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Activation of arachidonoyl-phosphatidylinositol and phosphatidylcholine turnover by K(+)-evoked stimulation of brain synaptosomes.

Neurochemistry international

Majewska MD, Sun GY.
PMID: 20487897
Neurochem Int. 1982;4(5):427-33. doi: 10.1016/0197-0186(82)90086-9.

The turnover of arachidonoyl groups in synaptosomal phospholipids after stimulation by K(+) was examined. Raising the K(+) concentration in the incubation medium from 5 to 55 mM caused a rapid hydrolysis of labeled arachidonate from the synaptosomal phospholipids. Under...

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Majewska MD, Sun GY. Activation of arachidonoyl-phosphatidylinositol and phosphatidylcholine turnover by K(+)-evoked stimulation of brain synaptosomes. Neurochem Int. 1982;4(5):427-33doi: 10.1016/0197-0186(82)90086-9.
Majewska, M. D., & Sun, G. Y. (1982). Activation of arachidonoyl-phosphatidylinositol and phosphatidylcholine turnover by K(+)-evoked stimulation of brain synaptosomes. Neurochemistry international, 4(5), 427-33. https://doi.org/10.1016/0197-0186(82)90086-9
Majewska, M D, and Sun, G Y. "Activation of arachidonoyl-phosphatidylinositol and phosphatidylcholine turnover by K(+)-evoked stimulation of brain synaptosomes." Neurochemistry international vol. 4,5 (1982): 427-33. doi: https://doi.org/10.1016/0197-0186(82)90086-9
Majewska MD, Sun GY. Activation of arachidonoyl-phosphatidylinositol and phosphatidylcholine turnover by K(+)-evoked stimulation of brain synaptosomes. Neurochem Int. 1982;4(5):427-33. doi: 10.1016/0197-0186(82)90086-9. PMID: 20487897.
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Diacylglycerol kinase and lipase activities in rat brain subcellular fractions.

Neurochemistry international

Strosznajder J, Wikiel H, Kelleher JA, Leu VS, Sun GY.
PMID: 20493049
Neurochem Int. 1986;8(2):213-21. doi: 10.1016/0197-0186(86)90166-x.

Phosphatidic acid synthesis via diacylglycerol kinase and free fatty acid release via diacylglycerol lipase were investigated in rat brain subcellular fractions using membrane-bound [I-(14)C]arachidonoyl-diacylglycerol as substrate. Labeled diacylglycerol was generated by incubating brain membranes containing [I-(14)C]arachidonoyl-phosphatidylinositols in the presence...

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Strosznajder J, Wikiel H, Kelleher JA, et al. Diacylglycerol kinase and lipase activities in rat brain subcellular fractions. Neurochem Int. 1986;8(2):213-21doi: 10.1016/0197-0186(86)90166-x.
Strosznajder, J., Wikiel, H., Kelleher, J. A., Leu, V. S., & Sun, G. Y. (1986). Diacylglycerol kinase and lipase activities in rat brain subcellular fractions. Neurochemistry international, 8(2), 213-21. https://doi.org/10.1016/0197-0186(86)90166-x
Strosznajder, J, et al. "Diacylglycerol kinase and lipase activities in rat brain subcellular fractions." Neurochemistry international vol. 8,2 (1986): 213-21. doi: https://doi.org/10.1016/0197-0186(86)90166-x
Strosznajder J, Wikiel H, Kelleher JA, Leu VS, Sun GY. Diacylglycerol kinase and lipase activities in rat brain subcellular fractions. Neurochem Int. 1986;8(2):213-21. doi: 10.1016/0197-0186(86)90166-x. PMID: 20493049.
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Serum Metabolic Alterations upon Zika Infection.

Frontiers in microbiology

Melo CFOR, Delafiori J, de Oliveira DN, Guerreiro TM, Esteves CZ, Lima EO, Pando-Robles V, Catharino RR.
PMID: 29067015
Front Microbiol. 2017 Oct 10;8:1954. doi: 10.3389/fmicb.2017.01954. eCollection 2017.

Zika virus (ZIKV) infection has recently emerged as a major concern worldwide due to its strong association with nervous system malformation (microcephaly) of fetuses in pregnant women infected by the virus. Signs and symptoms of ZIKV infection are often...

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Melo CFOR, Delafiori J, de Oliveira DN, et al. Serum Metabolic Alterations upon Zika Infection. Front Microbiol. 2017;8:1954doi: 10.3389/fmicb.2017.01954.
Melo, C. F. O. R., Delafiori, J., de Oliveira, D. N., Guerreiro, T. M., Esteves, C. Z., Lima, E. O., Pando-Robles, V., Catharino, R. R. (2017). Serum Metabolic Alterations upon Zika Infection. Frontiers in microbiology, 81954. https://doi.org/10.3389/fmicb.2017.01954
Melo, Carlos Fernando O R, et al. "Serum Metabolic Alterations upon Zika Infection." Frontiers in microbiology vol. 8 (2017): 1954. doi: https://doi.org/10.3389/fmicb.2017.01954
Melo CFOR, Delafiori J, de Oliveira DN, Guerreiro TM, Esteves CZ, Lima EO, Pando-Robles V, Catharino RR. Serum Metabolic Alterations upon Zika Infection. Front Microbiol. 2017 Oct 10;8:1954. doi: 10.3389/fmicb.2017.01954. eCollection 2017. PMID: 29067015; PMCID: PMC5641361.
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Locating Carbon-Carbon Double Bonds in Unsaturated Phospholipids by Epoxidation Reaction and Tandem Mass Spectrometry.

Analytical chemistry

Cao W, Ma X, Li Z, Zhou X, Ouyang Z.
PMID: 30095894
Anal Chem. 2018 Sep 04;90(17):10286-10292. doi: 10.1021/acs.analchem.8b02021. Epub 2018 Aug 23.

The presence of carbon-carbon double bonds (C═Cs) in unsaturated phospholipids is closely related to lipid conformations and physiochemical activities. Previously, we have demonstrated that epoxidation reaction facilitated by low-temperature plasma (LTP) enabled the structural analysis of unsaturated fatty acids...

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Cao W, Ma X, Li Z, et al. Locating Carbon-Carbon Double Bonds in Unsaturated Phospholipids by Epoxidation Reaction and Tandem Mass Spectrometry. Anal Chem. 2018;90(17):10286-10292doi: 10.1021/acs.analchem.8b02021.
Cao, W., Ma, X., Li, Z., Zhou, X., & Ouyang, Z. (2018). Locating Carbon-Carbon Double Bonds in Unsaturated Phospholipids by Epoxidation Reaction and Tandem Mass Spectrometry. Analytical chemistry, 90(17), 10286-10292. https://doi.org/10.1021/acs.analchem.8b02021
Cao, Wenbo, et al. "Locating Carbon-Carbon Double Bonds in Unsaturated Phospholipids by Epoxidation Reaction and Tandem Mass Spectrometry." Analytical chemistry vol. 90,17 (2018): 10286-10292. doi: https://doi.org/10.1021/acs.analchem.8b02021
Cao W, Ma X, Li Z, Zhou X, Ouyang Z. Locating Carbon-Carbon Double Bonds in Unsaturated Phospholipids by Epoxidation Reaction and Tandem Mass Spectrometry. Anal Chem. 2018 Sep 04;90(17):10286-10292. doi: 10.1021/acs.analchem.8b02021. Epub 2018 Aug 23. PMID: 30095894.
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Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila.

Biochemical and biophysical research communications

Zhang Q, Zhang B, Lim NKH, Zhang X, Meng S, Nyengaard JR, Huang F, Wang WA.
PMID: 34894559
Biochem Biophys Res Commun. 2021 Dec 03;589:71-77. doi: 10.1016/j.bbrc.2021.11.106. Epub 2021 Dec 03.

Hyccin/FAM126A mutations are linked to hypomyelination and congenital cataract disease (HCC), but whether and how Hyccin/FAM126A deficiency causes hypomyelination remains undetermined. This study shows Hyccin/FAM126A expression was necessary for the expression of other components of the PI4KIIIα complex in...

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Zhang Q, Zhang B, Lim NKH, et al. Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila. Biochem Biophys Res Commun. 2021;589:71-77doi: 10.1016/j.bbrc.2021.11.106.
Zhang, Q., Zhang, B., Lim, N. K. H., Zhang, X., Meng, S., Nyengaard, J. R., Huang, F., & Wang, W. A. (2021). Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila. Biochemical and biophysical research communications, 58971-77. https://doi.org/10.1016/j.bbrc.2021.11.106
Zhang, Qichao, et al. "Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila." Biochemical and biophysical research communications vol. 589 (2021): 71-77. doi: https://doi.org/10.1016/j.bbrc.2021.11.106
Zhang Q, Zhang B, Lim NKH, Zhang X, Meng S, Nyengaard JR, Huang F, Wang WA. Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila. Biochem Biophys Res Commun. 2021 Dec 03;589:71-77. doi: 10.1016/j.bbrc.2021.11.106. Epub 2021 Dec 03. PMID: 34894559.
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Insights into the inhibitory mechanism of triazole-based small molecules on phosphatidylinositol-4,5-bisphosphate binding pleckstrin homology domain.

Biochemistry and biophysics reports

Gorai S, Bagdi PR, Borah R, Paul D, Santra MK, Khan AT, Manna D.
PMID: 29124147
Biochem Biophys Rep. 2015 May 27;2:75-86. doi: 10.1016/j.bbrep.2015.05.007. eCollection 2015 Jul.

BACKGROUND: Phosphatidylinositol 4,5-bisphosphate [PI(4,5)PMETHODS: Surface plasmon resonance, molecular docking, circular dichroism, competitive Förster resonance energy transfer, isothermal titration calorimetric analyses and liposome pull down assay were used.RESULTS: In this study, we employed 1,2,3-triazol-4-yl methanol containing small molecule (CIPs) as...

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Gorai S, Bagdi PR, Borah R, et al. Insights into the inhibitory mechanism of triazole-based small molecules on phosphatidylinositol-4,5-bisphosphate binding pleckstrin homology domain. Biochem Biophys Rep. 2015;2:75-86doi: 10.1016/j.bbrep.2015.05.007.
Gorai, S., Bagdi, P. R., Borah, R., Paul, D., Santra, M. K., Khan, A. T., & Manna, D. (2015). Insights into the inhibitory mechanism of triazole-based small molecules on phosphatidylinositol-4,5-bisphosphate binding pleckstrin homology domain. Biochemistry and biophysics reports, 275-86. https://doi.org/10.1016/j.bbrep.2015.05.007
Gorai, Sukhamoy, et al. "Insights into the inhibitory mechanism of triazole-based small molecules on phosphatidylinositol-4,5-bisphosphate binding pleckstrin homology domain." Biochemistry and biophysics reports vol. 2 (2015): 75-86. doi: https://doi.org/10.1016/j.bbrep.2015.05.007
Gorai S, Bagdi PR, Borah R, Paul D, Santra MK, Khan AT, Manna D. Insights into the inhibitory mechanism of triazole-based small molecules on phosphatidylinositol-4,5-bisphosphate binding pleckstrin homology domain. Biochem Biophys Rep. 2015 May 27;2:75-86. doi: 10.1016/j.bbrep.2015.05.007. eCollection 2015 Jul. PMID: 29124147; PMCID: PMC5668642.
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Changes in Meibum Lipid Composition With Ocular Demodex Infestation.

Translational vision science & technology

Gao H, Chen H, Xie HT, Xu KK, Shi BJ, Huang YK.
PMID: 34874449
Transl Vis Sci Technol. 2021 Dec 01;10(14):6. doi: 10.1167/tvst.10.14.6.

PURPOSE: The purpose of this study was to understand the impact of Demodex infection in the lipid component of meibum in patients.METHODS: The meibum samples were collected from four groups of subjects: (1) Demodex-negative with non-MGD (D-M-; n =...

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Gao H, Chen H, Xie HT, et al. Changes in Meibum Lipid Composition With Ocular Demodex Infestation. Transl Vis Sci Technol. 2021;10(14):6doi: 10.1167/tvst.10.14.6.
Gao, H., Chen, H., Xie, H. T., Xu, K. K., Shi, B. J., & Huang, Y. K. (2021). Changes in Meibum Lipid Composition With Ocular Demodex Infestation. Translational vision science & technology, 10(14), 6. https://doi.org/10.1167/tvst.10.14.6
Gao, Hui, et al. "Changes in Meibum Lipid Composition With Ocular Demodex Infestation." Translational vision science & technology vol. 10,14 (2021): 6. doi: https://doi.org/10.1167/tvst.10.14.6
Gao H, Chen H, Xie HT, Xu KK, Shi BJ, Huang YK. Changes in Meibum Lipid Composition With Ocular Demodex Infestation. Transl Vis Sci Technol. 2021 Dec 01;10(14):6. doi: 10.1167/tvst.10.14.6. PMID: 34874449; PMCID: PMC8662575.
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Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver.

Journal of lipid research

Xia M, Chandrasekaran P, Rong S, Fu X, Mitsche MA.
PMID: 32859645
J Lipid Res. 2021;62:100031. doi: 10.1194/jlr.RA120000856. Epub 2021 Feb 06.

Genetic variants that increase the risk of fatty liver disease and cirrhosis have recently been identified in the proximity of membrane-bound O-acyltransferase domain-containing 7 (MBOAT7). To elucidate the link between these variants and fatty liver disease, we characterized Mboat7...

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Xia M, Chandrasekaran P, Rong S, et al. Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver. J Lipid Res. 2021;62:100031doi: 10.1194/jlr.RA120000856.
Xia, M., Chandrasekaran, P., Rong, S., Fu, X., & Mitsche, M. A. (2021). Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver. Journal of lipid research, 62100031. https://doi.org/10.1194/jlr.RA120000856
Xia, Mingfeng, et al. "Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver." Journal of lipid research vol. 62 (2021): 100031. doi: https://doi.org/10.1194/jlr.RA120000856
Xia M, Chandrasekaran P, Rong S, Fu X, Mitsche MA. Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver. J Lipid Res. 2021;62:100031. doi: 10.1194/jlr.RA120000856. Epub 2021 Feb 06. PMID: 32859645; PMCID: PMC8022244.
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The Vacuolar Protein Sorting-38 Subunit of the .

Frontiers in plant science

Liu F, Hu W, Vierstra RD.
PMID: 29967628
Front Plant Sci. 2018 Jun 18;9:781. doi: 10.3389/fpls.2018.00781. eCollection 2018.

The family of phosphatidylinositols (PtdIns) plays essential roles in membrane identity and intracellular trafficking events. In animals and yeast, PtdIn-3-phosphate, which is particularly important for endosomal sorting, lysosomal/vacuolar transport and autophagy, is assembled by two conserved kinase complexes comprised...

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Liu F, Hu W, Vierstra RD. The Vacuolar Protein Sorting-38 Subunit of the . Front Plant Sci. 2018;9:781doi: 10.3389/fpls.2018.00781.
Liu, F., Hu, W., & Vierstra, R. D. (2018). The Vacuolar Protein Sorting-38 Subunit of the . Frontiers in plant science, 9781. https://doi.org/10.3389/fpls.2018.00781
Liu, Fen, et al. "The Vacuolar Protein Sorting-38 Subunit of the ." Frontiers in plant science vol. 9 (2018): 781. doi: https://doi.org/10.3389/fpls.2018.00781
Liu F, Hu W, Vierstra RD. The Vacuolar Protein Sorting-38 Subunit of the . Front Plant Sci. 2018 Jun 18;9:781. doi: 10.3389/fpls.2018.00781. eCollection 2018. PMID: 29967628; PMCID: PMC6016017.
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Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila.

Biochemical and biophysical research communications

Zhang Q, Zhang B, Lim NKH, Zhang X, Meng S, Nyengaard JR, Huang F, Wang WA.
PMID: 34894559
Biochem Biophys Res Commun. 2021 Dec 03;589:71-77. doi: 10.1016/j.bbrc.2021.11.106. Epub 2021 Dec 03.

Hyccin/FAM126A mutations are linked to hypomyelination and congenital cataract disease (HCC), but whether and how Hyccin/FAM126A deficiency causes hypomyelination remains undetermined. This study shows Hyccin/FAM126A expression was necessary for the expression of other components of the PI4KIIIα complex in...

Cite
Zhang Q, Zhang B, Lim NKH, et al. Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila. Biochem Biophys Res Commun. 2021;589:71-77doi: 10.1016/j.bbrc.2021.11.106.
Zhang, Q., Zhang, B., Lim, N. K. H., Zhang, X., Meng, S., Nyengaard, J. R., Huang, F., & Wang, W. A. (2021). Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila. Biochemical and biophysical research communications, 58971-77. https://doi.org/10.1016/j.bbrc.2021.11.106
Zhang, Qichao, et al. "Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila." Biochemical and biophysical research communications vol. 589 (2021): 71-77. doi: https://doi.org/10.1016/j.bbrc.2021.11.106
Zhang Q, Zhang B, Lim NKH, Zhang X, Meng S, Nyengaard JR, Huang F, Wang WA. Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila. Biochem Biophys Res Commun. 2021 Dec 03;589:71-77. doi: 10.1016/j.bbrc.2021.11.106. Epub 2021 Dec 03. PMID: 34894559.
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Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver.

Journal of lipid research

Xia M, Chandrasekaran P, Rong S, Fu X, Mitsche MA.
PMID: 32859645
J Lipid Res. 2021;62:100031. doi: 10.1194/jlr.RA120000856. Epub 2021 Feb 06.

Genetic variants that increase the risk of fatty liver disease and cirrhosis have recently been identified in the proximity of membrane-bound O-acyltransferase domain-containing 7 (MBOAT7). To elucidate the link between these variants and fatty liver disease, we characterized Mboat7...

Cite
Xia M, Chandrasekaran P, Rong S, et al. Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver. J Lipid Res. 2021;62:100031doi: 10.1194/jlr.RA120000856.
Xia, M., Chandrasekaran, P., Rong, S., Fu, X., & Mitsche, M. A. (2021). Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver. Journal of lipid research, 62100031. https://doi.org/10.1194/jlr.RA120000856
Xia, Mingfeng, et al. "Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver." Journal of lipid research vol. 62 (2021): 100031. doi: https://doi.org/10.1194/jlr.RA120000856
Xia M, Chandrasekaran P, Rong S, Fu X, Mitsche MA. Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver. J Lipid Res. 2021;62:100031. doi: 10.1194/jlr.RA120000856. Epub 2021 Feb 06. PMID: 32859645; PMCID: PMC8022244.
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Phosphoinositides signaling modulates microglial actin remodeling and phagocytosis in Alzheimer's disease.

Cell communication and signaling : CCS

Desale SE, Chinnathambi S.
PMID: 33627135
Cell Commun Signal. 2021 Feb 24;19(1):28. doi: 10.1186/s12964-021-00715-0.

Alzheimer's disease is one of the neurodegenerative diseases, characterized by the accumulation of abnormal protein deposits, which disrupts signal transduction in neurons and other glia cells. The pathological protein in neurodegenerative diseases, Tau and amyloid-β contribute to the disrupted...

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Desale SE, Chinnathambi S. Phosphoinositides signaling modulates microglial actin remodeling and phagocytosis in Alzheimer's disease. Cell Commun Signal. 2021;19(1):28doi: 10.1186/s12964-021-00715-0.
Desale, S. E., & Chinnathambi, S. (2021). Phosphoinositides signaling modulates microglial actin remodeling and phagocytosis in Alzheimer's disease. Cell communication and signaling : CCS, 19(1), 28. https://doi.org/10.1186/s12964-021-00715-0
Desale, Smita Eknath, and Chinnathambi, Subashchandrabose. "Phosphoinositides signaling modulates microglial actin remodeling and phagocytosis in Alzheimer's disease." Cell communication and signaling : CCS vol. 19,1 (2021): 28. doi: https://doi.org/10.1186/s12964-021-00715-0
Desale SE, Chinnathambi S. Phosphoinositides signaling modulates microglial actin remodeling and phagocytosis in Alzheimer's disease. Cell Commun Signal. 2021 Feb 24;19(1):28. doi: 10.1186/s12964-021-00715-0. PMID: 33627135; PMCID: PMC7905611.
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Showing 25 to 36 of 52 entries