DNA helicase


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BLM

A gene on chromosome 15q26.1 that encodes a DExH box-containing DNA helicase with both DNA-stimulated ATPase and ATP-dependent DNA helicase activities, which is thought to suppress inappropriate recombination events.
 
Molecular pathology
BLM mutations cause Bloom syndrome.
References in periodicals archive ?
Instead, in vivo DNA replication methods for most organisms rely on a class of enzymes known as DNA helicases, which act to locally unwind dsDNA to create small ssDNA regions suitable for polymerase activity.
A set of four LAMP primers (JF3 and JB3, JBIP and JFIP) recognizing six distinct regions in the viral putative DNA helicase gene sequence (GenBank accession KC245087) was designed by using the Primer Explorer version 4 (http://primerexplorer.Jp/elamp4.0.0/index.html).
presented another line of evidence suggesting that the abundance of MCM proteins must be meant for functions other than DNA helicase activity.
Disease variants of the human mitochondrial DNA helicase encoded by C10orf2 differentially alter protein stability, nucleotide hydrolysis and helicase activity.
Mutations in any one of these genes, such as in the DNA helicase gene associated with Werner's syndrome, may trigger major portions of the aging phenotype.
These patients are homozygous for the BLM gene on the long arm of chromosome 15, which has also been recently shown to encode a DNA helicase [49].
Tamura, "A rat RuvB-like protein, TIP49a, is a germ cell-enriched novel DNA helicase," Journal of Biological Chemistry, vol.
Interactions between DNA helicases and frozen topoisomerase IV-quinolone-DNA ternary complexes.
To date, several genetic and biochemical studies have revealed the molecular and physiological functions of dna helicases. Moreover, protein three-dimension structural studies coupled with single molecule biophysical approaches have provided insights into structure-function relationships and reaction mechanisms of some key dna helicases.
The XP-B and XP-D DNA helicases unwind the region surrounding the damaged site, along with the XP-A, XP-G, and replication protein A (RPA) [14].
It is caused by null mutations at WRN locus, which codes for a member of RecQ family of DNA helicases.6-9,11 The disease is associated with excessive synthesis of collagen type I and III which is dependent on elevated messenger RNA(mRNA) levels.6 The locus of Werner Syndrome has been found on the short arm of chromosome 8 in both Japanese and non Japanes.5,7,11 Fibroblasts isolated from WS patients exhibit genomic instability, increased sensitivity to specific DNA damaging agents, slow proliferation, lengthened S-phase, and accelerated replicative senescence.5,7,16
Other topics include mediation and modulation of membrane-cytoskeleton interactions, metal binding affinity and selectivity in metalloproteins, translocation and unwinding mechanisms of RNA and DNA helicases, and the structure of eukaryotic RNA polymerases.