trinucleotide


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tri·nu·cle·o·tide

(trī-nū'klē-ō-tīd),
A combination of three adjacent nucleotides, free or in a polynucleotide or nucleic acid molecule; often used with specific reference to the unit (codon or anticodon) specifying a particular amino acid in expression of the genetic code.

trinucleotide

(trī-no͞o′klē-ə-tīd′, -nyo͞o′-)
n.
A triplet of nucleotides; a codon.

tri·nu·cle·o·tide

(trī-nū'klē-ō-tīd)
A combination of three adjacent nucleotides, free or in a polynucleotide or nucleic acid molecule; often used with specific reference to the unit (codon or anticodon) specifying a particular amino acid in expression of the genetic code.
References in periodicals archive ?
We genotyped 30 individuals of Meridiastra calcar from one population (Shell Harbour, New South Wales) at seven polymorphic trinucleotide loci (B202, B236, C8, C112, C114, C204a, C232), and 48 individuals of Patiria miniata from one population (Bamfield, British Columbia) at two of the same loci (B202, C8) plus five others (B11, B201, B209, C113, C210).
The relationship between Trinucleotide (GAA) Repeat Length and Clinical Features in Friedreich Ataxia.
The identification of microsatellite loci with trinucleotide and higher motif lengths is of particular interest as they are more easily resolvable with standard agarose-gel electrophoresis techniques, and thus, best meet the criteria required for the transfer of marker technology to research laboratories in developing countries.
Within a normal copy of the gene is a trinucleotide (CAG) that is repeated up to 29 times (Kremer et al., 1994).
Huntington's disease-like phenotype due to trinucleotide repeat expansion in the TBP and JPH3 genes.
Genes in normal individuals contain short lengths of trinucleotide repeats in which a combination of nucleotides, the building blocks of DNA, are repeated several times.
Hayden, "Patients' Rights to Laboratory Data: Trinucleotide Repeat Length in Huntington Disease" (1996) 62 Am.
It was reported in 1993 that HD is caused by an expanded trinucleotide repeat sequence on the short arm of chromosome 4.[7] Although several theories exist, it is not yet known how this mutation causes neuronal cell death and brain atrophy.
Both gene mutations involve a trinucleotide cytosine-guanine-guanine (CGG) repeat expansion (Verkerk et al., 1991; Knight et al., 1993; Gecz, Gedeon, Sutherland, & Mulley, 1996; Gu, Shen, Gibbs, & Nelson, 1996) that varies in size among both normal and mutated genes.
This disorder, as is the case with several other neurologic disorders including Huntington's Disease, results from an abnormally large number of repeats, i.e., expansion of a trinucleotide sequence (Orr H, Chung M, Banff S, et al, 1993), in the DNA of the SCA1 gene on chromosome 6 (Ranum LPW, Duvick LA, Rich SS, et al, 1991).
New facts about basic genetic phenomena are being discovered--e.g., five human genetic disorders have been found that are based on mutations involving expandable and contractible trinucleotide repeats.
We used seven pairs of trinucleotide microsatellite primers for P.