Evidence map›Paper›PMID 24001773›Full record

ArticleMolecular and cellular biology2013

G-quadruplex structures formed at the HOX11 breakpoint region contribute to its fragility during t(10;14) translocation in T-cell leukemia.

Mridula Nambiar, Mrinal Srivastava, Vidya Gopalakrishnan, Sritha K Sankaran, Sathees C Raghavan

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Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

The trial behind it

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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

28 citing papers in PubMed, 53 citations in OpenAlex.

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  5. Mutations atMolecular and cellular biology · 2024
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  11. Characterization of G-quadruplex antibody reveals differential specificity for G4 DNA forms.DNA research : an international journal for rapid publication of reports on genes and genomes · 2020
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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Mridula NambiarDepartment of Biochemistry, Indian Institute of Science, Bangalore, India.
Mrinal Srivastava
Vidya Gopalakrishnan
Sritha K Sankaran
Sathees C Raghavan
Indian Institute of Science Bangalore · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The t(10;14) translocation involving the HOX11 gene is found in several T-cell leukemia patients. Previous efforts to determine the causes of HOX11 fragility were not successful. The role of non-B DNA structures is increasingly becoming an important cause of genomic instability. In the present study, bioinformatics analysis revealed two G-quadruplex-forming motifs at the HOX11 breakpoint cluster. Gel shift assays showed formation of both intra- and intermolecular G-quadruplexes, the latter being more predominant. The structure formation was dependent on four stretches of guanines, as revealed by mutagenesis. Circular dichroism analysis identified parallel conformations for both quadruplexes. The non-B DNA structure could block polymerization during replication on a plasmid, resulting in consistent K(+)-dependent pause sites, which were abolished upon mutation of G-motifs, thereby demonstrating the role of the stretches of guanines even on double-stranded DNA. Extrachromosomal assays showed that the G-quadruplex motifs could block transcription, leading to reduced expression of green fluorescent protein (GFP) within cells. More importantly, sodium bisulfite modification assay showed the single-stranded character at regions I and II of HOX11 in the genome. Thus, our findings suggest the occurrence of G-quadruplex structures at the HOX11 breakpoint region, which could explain its fragility during the t(10;14) translocation.

Indexed as

Chromosome FragilityG-QuadruplexesTranslocation, GeneticBase SequenceChromosome BreakpointsChromosome Fragile SitesChromosomes, Human, Pair 10Chromosomes, Human, Pair 14DNA ReplicationDNA, Single-StrandedGC Rich SequenceGene ExpressionGreen Fluorescent ProteinsHomeodomain ProteinsHumansK562 CellsDNA, Single-Strandedenhanced green fluorescent proteinGreen Fluorescent ProteinsHomeodomain ProteinsProto-Oncogene ProteinsTLX1 protein, human

Identifiers

PMID24001773
PMCPMC3811900
OpenAlexW1975763088

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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.