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Computational characterization and integrative analysis of proteins involved in spermatogenesis
Published in C. Yan Cheng, Spermatogenesis, 2018
Pranitha Jenardhanan, Manivel Panneerselvam, Premendu P. Mathur
On the other hand, proteins such as keratin, type II cytoskeletal 1 (KRT1), isoaspartyl peptidase/lasparaginase (ASRGL1), and clusterin (CLU) were enriched in asthenozoospermia data set. Besides the ASRGL1 and SPANXB proteins, the remaining 12 proteins were assigned to five functional classes: (1) sperm movement and structural organization (TUBB2B, ODF2, AKAP4, KRT1, and CLU); (2) energy and metabolism (COX6B, GAPDS, PHGPx), (3) stress response and turnover (HSPA2, HSPA9), (4) signaling and transportation (VDAC2), and (5) antioxidant activity (GSTMu3).
The relevant targets of anti-oxidative stress: a review
Published in Journal of Drug Targeting, 2021
The protective effect of ischaemic preconditioning on myocardium has been confirmed by a large number of experiments. Recent studies have shown that short-term myocardial ischemia-reperfusion can induce the up-regulation of many protective genes, such as antioxidant enzyme genes and NO synthase. Regulating the functional and metabolic changes of myocardium after ischemia-reperfusion is an important part of the myocardial endogenous protective mechanism, and it is also one of the important molecular bases for the myocardial protection of ischaemic preconditioning. Based on rat myocardial ischemia-reperfusion animal model, Jiang et al. screened the possible interaction proteins of MIP2 and identified voltage-dependent anion channel (VDAC), including VDAC1, VDAC2 and VDAC3 [120]. They found that VDAC1 might be a potential target for MIP2, and WD40 at the C-terminal of MIP2 is a domain that interacts with VDAC1. MIP2 can inhibit the reduction of mitochondrial membrane potential and cell death of cardiomyocytes induced by oxidative stress, and its mechanism may be related to the regulation of VDAC1.
Evolution of proteomics technologies for understanding respiratory syncytial virus pathogenesis
Published in Expert Review of Proteomics, 2021
In 2010, Munday, et al. published two papers employing SILAC to quantify RSV-induced changes to both the cytoplasmic and nuclear proteomes of Hep2 cells [78,79]. In these studies, the authors identified concerted reductions to the abundances of mitochondrial proteins such as the Translocase of the Outer Mitochondrial membrane (TOM) complex (e.g. Tom20, Tom22, Tom40, Tom70), as well as Voltage-dependent Anion Channels (VDACs; e.g. VDAC-1, VDAC2, VDAC-3). These changes were induced by both RSV subtypes, although no direct comparison of the two was conducted. Their findings led the investigators to propose that RSV infection altered the permeability of mitochondrial transition pores; a hypothesis that they then confirmed using a live-cell mitochondrial permeability assay. These results suggested that mitochondrial dysfunction may contribute to RSV-induced oxidative damage. A third study from this group applied SILAC to mitochondrial extracts from RSV-infected A549 cells, and confirmed that infection altered the abundances of TOM proteins [80]. The authors demonstrated that knockdown of Tom70 increased viral titer, further indicating a role for these proteins during viral infection.
Shining a light on defective autophagy by proteomics approaches: implications for neurodegenerative illnesses
Published in Expert Review of Proteomics, 2019
Fabio Di Domenico, Ilaria Zuliani, Antonella Tramutola
Proteomics represents a valuable tool to gain insight into the substantial changes that occur into the brain during the aging process. Phospho-proteomic analysis of differently aged naked mole rats identified changes in specific isoforms of voltage-dependent anion channels (VDACs), the major outer mitochondrial membrane porins; levels of both VDAC2 and VDAC3 were increase as a function of age while phosphorylation levels decreased with age for all VDACs [70]. Naked mole rats demonstrate a more robust functionality of the ubiquitin-proteasome and autophagy-lysosomal systems when compared to shorter-lived rodents [118]. As decreased levels of VDACs are known to increase the presence of malfunctioning mitochondria, the age-dependent increase of their levels in aged-rodents suggest an increase monitoring of mitochondrial function that could be linked with their incredibly long lifespan. Further, VDAC are known to be phosphorylated by different kinases: phosphorylation of VDAC1 by Nek1 has been reported to open the channel [119], while VDAC phosphorylation by GSK3β or PKA increases the interaction between VDAC and tubulin, blocking the channel [120]. The consequences of the decreased phosphorylation levels of VDAC2 and VDAC3 in brain from aged rodents are unclear and may reflect the greater proportion of breeding animals in the older samples [70]. These evidences are useful to understand the compensatory mechanisms necessary to maintain protein homeostasis in this long-lived animal model.