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Telomeric Sequences (telomeric + sequence)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

Small-Molecule Binding to the Nonquadruplex Form of the Human Telomeric Sequence

CHEMBIOCHEM, Issue 7 2007
Yuki Goto
The single-stranded region of the d(TTAGGG) repeat is known to form a G-quadruplex structure in vitro. We report here a novel naphthyridine tetramer (NT) ligand that induces a nonquadruplex structure in the single-stranded region of the human telomeric sequence. [source]

Comprehensive karyotyping of the HT-29 colon adenocarcinoma cell line

GENES, CHROMOSOMES AND CANCER, Issue 1 2002
Kanji Kawai
The tumor cell line HT-29 was derived from a primary adenocarcinoma of the rectosigmoid colon. HT-29 is hypertriploid (3n+) and has accumulated numerous chromosomal structural aberrations. To identify material involved in chromosome rearrangements, we performed a comprehensive cytogenetic analysis using G-banding, spectral karyotyping (SKY), and fluorescence in situ hybridization (FISH). The combination of molecular cytogenetic techniques enabled us to define the first comprehensive karyotype for HT-29. Seventeen marker chromosomes were found in 75,100% of metaphase cells, generally in a single copy per cell. We confirmed the composition of eight previously described markers, refined the classification of seven others, and identified two novel marker chromosomes. Notable aberrations included a reciprocal translocation between chromosomes 6 and 14 and an unusual, large derivative chromosome 8 composed entirely of 8q material. The telomere status, evaluated by FISH, revealed telomeric signals at the termini of all chromosomes. No interstitial telomeric sequences were observed in any cell. Although numerous chromosomal aberrations are present in HT-29, the cell line appears to have retained a high level of genomic stability during passage in culture since undergoing transformation. The excellent resolving power of SKY, coupled with additional information obtained from molecular cytogenetic analyses, will improve our ability to identify genetic lesions characteristic of cancer. © 2002 Wiley-Liss, Inc. [source]

Ageing mechanisms: the role of telomere loss

CLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 7 2001
P. Boukamp
The ends of the chromosomes are capped by specialized structures, the telomeres. These are comprised of tracts of hexanucleotid sequences and, in combination with specific proteins, protect the chromosome against degradation, fusion events and as being recognized as 'damaged' DNA; thus, they guarantee chromosomal integrity. Due to deficiencies during DNA replication, the telomeres continuously loose part of their sequences and it has been proposed that this loss is the liming factor for the replicative capacity of a cell, i.e. telomeric loss is the counting mechanism - the internal clock of ageing. In order to proliferate indefinitely, the cells must prevent telomere erosion and this is mostly achieved by upregulation or de novo expression of the ribonucleoprotein complex telomerase. This enzyme, which has a reverse-transcriptase activity, is able to add telomeric sequences to the outer most ends off the telomeres and thereby stabilize or even elongate the telomeres. As telomerase is expressed in about 90% of all tumours while expression is absent in many somatic tissues, it is not surprising that the causal role of telomere erosion is presently the most favoured hypothesis of cellular ageing. [source]