Publications by authors named "W Krzeptowski"

Heme oxygenase-1 (HO-1, HMOX1) degrades heme protecting cells from heme-induced oxidative damage. Beyond its well-established cellular functions, heme has emerged as a stabilizer of G-quadruplexes. These secondary DNA structures interfere with DNA replication.

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Article Synopsis
  • Mesencephalic Astrocyte-derived Neurotrophic Factor (MANF), specifically DmMANF in fruit flies, is found in various clusters of clock neurons but its precise role is not well understood.! -
  • The study reveals that while DmMANF is present in several types of neurons, its expression in particular ventral lateral neurons is independent of the circadian clock but silencing it disrupts locomotor rhythms in different lighting conditions.! -
  • DmMANF is essential for the normal structure of specific interneurons in the visual system and plays a key role in maintaining the circadian adaptability of their dendritic structures.!
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DmMANF, Drosophila melanogaster mesencephalic astrocyte-derived neurotrophic factor (DmMANF) is an evolutionarily conserved orthologue of mammalian MANF. This neurotrophic factor exerts many functions in the Drosophila brain, particularly those dependent on glial cells. As we found in our earlier study, downregulation of DmMANF in glia induces degeneration of glial cells in the first optic neuropil (lamina) where DmMANF abundance is especially high.

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G-quadruplexes (G4) are stacked nucleic acid structures that are stabilized by heme. In cells, they affect DNA replication and gene transcription. They are unwound by several helicases but the composition of the repair complex and its heme sensitivity are unclear.

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Jackson toxic milk mutant mice (tx-J) carrying a missense mutation in the Atp7b gene are animal models of the Wilson disease. In both the Wilson patients and the tx-J mice, mutations in the ATP7B/Atp7b gene lead to disturbances in copper metabolism. The dysfunction of ATP7B/Atp7b leads to a reduction in the incorporation of copper into apoceruloplasmin; this decreases the ferroxidase activity of ceruloplasmin necessary for the efflux of iron from cells and reduces the release of copper from hepatocytes to the bile; this results in a massive hepatic copper accumulation.

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