ArticleBlood2006
JAZ mediates G1 cell-cycle arrest and apoptosis by positively regulating p53 transcriptional activity.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Methylation-regulated ZNF545 inhibits growth of the p53-mutant KYSE150 cell line by inducing p21 and Bax.Experimental and therapeutic medicine · 2019Article
- Trichinella spiralis and Tumors: Cause, Coincidence or Treatment?Anti-cancer agents in medicinal chemistry · 2018Review
- JAZ (Znf346), a SIRT1-interacting protein, protects neurons by stimulating p21 (WAF/CIP1) protein expression.The Journal of biological chemistry · 2014Article
- Structural characterization of interactions between the double-stranded RNA-binding zinc finger protein JAZ and nucleic acids.Biochemistry · 2014Article
- Genomic analysis of wig-1 pathways.PloS one · 2012Article
- The p53 target Wig-1: a regulator of mRNA stability and stem cell fate?Cell death and differentiation · 2011Review
- JAZ mediates G1 cell cycle arrest by interacting with and inhibiting E2F1.Cell cycle (Georgetown, Tex.) · 2011Article
- Activation of tumor suppressor protein p53 is required for Theiler's murine encephalomyelitis virus-induced apoptosis in M1-D macrophages.Journal of virology · 2009Article
- The p53 target Wig-1 regulates p53 mRNA stability through an AU-rich element.Proceedings of the National Academy of Sciences of the United States of America · 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
4 authors at 1 institution in 1 country.
Funding
Abstract
We previously identified JAZ as a novel zinc finger (ZF) protein by screening a murine interleukin-3 (IL-3)-dependent NFS/N1.H7 myeloid cell cDNA library. JAZ is a member of a new class of ZFPs that is evolutionarily conserved and preferentially binds to dsRNA, but its function was unknown. Now, we report that the stress of IL-3 growth factor withdrawal up-regulates JAZ expression in hematopoietic cells in association with p53 activation and induction of cell death. Biochemical analysis reveals that JAZ associates with p53 to stimulate its transcriptional activity in p53-expressing cells, but not in p53-null cells unless complemented with p53. JAZ functions to mediate G1 cell-cycle arrest followed by apoptosis in a p53-dependent mechanism that is associated with up-regulation of p21 and BAX, dephosphorylation of Rb, and repression of cyclin A. Of importance, siRNA "knockdown" of endogenous JAZ inhibits p53 transcriptional activity, decreases the G1/G0 population, and attenuates stress-induced cell death. While JAZ directly binds p53 in vitro in a mechanism requiring p53's C-terminal regulatory domain but independent of dsRNA, the dsRNA-binding ZF domains are required for JAZ's stimulatory role of p53 in vivo by dictating its nuclear localization. Thus, JAZ is a novel negative regulator of cell growth by positively regulating p53.
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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.