Dodatkowe przykłady dopasowywane są do haseł w zautomatyzowany sposób - nie gwarantujemy ich poprawności.
This exchange between homologues is most likely due to homologous sequences containing low copy repeats.
Smith-Magenis syndrome is a chromosomal condition related to low copy repeats of specific segments of chromosome 17.
CNVs occur due to non-allelic homologous recombination mediated by low copy repeats (sequentially similar regions).
Most gene duplications exist as low copy repeats (LCRs), rather highly repetitive sequences like transposable elements.
This sequence, while short, does not correspond to any of the known chromosome 15q11-q13 duplicon sequences, and therefore could represent a novel class of such low copy repeats.
It usually occurs between sequences of DNA that have been previously duplicated through evolution, and therefore have low copy repeats (LCRs).
Low copy repeats (LCRs), also known as segmental duplications (SDs), are highly homologous sequence elements within the eukaryotic genome.
Low copy repeats (LCRs), which are region-specific repeat sequences, are susceptible to such genomic rearrangements resulting in CNVs.
Segmental duplications give rise to low copy repeats (LCRs) and are believed to have played a role in creating new primate genes as reflected in human genetic variation.
Unique DNA sequences, known as low copy repeats, occur in the pericentric region of the p arm, so a crossover event in that area can create a dicentric isochromosome through U-type strand exchange.
The orientation of low copy repeats flanking the deleted segment, suggests the inversion in the parental chromosome influences the deletion in the child's chromosome via a non-allelic homologous recombination (NAHR) mechanism.
