TelAP2 links TelAP1 to the telomere complex in Trypanosoma brucei.

The extracellular parasite Trypanosoma brucei evades the immune system of the mammalian host by periodically exchanging its variant surface glycoprotein (VSG) coat. Hereby, only one VSG gene is transcribed from one of 15 subtelomeric so-called bloodstream form expression sites (BES) at any given timepoint, while all other BESs are silenced. VSG gene expression is altered by homologous recombination using a large VSG gene repertoire or by a so-called in situ switch, which activates a previously silent BES.

ZNF524 directly interacts with telomeric DNA and supports telomere integrity.

Telomeres are nucleoprotein structures at the ends of linear chromosomes. In humans, they consist of TTAGGG repeats, which are bound by dedicated proteins such as the shelterin complex. This complex blocks unwanted DNA damage repair at telomeres, e.

RISK FACTORS OF IN-HOSPITAL INFECTIONS OCCURRENCE IN HEALTHCARE INSTITUTIONS IN UKRAINE AND EU COUNTRIES.

The rapid development of modern scientific medicine and practice (development of genetic engineering, coronary angiography, use of microprocessors (microminiature implant in eye retina, 3D-print of implants, prostheses) is connected with the scientific-technical progress in recent years, which gave impetus to introduction of extremely complex treatment and diagnostic methods. The use of high-tech medical equipment requires the implementation of modern sanitary and anti-epidemic measures of disinfection and sterilization after each manipulation to prevent in-hospital infection/infectious diseases which are related to the grant of medicare (IHI/IPNMD). Every year in the USA, up to 2 million patients who received medical services are registered with IHI/IPNMD cases.

Selective pericentromeric heterochromatin dismantling caused by TP53 activation during senescence.

Cellular senescence triggers various types of heterochromatin remodeling that contribute to aging. However, the age-related mechanisms that lead to these epigenetic alterations remain elusive. Here, we asked how two key aging hallmarks, telomere shortening and constitutive heterochromatin loss, are mechanistically connected during senescence.

The Telomeric Protein TRF2 Regulates Replication Origin Activity within Pericentromeric Heterochromatin.

Heterochromatic regions render the replication process particularly difficult due to the high level of chromatin compaction and the presence of repeated DNA sequences. In humans, replication through pericentromeric heterochromatin requires the binding of a complex formed by the telomeric factor TRF2 and the helicase RTEL1 in order to relieve topological barriers blocking fork progression. Since TRF2 is known to bind the Origin Replication Complex (ORC), we hypothesized that this factor could also play a role at the replication origins (ORI) of these heterochromatin regions.