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Grass pollen allergens
Published in Richard F. Lockey, Dennis K. Ledford, Allergens and Allergen Immunotherapy, 2020
PCGs released by the grass pollen grain are recognized as a source of specific allergens playing a role in triggering asthma symptoms [100,106,132,133]. A comprehensive proteomic analysis was conducted to characterize allergens intrinsic to the PCGs [141]. Among those already known grass pollen allergens, seven are associated with PCGs: Phl p 1, 3, 4, 5, 6, 11, and 12. Three novel IgE-reactive proteins were identified: an alcohol dehydrogenase unique to the PCGs, an ascorbic reductase detected in both the whole pollen grain as well as the PCGs, and a β-glucosidase detected only in pollen extracts. Five additional proteins were identified in PCGs which might be potential allergens: enolase, triosephosphate isomerase, legumin-like protein, UDP-glucose pyrophosphorylase, and a phosphomutase.
Modulation of Lipid Biosynthesis by Stress in Diatoms
Published in Gokare A. Ravishankar, Ranga Rao Ambati, Handbook of Algal Technologies and Phytochemicals, 2019
Bing Huang, Virginie Mimouni, Annick Morant-Manceau, Justine Marchand, Lionel Ulmann, Benoit Schoefs
It is well documented that TAG accumulation is a consequence of re-allocation of carbon from intermediates of the TCA cycle but also from the degradation of chrysolaminarin (Zhu et al., 2016). Diatoms can produce both lipids and chrysolaminarin as energy reserves, with lipid-to-chrysolaminarin ratios that depend on growth conditions. In the most common situation, chrysolaminarin is the primary energy compound, but how its production switches to FAs or TAG under specific conditions is not completely understood. Daboussi et al. (2014) were the first to report that a block of the chrysolaminarin pathway by disruption of the UDP-glucose pyrophosphorylase gene (UGPase) using nucleases (meganucleases and TALEN) in P. tricornutum resulted in a 45-fold increase in TAG accumulation. Zhu et al. (Zhu et al., 2016), by knocking down the same gene in P. tricornutum (69% of the UGPase activity was inactivated), highlighted a significant decrease in chrysolaminarin content and an increase in lipid synthesis. In T. pseudonana, Hildebrand, Manandhar-Shrestha and Abbriano (2017) demonstrated that knockdown transformants were accumulating less chrysolaminarin and increased their TAG level, suggesting that UGPase plays an important role in carbon allocation. Their data also suggest that the effect of chrysolaminarin levels on TAG accumulation is triggered by growth cessation and is transient. Silencing nitrate assimilation can also be a strategy to direct the carbon flux toward lipids since they require little nitrogen (Levitan et al., 2015b). In diatoms, the rate‐limiting reaction in the assimilation of nitrate is the reduction of the molecule to nitrite, a reaction catalyzed by the nitrate reductase. The silencing of the nitrate reductase in P. tricornutum revealed an accumulation of over 40% more fatty acids with a 50% lower expression and activity of the enzyme in the transformants compared to the wild type. In contrast to nitrogen‐stressed WT cells, which grow at about 20% of the rate of nitrogen‐replete cells, growth of the transformants was only reduced by about 30% (Levitan et al., 2015b).
Liver cancer-associated changes to the proteome: what deserves clinical focus?
Published in Expert Review of Proteomics, 2018
José M. Mato, Félix Elortza, Shelly C. Lu, Virginie Brun, Alberto Paradela, Fernando J. Corrales
Cancer cell metastasis is a major cause of cancer fatality, yet the underlying molecular mechanisms remain poorly understood. HCC cell lines with different metastatic capacities have been studied to address this question using several large-scale approaches. The metastatic potential of four HCC cell lines was analysed by IEF prefractionation and LC-MS/MS leading to the identification of deregulated proteins involved in the maintenance of extracellular matrix homeostasis in the secretome that might explain their differential aggressiveness [37]. Protein–protein interaction network analysis revealed statistically enriched nodes integrating many well-known oncogene and tumor-supressor proteins pointing at severe metabolic and cytoskeleton reshaping [38]. In agreement with these observations, multi-omic studies on Huh7, MHCC97L, HCCLM3 HCC cell lines (low, medium and high metastatic potential respectively), revealed specific metabolic profiles correlating with their metastatic potential, with a principal role of UDP-glucose pyrophosphorylase 2 (UGP2), a critical enzyme for glycogen synthesis [39].
Molecular mechanism and research progress on pharmacology of traditional Chinese medicine in liver injury
Published in Pharmaceutical Biology, 2018
Hong Yang Zhang, Hong Ling Wang, Guo Yue Zhong, Ji Xiao Zhu
d-GalN is a hepatotoxic and liver-damaging drug that has been extensively used as an animal model for the induction of experimental liver failure. The induced mechanism is similar to that of CCl4-induced liver injury. d-GalN causes glucosamine accumulation, combines with the uridine diphosphate (UDP), induces deficiency of uridine triphosphate (UTP), and suppress the activation and amount of UDP glucose pyrophosphorylase (UDPase), which result in the metabolic inhibition of carbohydrate and phospholipids. d-GalN also suppresses the synthesis of RNA and proteins in liver cells, while increasing the loss of membrane and further lead to necrocytosis. Meanwhile, Kupffer cells and liver sinusoidal endothelial cells release cytokines that enhance the expression of various enzymes and inflammatory factors. d-GalN can also combine with specific parenchymal hepatic cells and affect its integrity. A large amount of calcium ions can damage calcium homeostasis, which subsequently leads to metabolic disorders. Apart from that, it also causes the depletion of glutathione (GSH) that prohibits carbohydrate and lipid metabolisms, induces free radicals and disturbs redox balance, releases TNF-α and induces apoptosis. Therefore, d-GalN is a hepatotoxic agent that causes panlobular focal hepatocyte necrosis, polymorphonuclear cell infiltration and macrophages enlargement, which closely resembles human viral hepatitis infection. Due to its unique propensity, d-GalN has been widely used in inflammatory liver injury models to screen for potential hepatoprotective agents (Wang et al. 2016).
Repurposing drugs for the treatment of galactosemia
Published in Expert Opinion on Orphan Drugs, 2019
The molecular causes of these movement disorders remain unknown. Work on the D. melanogaster model suggests that galactose 1-phosphate accumulation is not required for the development of this aspect of the galactosemic phenotype [91]. Disturbances to the UDP-sugar pools and subsequent disruption of the glycosylation of neuronal proteins may be important in this model [92,93]. UDP-glucose pyrophosphorylase (UGP; EC 2.7.7.9) has been suggested as a possible drug target based on these studies [93]. Currently, no drugs are in clinical use which target this enzyme.