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Copy-number variants (CNVs) are an important class of genetic variation that can mediate rapid adaptive evolution. Whereas CNVs can increase the relative fitness of the organism, they can also incur a cost due to the associated increased gene expression and repetitive DNA. We previously evolved populations of Saccharomyces cerevisiae over hundreds of generations in glutamine-limited (Gln-) chemostats and observed the recurrent evolution of CNVs at the GAP1 locus.

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A novel bacterium, designated 19SA41, was isolated from the air of the Icelandic volcanic island Surtsey. Cells of strain 19SA41 are Gram-stain-negative, strictly aerobic, non-motile rods and form pale yellow-pigmented colonies. The strain grows at 4-30 °C (optimum, 22 °C), at pH 6-10 (optimum, pH 7.

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Background: The effects of ionizing radiation (IR) involve a highly orchestrated series of events in cells, including DNA damage and repair, cell death, and changes in the level of proliferation associated with the stage of the cell cycle. A large number of existing studies in literature have examined the activity of genes and their regulators in mammalian cells in response to high doses of ionizing radiation. Although there are many studies, the research in effect of low doses of ionizing radiation remains limited.

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Metagenomes present a source for novel enzymes, but under 1% of environmental microbes are cultivatable. Because of its useful properties, Escherichia coli has been used as a host organism in functional genomic screens. However, due to differing expression machineries in the expression host compared to the source organism of the DNA sequences, screening outcomes can be biased.

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DNA Damage-Induced Ferroptosis: A Boolean Model Regulating p53 and Non-Coding RNAs in Drug Resistance.

Proteomes

January 2025

Instituto de Matemática e Estatística, Departamento de Ciência da Computação, Universidade de São Paulo, Rua do Matão 1010, São Paulo 05508-090, SP, Brazil.

The tumor suppressor p53, in its wild-type form, plays a central role in cellular homeostasis by regulating senescence, apoptosis, and autophagy within the DNA damage response (DDR). Recent findings suggest that wild-type p53 also governs ferroptosis, an iron-dependent cell death process driven by lipid peroxidation. Post-translational modifications of p53 generate proteoforms that significantly enhance its functional diversity in regulating these mechanisms.

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