Publications by authors named "D Cervia"
Article Synopsis
- Most mammalian mRNAs have a 5' cap that usually binds to a protein called eIF4E for translation initiation.
- Even when eIF4E is inhibited, mRNAs remain capped, indicating that other mechanisms can facilitate translation.
- This study reveals that the ribosomal protein RACK1 can replace eIF4E by recruiting another protein, eIF3d, when a certain active form of PKCBII is present.
Receptors for activated C kinases (RACKs) have been shown to coordinate PKC-mediated hypertrophic signalling in mice. However, little information is available on its participation in embryonic gene expression. This study investigated the involvement of RACK1 in the expression of embryonic genes in a zebrafish (ZF) ex vivo heart culture model by using phenylephrine (PE) or a growth factors cocktail (GFs) as a prohypertrophic/regeneration stimulus.
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- Duchenne muscular dystrophy (DMD) is a muscle-wasting disease that requires additional supportive therapies alongside gene treatments to improve patients' quality of life.
- Plumbagin, a natural compound similar to vitamin K3, has shown promise in reducing chronic inflammation and improving muscle function in studies conducted on dystrophic fruit flies and mdx mice.
- The research found that plumbagin enhanced muscle performance and morphology while activating specific pathways to reduce oxidative stress and inflammation, suggesting potential for further exploration as a human therapy.
Alzheimer's disease (AD) brains are histologically marked by the presence of intracellular and extracellular amyloid deposits, which characterize the onset of the disease pathogenesis. Increasing evidence suggests that certain nutrients exert a direct or indirect effect on amyloid β (Aβ)-peptide production and accumulation and, consequently, on AD pathogenesis. We exploited the fruit fly model of AD to evaluate in vivo the beneficial properties of Lisosan G, a fermented powder obtained from organic whole grains, on the intracellular Aβ-42 peptide accumulation and related pathological phenotypes of AD.
View Article and Find Full Text PDFDuchenne muscular dystrophy (DMD) is a genetic progressive muscle-wasting disorder that leads to rapid loss of mobility and premature death. The absence of functional dystrophin in DMD patients reduces sarcolemma stiffness and increases contraction damage, triggering a cascade of events leading to muscle cell degeneration, chronic inflammation, and deposition of fibrotic and adipose tissue. Efforts in the last decade have led to the clinical approval of novel drugs for DMD that aim to restore dystrophin function.
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