ArticleMolecular and cellular biology2003
Regulation of RelA (p65) function by the large subunit of replication factor C.
Article in Molecular and cellular biology, 2003. 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, 25 citations in OpenAlex.
- A Hypothesis-Generating Pharmacologic Profile for Sargramostim Treatment of Parkinson's Disease.Cellular and molecular neurobiology · 2026Trial
- Participation of host cell proteins in inclusion bodies of non-segmented RNA virus infected cells: a molecular insight.Virology journal · 2025Review
- Disruption of the moonlighting function of CTF18 in a patient with T-lymphopenia.Frontiers in immunology · 2025Article
- Temporal modulation of the NF-κB RelA network in response to different types of DNA damage.The Biochemical journal · 2021Article
- Review
- Overexpression of RFC3 is correlated with ovarian tumor development and poor prognosis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Evolutionary conserved regulation of HIF-1β by NF-κB.PLoS genetics · 2011Article
- Adenomatous polyposis coli and hypoxia-inducible factor-1{alpha} have an antagonistic connection.Molecular biology of the cell · 2010Article
- IKK and NF-kappaB-mediated regulation of Claspin impacts on ATR checkpoint function.The EMBO journal · 2010Article
- Regulation of hypoxia-inducible factor-1alpha by NF-kappaB.The Biochemical journal · 2008Article
- Proenkephalin assists stress-activated apoptosis through transcriptional repression of NF-kappaB- and p53-regulated gene targets.Cell death and differentiation · 2007Article
- Recruitment of DNA repair synthesis machinery to sites of DNA damage/repair in living human cells.Nucleic acids research · 2007Article
- The FHA domain protein SNIP1 is a regulator of the cell cycle and cyclin D1 expression.Oncogene · 2004Article
- Association of differentially expressed genes with activation of mouse hepatic stellate cells by high-density cDNA microarray.World journal of gastroenterology · 2004Article
- The p53-inhibitor pifithrin-alpha inhibits firefly luciferase activity in vivo and in vitro.BMC molecular biology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The RelA (p65) subunit of NF-kappaB is an important regulator of inflammation, proliferation, and apoptosis. We have discovered that the large subunit, p140, of replication factor C (RFC) can function as a regulator of RelA. RFC is a clamp loader, facilitating the addition and removal of proliferating-cell nuclear antigen from DNA during replication and repair but can also interact directly with the retinoblastoma tumor suppressor protein and the transcription factor C/EBPalpha. We find that RFC (p140) interacts with RelA both in vitro and in vivo and stimulates RelA transactivation. In contrast, coexpression of fragments of RFC (p140) that mediate the interaction with RelA results in transcriptional inhibition. The significance of this regulation was confirmed by using short interfering RNA oligonucleotides targeted to RFC (p140). Down regulation of endogenous RFC (p140) inhibits expression from a chromosomally integrated reporter plasmid induced by endogenous, TNF-alpha-activated NF-kappaB. Dominant negative fragments of RFC (p140) also cooperate with overexpressed RelA to induce cell death. Interestingly, RFC (p140) also interacts with the tumor suppressor p53. Taken together, these observations suggest that, in addition to its previously described function in DNA replication and repair, RFC (p140) has an important role as a regulator of transcription and NF-kappaB activity.
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.