Evidence map›Paper›PMID 11134351›Full record

ArticleMolecular and cellular biology2001

A novel 16-kilodalton cellular protein physically interacts with and antagonizes the functional activity of c-myc promoter-binding protein 1.

A K Ghosh, M Majumder, R Steele, R A White, R B Ray

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In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 41 citations in OpenAlex.

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  12. Evolutionary fate of retroposed gene copies in the human genome.Proceedings of the National Academy of Sciences of the United States of America · 2006
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

A K GhoshDepartments of Pathology, Saint Louis University, St. Louis, Missouri 63104, USA.
M Majumder
R Steele
R A White
R B Ray
Children's Mercy Hospital · USSaint Louis University · ESUniversity of Missouri–St. Louis · US

Funding

FUNCTIONAL ROLE OF MBP 1R01CA052799 · NCI · SAINT LOUIS UNIVERSITY · PI RAY, RATNA B. · 1997 to 2006
$1.2M
CLONING &CHARACTER OF C-MYC PROMOTER BINDING PROTEINR29CA052799 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RAY, RATNA B · 1991 to 1996
–
NCI NIH HHS CA52799NCI NIH HHS R01 CA052799
6 · The paper itself

Abstract

We initially identified c-myc promoter-binding protein 1 (MBP-1) from a human cervical carcinoma cell expression library which negatively regulates c-myc promoter activity. A recent study demonstrated that MBP-1 acts as a general transcriptional repressor (A. K. Ghosh, R. Steele, and R. B. Ray, Mol. Cell. Biol. 19:2880-2886, 1999). In order to identify the cellular protein(s) interacting with MBP-1 for transcriptional regulation, a HeLa cell cDNA expression library was screened using a yeast two-hybrid system. An MBP-1-interacting cDNA encoding a polypeptide of 140 amino acid residues with an approximate molecular mass of 16 kDa was identified and named MBP-1 interacting protein-2A (MIP-2A). MIP-2A has a sequence similarity with an unknown mRNA and SEDL. Mutations in the SEDL gene, located at human chromosome Xp22, has recently been implicated with an X-linked genetic disease, although the function of SEDL gene product was not determined (A. K. Gedeon et al., Nat. Genet. 22:400-404, 1999). However, our results suggested the localization of MIP-2A at human chromosome 19. The specificity of interaction between MBP-1 and MIP-2A was verified by an in vitro glutathione S-transferase pulldown experiment, a mammalian two-hybrid analysis, and in vivo coimmunoprecipitation assays. Further analysis revealed that the amino-terminal domain of MBP-1 (amino acids 1 to 95) interacts with MIP-2A. Immunofluorescent staining suggested colocalization of MIP-2A and MBP-1 primarily in the perinuclear membrane of cells. Functional analysis demonstrated that MIP-2A relieves MBP-1 mediated transcriptional repression on c-myc promoter. Additionally, MIP-2A antagonizes cell growth regulatory role of MBP-1. Taken together, these results suggest the functional interaction of MIP-2A and MBP-1 in cell growth regulation.

Indexed as

DNA-Binding ProteinsGene Expression RegulationPhosphopyruvate HydrataseTumor Suppressor Proteins3T3 CellsAnimalsBinding SitesBiomarkers, TumorCell DeathCell DivisionChromosomes, Human, Pair 19Fluorescent Antibody TechniqueGenes, mycGenes, ReporterHeLa CellsHumansBiomarkers, TumorDNA-Binding ProteinsENO1 protein, humanMembrane Transport ProteinsNeoplasm ProteinsPhosphopyruvate HydrataseRepressor ProteinsTranscription FactorsTRAPPC2 protein, humanTumor Suppressor Proteins

Identifiers

PMID11134351
PMCPMC86643
OpenAlexW2136630287

What OpenQuestion holds

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Registered trials

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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.