Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coagulase-negative staphylococci are now the major cause of bacteremia in neonatal intensive care units. To date, coagulase-negative staphylococci causing neonatal infections have been found to be distinct when typed by standard techniques. To determine whether or not an endemic strain could be identified using more discriminatory techniques, we characterized coagulase-negative staphylococci isolates obtained from a prospective study of coagulase-negative staphylococci bacteremia in a neonatal intensive care unit during 1984 through 1985, by standard techniques supplemented with DNA-DNA hybridization and restriction endonuclease analysis. We typed 58 strains that were isolated from 52 episodes of bacteremia in 38 neonates. There were 46 isolates of Staphylococcus epidermidis. Three pairs of strains were identical, and each strain was from a different patient. There were 12 isolates of Staphylococcus haemolyticus. Ten were identical, referred to as strain TOR-35, and had been isolated from eight different infants. Characterization of strains obtained in 1986 from a prospective study of coagulase-negative staphylococci-colonizing neonates admitted to the same neonatal intensive care unit found the TOR-35 strain had colonized 6 of 17 neonates by day seven. A point prevalence survey of all neonates in the same neonatal intensive care unit in 1990 found 5 of 30 neonates to be colonized with the TOR-35 strain. Therefore, we were able to identify an endemic strain of S haemolyticus that caused multiple episodes of bacteremia during a 6-month period and remained present in the same environment for a 5-year period.
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PMID:An endemic strain of Staphylococcus haemolyticus colonizing and causing bacteremia in neonatal intensive care unit patients. 155 64

VMA1-derived endonuclease (VDE), a site-specific endonuclease in Saccharomyces cerevisiae, enters the nucleus to generate a double-strand break in the VDE-negative allelic locus, mediating the self-propagating gene conversion called homing. Although VDE is excluded from the nucleus in mitotic cells, it relocalizes at premeiosis, becoming localized in both the nucleus and the cytoplasm in meiosis. The nuclear localization of VDE is induced by inactivation of TOR kinases, which constitute central regulators of cell differentiation in S. cerevisiae, and by nutrient depletion. A functional genomic approach revealed that at least two karyopherins, Srp1p and Kap142p, are required for the nuclear localization pattern. Genetic and physical interactions between Srp1p and VDE imply direct involvement of karyopherin-mediated nuclear transport in this process. Inactivation of TOR signaling or acquisition of an extra nuclear localization signal in the VDE coding region leads to artificial nuclear localization of VDE and thereby induces homing even during mitosis. These results serve as evidence that VDE utilizes the host systems of nutrient signal transduction and nucleocytoplasmic transport to ensure the propagation of its coding region.
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PMID:Karyopherin-mediated nuclear import of the homing endonuclease VMA1-derived endonuclease is required for self-propagation of the coding region. 1258 91