Background: Peptidases are key proteins involved in essential plant physiological processes. Although protein peptidase inhibitors are essential molecules that modulate peptidase activity, their global presence in different plant species remains still unknown. Comparative genomic analyses are powerful tools to get advanced knowledge into the presence and evolution of both, peptidases and their inhibitors across the Viridiplantae kingdom.
Results: A genomic comparative analysis of peptidase inhibitors and several groups of peptidases in representative species of different plant taxonomic groups has been performed. The results point out: i) clade-specific presence is common to many families of peptidase inhibitors, being some families present in most land plants; ii) variability is a widespread feature for peptidase inhibitory families, with abundant species-specific (or clade-specific) gene family proliferations; iii) peptidases are more conserved in different plant clades, being C1A papain and S8 subtilisin families present in all species analyzed; and iv) a moderate correlation among peptidases and their inhibitors suggests that inhibitors proliferated to control both endogenous and exogenous peptidases.
Conclusions: Comparative genomics has provided valuable insights on plant peptidase inhibitor families and could explain the evolutionary reasons that lead to the current variable repertoire of peptidase inhibitors in specific plant clades.
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http://dx.doi.org/10.1186/1471-2164-15-812 | DOI Listing |
Endocrine
January 2025
Unit of Endocrinology, Department of Clinical and Molecular Medicine, ENETS Center of Excellence, Sapienza University of Rome, Rome, Italy.
Diabetes mellitus (DM) and neuroendocrine tumors (NET) can exert unfavorable effects on each other prognosis. In this narrative review, we evaluated the effects of NET therapies on glycemic control and DM management and the effects of anti-diabetic therapies on NET outcome and management. For this purpose, we searched the PubMed, Science Direct, and Google Scholar databases for studies reporting the effects of NET therapy on DM as well as the effect of DM therapy on NET.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by hallmark pathologies that affect many brain regions, including the cellular microenvironment with the hippocampus, ultimately leading to profound deficits in cognition. Surprising recent work has shown that factors in the systemic environment regulate the hippocampal cellular niche; age-associated blood-borne factors exacerbate brain aging phenotypes, whereas youth-associated blood-borne factors, including tissue inhibitor of metalloproteinases 2 (TIMP2), reverse or ameliorate features of brain aging. As aging serves as the major risk factor for AD, and recent work shows that systemic factors can regulate AD pathology, we sought to characterize mechanisms by which the systemic environment regulates CNS phenotypes relevant to AD pathology through changes in neuroinflammation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Barcelonaβeta Brain Research Center (BBRC), Pasqual Maragall Foundation, Barcelona, Spain.
Background: Murine studies have identified blood proteins that influence brain aging, but translating these findings to humans remains challenging. We used an innovative approach to investigate whether genetically predicted blood levels of proteins linked to brain aging in animal models are associated with cognitive performance in individuals at risk of Alzheimer's disease (AD) [Figure 1].
Method: Through systematic review, we identified 13 circulating proteins with an aging/rejuvenating effect on the mouse brain.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
December 2024
Department of Oncology, Renmin Hospital of Wuhan University, Wuhan 430000, China.
Objective To investigate the effects of evodiamine (EVO) on Natural Killer (NK) cell-mediated killing in small cell lung cancer (SCLC) cells via affecting baculoviral inhibitor of apoptosis repeat containing 5 (BIRC5). Methods H446 cells and NK-92 cells were treated with EVO at different concentrations, and cell proliferation was detected using the MTT (3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) assay, while cell invasion was assessed using the Transwell assay. NK-92 cells and H446 cells were co-cultured at different effector-to-target ratios to detect the cytotoxicity of NK cells against H446 cells and the level of degranulation in NK-92 cells.
View Article and Find Full Text PDFDrug Dev Res
February 2025
Department of Biology and Biotechnologies 'Charles Darwin', Sapienza University of Rome, Rome, Italy.
Familial encephalopathy with neuroserpin inclusion bodies (FENIB) is a neurodegenerative pathology caused by accumulation of mutant neuroserpin (NS) polymers inside the endoplasmic reticulum (ER) of neurons, leading to cellular toxicity and neuronal death. To date, there is no cure for FENIB, and only palliative care is available for FENIB patients, underlining the urgency to develop therapeutic strategies. The purpose of this work was to create a cellular system designed for testing small molecules able to reduce the formation of NS polymers.
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