroxyurea. These results suggest that Jab1 is an important regulator for the stability of protein 9-1-1 control in cells, which may provide novel information on the involvement of Jab1 in the checkpoint and DNA repair signaling in response to DNA damage.
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.