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Vanadium Toxicity Revisited
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Rituparna Ghosh, Ahana Das, Arnab Bandyopadhyay, Rajib Majumder, Samudra Prosad Banik
Vanadium in the form of pentavalent orthovanadate acts as a reversible competitive inhibitor of PTP owing to its resemblance with phosphate group (Crans et al. 2004). Binding of vanadate into the PTP active site is facilitated by hydrogen bonds (Peters et al. 2003) which make it a strong inhibitor. Due to the sequence conservation of PTP active site, vanadium has evolved as a universal inhibitor of the pan PTP superfamily of enzymes (Gordon 1991). Some vanadium compounds, such as the peroxidovanadium complexes, can also bring about permanent irreversible inhibition of the active site by oxidizing critical cysteine residues (Evangelou 2002, Scrivens et al. 2003). This has enlarged the domain of metallotherapeutics and has led to the synthesis of several new oxovanadium-based compounds such as bis(maltolato)oxidovanadium (IV) (BMOV) as an inhibitor of class II LMW-PTP (Peters et al. 2003). Inhibition of PTPs is also implicated in treating diabetes, a long-recognized potential of vanadium-based compounds. Autophosphorylation of insulin receptors upon insulin binding causes docking and simultaneous activation of insulin receptor substrate 1 (IRS-1). This, in turn, initiates a signal cascade which culminates into deployment of GLUT-4 channels to the cell membrane resulting in increased uptake of glucose. In diabetic individuals, insulin doesn’t function properly; therefore, subsequent glucose uptake ceases to occur efficiently. Vanadium-based compounds cause inhibition of PTPs thus resulting in sustained signal transmission by phosphotyrosine residues and consequent activation of IRS-1 (Heyliger et al. 1985). In this way, vanadium mimics insulin and is able to lower blood glucose significantly. Structural analogy with phosphate has enabled vanadium to be used in other non-PTP inhibitor-based therapeutic formulations also.
Medium Design for Cell Culture Processing
Published in Wei-Shou Hu, Cell Culture Bioprocess Engineering, 2020
Both insulin and IGF-1 bind to the insulin receptor (IR) and IGF receptor (IGF1R), but with different affinities. After insulin binding, IR or IGF1R is phosphorylated, leading to activation of an insulin receptor substrate (IRS). There are multiple isoforms of IRS that are distributed differently in cells of different tissues. The signal is then relayed to downstream signaling pathways.
Transcriptome analysis of Takifugu obscurus liver in response to acute retene exposure
Published in Journal of Environmental Science and Health, Part A, 2020
Shulun Jiang, Di-an Fang, Dongpo Xu
The insulin receptor substrate (IRS) proteins are a family of cytoplasmic proteins composed of six members (IRS1-6). This gene family integrates and coordinates the signal transmission from the extracellular to the intracellular environment, which then regulates cell growth, metabolism, survival, and proliferation.[54] IRS proteins are the major molecules that mediate responses to insulin, insulin-like growth factor 1 (IGF1) stimulation, and environmental stimuli.[15] After phosphorylation, IRS proteins bind to Src homology (SH2) domain-containing proteins like phosphatidylinositol 3-kinase (PI3K), with the consequent activation of AKT, and mediate various signaling pathways. In this study, IRS2 and IRS4 were upregulated 3.8 and 4.2 times, respectively, after RET exposure (Table A3). These changes were consistent with the outcome predicted by the upregulation of LPIN1 and LPIN2. Previous studies indicate that disruption of the IRS2 gene in mice resulted in pathological alterations similar to metabolic syndrome, including insulin resistance, hyperinsulinemia, glucose intolerance, obesity, hypertension, and moderate hyperlipidemia.[15] Mice with IRS4 knockout exhibited mild defects in growth, reproduction, and glucose homeostasis, but overexpression of IRS4 reversed the effects of IRS2 knockout in rodent cells.[55]
Instance-based learning of marker proteins of carcinoma cells for cell death/ survival
Published in Computer Methods in Biomechanics and Biomedical Engineering: Imaging & Visualization, 2020
Initially authors have considered Mitogen-activated protein kinase-activated protein kinase 2 (MK2), c-jun N-terminal kinases(JNK), Forkhead transcription factor (FKHR), Mitogen-activated protein kinase and extracellular-regulated kinase (MEK), Extracellular-regulated kinase (ERK), Insulin receptor substrate (IRS), AkT, IKK, Phospho-to-total EGFR (ptEGFR), Phospho-to-total Akt (ptAkt), and pAkT proteins that are due to the combination of three input proteins (Jain et al. 2012). To make data consistent, outlier and erroneous data were removed. The signal values were normalised (1: red; 0.5: black; 0: green) to the maximum. Authors have calculated different statistical parameters like harmonic mean, geometric mean, standard error, median, mode, sum, minimum value, maximum values, and coefficient variance. Figure 5 represents the P-P plot, box plot and Kolmogorov–Smirnov (KS) plot, p-value of a normal distribution of FKHR protein (Jain 2017b). Due to the constraint of space, data of FKHR protein are shown in the Figure. Based on the calculation of different statistical parameters and different plots, it is seen that AkT, EGFR, IRS, MEK, ERK, JNK, and FKHR yields better results which was also validated experimentally as shown in Figure 3. All the selected proteins are used for further analysis except AkT. Author has already done all simulations using AkT in (Jain and Salau 2019).
Lipogenesis inhibition and adipogenesis regulation via PPARγ pathway in 3T3-L1 cells by Zingiber cassumunar Roxb. rhizome extracts
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Natthawut Wong-a-nan, Kewalin Inthanon, Aroonchai Saiai, Angkhana Inta, Wutigri Nimlamool, Siriwadee Chomdej, Prasat Kittakoop, Weerah Wongkham
In this study, we focused on 4 groups of genes i.e. those involved in the following processes: 1) adipocyte differentiation (C/EBPα (CCAAT/enhancer binding protein alpha), PPARγ (Peroxisome proliferator-activated receptor gamma), ADD-1 (Adipocyte determination and differentiation-dependent factor 1) and Pref-1 (Pre-adipocyte factor 1)); 2) glucose uptake (IRS-1 (Insulin receptor substrate 1), GLUT4 (Glucose transporter type 4) and Adiponectin); 3) lipid metabolism (FAS (Fatty acid synthase) and aP2 (Adipocyte protein 2)) and 4) fatty acid oxidation (ATGL (Adipose triglyceride lipase), HSL (Hormone sensitive lipase) and PGC-1β (PPARγ coactivator 1 beta)). The relative mRNA expression of real-time PCR products was evaluated. ZCE and ZCW extracts were chosen in this work, since other solvents pose human health hazards and are not used in traditional medicine.