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Phosphoinositide Metabolism
Published in Enrique Pimentel, Handbook of Growth Factors, 2017
Phosphoinositide kinases catalyze the phosphorylation of the inositol ring of phosphatidylinositol at different positions including the D3 hydroxyl position (phosphatidylinositol 3-kinase), the D4 position (phosphatidylinositol 4-kinase), and the D5 position (phosphatidylinositol 5-kinase).111
BCL11B depletion induces the development of highly cytotoxic innate T cells out of IL-15 stimulated peripheral blood αβ CD8+ T cells
Published in OncoImmunology, 2022
Hannes Forkel, Piotr Grabarczyk, Maren Depke, Sascha Troschke-Meurer, Stefan Simm, Elke Hammer, Stephan Michalik, Christian Hentschker, Björn Corleis, Lucie Loyal, Maxi Zumpe, Nikolai Siebert, Anca Dorhoi, Andreas Thiel, Holger Lode, Uwe Völker, Christian A. Schmidt
Moreover, the concomitant flow cytometry analysis showed upregulation of ITA1 and ITAX. Both integrins co-operate with other adhesome factors in forming bidirectional signaling hubs and play a critical role in NK cell activation48 (Figure 4(c)). We further observed the varying influence of BCL11B deletion on signaling events downstream of the membrane/cytoskeleton level. Phosphatidylinositol 4-kinase alpha (PI4KA) and the inositol polyphosphate-4-phosphatase type I A (INP4A), both participating in phosphatidylinositol signaling and inositol phosphate metabolism, were significantly upregulated in BCL11B knock-out cells. In contrast, kinases of the MAPK cascade system acting upstream of PAK1 were downregulated47 (Figure 4(b)). The downregulation of the antigen processing and presentation-related factors revealed earlier by expression profiling was confirmed on the proteome level: both HLA class I molecules (HLA-E) and HLA class II molecules (HLA-DR and HLA-DQ) were reduced due to BCL11B removal (Figure 4(a, b)).
Dual role of quercetin in enhancing the efficacy of cisplatin in chemotherapy and protection against its side effects: a review
Published in Archives of Physiology and Biochemistry, 2022
Masoud Najafi, Shima Tavakol, Ali Zarrabi, Milad Ashrafizadeh
Ovarian cancer (OC) is one of the most malignant tumours among women and claims the eighth place among other cancers in females (Angeli et al.2020). Currently, there is no cure for effective eradication of OC and because of its high incidence rate, it is considered as one of the major public health issues (Mahalaxmi et al.2019). Chemotherapy and radiotherapy are common non-invasive and minimal invasive strategies in OC therapy (Revaux et al.2020). Notably, the resistance of OC cells has significantly reduced the efficacy of chemotherapy. The co-administration of quercetin and CP has more inhibitory impact on the growth and proliferation of OC cells compared to CP alone (Scambia et al. 1990). It is said that dose-dependent cytotoxicity of quercetin sensitises OC cells into CP chemotherapy (Scambia et al.1990). The capability of quercetin in induction of cell cycle arrest at G1 and S phases exerts anti-proliferative activity in OC cells. This effect on the proliferation is mediated through suppressing phosphatidylinositol conversion into IP3 via down-regulation of 1-phosphatidylinositol 4-kinase (Shen and Weber 1997).
Type II phosphatidylinositol 4-kinase regulates nerve terminal growth and synaptic vesicle recycling
Published in Journal of Neurogenetics, 2018
Kristyn C. Cantarutti, Jason Burgess, Julie A. Brill, Jeffrey S. Dason
Phosphoinositides affect a vast array of processes at synapses (reviewed in Frere, Chang-Ileto, & Di Paolo, 2012; Lauwers, Goodchild, & Verstreken, 2016). Phosphatidylinositol (4,5)-bisphosphate (PI(4,5)P2) regulates axonal growth (Khuong, Habets, Slabbaert, & Verstreken, 2010), ion channel function (Suh, Leal, & Hille, 2010; Suh & Hille, 2002) and several steps of the synaptic vesicle (SV) cycle (Di Paolo et al., 2004; Verstreken et al., 2009; Walter et al., 2017). The role of the PI(4,5)P2 precursor phosphatidylinositol 4-phosphate (PI4P) at the synapse is less clear. Mounting evidence suggests that PI4P is functionally important and not simply a precursor for PI(4,5)P2 ( reviewed in D'Angelo, Vicinanza, Di Campli, & De Matteis, 2008; De Matteis, Wilson, & D'Angelo, 2013; Tan & Brill, 2014 ). Phosphatidylinositol 4-kinase (PI4K) is responsible for the synthesis of PI4P, which is subsequently converted to PI(4,5)P2 by phosphatidylinositol 4-phosphate 5-kinase (PI4P5K).