ArticleMolecular biology reports2013
Human TTC5, a novel tetratricopeptide repeat domain containing gene, activates p53 and inhibits AP-1 pathway.
Article in Molecular biology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 5 citations in OpenAlex.
- TTC5 syndrome: Clinical and molecular spectrum of a severe and recognizable condition.American journal of medical genetics. Part A · 2022Article
- Evaluation of the Role of p53 Tumour Suppressor Posttranslational Modifications and TTC5 Cofactor in Lung Cancer.International journal of molecular sciences · 2021Article
- The Effect of Wenxin Keli on the mRNA Expression Profile of Rabbits with Myocardial Infarction.Evidence-based complementary and alternative medicine : eCAM · 2016Article
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
The transcription factor p53 and AP-1 play an important role in cellular proliferation, transformation and death. In this study, we investigated the role of a novel human gene, TTC5 (tetratricopeptide repeat domain 5), in the regulation of cell signaling pathway and cell viability. TTC5 is a member of the TTC family of proteins and has previously been shown to participate in cellular stress response. Here we demonstrate for the first time that TTC5 significantly activates p53 pathway and inhibits AP-1 transcriptional activity. Further investigation revealed that overexpression of TTC5 up-regulated p53 and p21 expression, and significantly inhibited transcriptional activity, expression and phosphorylation of c-Jun. As for the upstream of signaling pathway of AP-1, our study demonstrated that overexpression of TTC5 significantly down-regulated the expression and phosphorylation of JNK/SAPK. Moreover, overexpression of TTC5 repressed cell proliferation and induced S phase cell cycle arrest. These results indicated that TTC5 may regulate cell viability by p53 and AP-1 signaling pathway.
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.