Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome.

PLoS genetics - 1 Dec 2016

Hudson Damien F, Amor David J, Boys Amber, Butler Kathy, Williams Lorna, Zhang Tao, Kalitsis Paul

Abstract excerpt

Bloom syndrome is a recessive human genetic disorder with features of genome instability, growth deficiency and predisposition to cancer. The only known causative gene is the BLM helicase that is a member of a protein complex along with topoisomerase III alpha, RMI1 and 2, which maintains replication fork stability and dissolves double Holliday junctions to prevent genome instability. Here we report the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Bloom Syndrome
Share to Chromosomal Instability
Share to DNA Helicases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fanconi Anemia Complementation Group D2 Protein

Share to Genomic Instability

Share to Multiprotein Complexes

Share to Nuclear Proteins

Share to Sister Chromatid Exchange

Source

Open in PubMed Open full text

Identifiers

PMID: 27977684
DOI: 10.1371/journal.pgen.1006483
PMCID: PMC5157948

Genes

RMI2
BLM
FANCD2
RMI1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome.PMID 27977684Read ↗

The BLM-TOP3A-RMI1-RMI2 proximity map reveals that RAD54L2 suppresses sister chromatid exchangesSemantic proximity Read ↗

Mechanism of Bloom syndrome complex assembly required for double Holliday junction dissolution and genome stability.Semantic proximity Read ↗

Bloom helicase and DNA topoisomerase IIIalpha are involved in the dissolution of sister chromatids.Semantic proximity Read ↗

More complexity to the Bloom's syndrome complex.Semantic proximity Read ↗

Structure and cellular roles of the RMI core complex from the bloom syndrome dissolvasome.Semantic proximity Read ↗

Genomic instability and cancer: lessons from analysis of Bloom's syndrome.Semantic proximity Read ↗

Depletion of the bloom syndrome helicase stimulates homology-dependent repair at double-strand breaks in human chromosomes.Semantic proximity Read ↗

Bloom syndrome and the underlying causes of genetic instability.Semantic proximity Read ↗

Aberrant chromosome morphology in human cells defective for Holliday junction resolution.Semantic proximity Read ↗

FANCD2 regulates BLM complex functions independently of FANCI to promote replication fork recoverySemantic proximity Read ↗

The toposiomerase IIIalpha-RMI1-RMI2 complex orients human Bloom’s syndrome helicase for efficient disruption of D-loopsSemantic proximity Read ↗

The Bloom's syndrome protein (BLM) interacts with MLH1 but is not required for DNA mismatch repair.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.