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Showing 1 to 12 of 52 entries
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Synthesis and Kinetic Evaluation of Inhibitors of the Phosphatidylinositol-Specific Phospholipase C from Bacillus cereus.

The Journal of organic chemistry

Martin SF, Wagman AS.
PMID: 11667784
J Org Chem. 1996 Nov 15;61(23):8016-8023. doi: 10.1021/jo960850q.

Substrate analogues of phosphatidylinositol (1) were synthesized and evaluated as potential inhibitors of the bacterial phosphatidylinositol-specific phospholipase C (PI-PLC) from Bacillus cereus. The chiral analogues of the water-soluble phospholipid substrate 5 were designed to probe the effects of varying...

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Martin SF, Wagman AS. Synthesis and Kinetic Evaluation of Inhibitors of the Phosphatidylinositol-Specific Phospholipase C from Bacillus cereus. J Org Chem. 1996;61(23):8016-8023doi: 10.1021/jo960850q.
Martin, S. F., & Wagman, A. S. (1996). Synthesis and Kinetic Evaluation of Inhibitors of the Phosphatidylinositol-Specific Phospholipase C from Bacillus cereus. The Journal of organic chemistry, 61(23), 8016-8023. https://doi.org/10.1021/jo960850q
Martin, Stephen F., and Wagman, Allan S.. "Synthesis and Kinetic Evaluation of Inhibitors of the Phosphatidylinositol-Specific Phospholipase C from Bacillus cereus." The Journal of organic chemistry vol. 61,23 (1996): 8016-8023. doi: https://doi.org/10.1021/jo960850q
Martin SF, Wagman AS. Synthesis and Kinetic Evaluation of Inhibitors of the Phosphatidylinositol-Specific Phospholipase C from Bacillus cereus. J Org Chem. 1996 Nov 15;61(23):8016-8023. doi: 10.1021/jo960850q. PMID: 11667784.
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The interactome of the amyloid beta precursor protein family members is shaped by phosphorylation of their intracellular domains.

Molecular neurodegeneration

Tamayev R, Zhou D, D'Adamio L.
PMID: 19602287
Mol Neurodegener. 2009 Jul 14;4:28. doi: 10.1186/1750-1326-4-28.

BACKGROUND: Brain tissue from patients with Alzheimer's disease has shown an increase of phosphorylation of Tyr-682, located on the conserved Y682ENPTY motif, and Thr-668 residues, both in the intracellular domain (AID) of amyloid beta precursor protein (APP), although the...

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Tamayev R, Zhou D, D'Adamio L. The interactome of the amyloid beta precursor protein family members is shaped by phosphorylation of their intracellular domains. Mol Neurodegener. 2009;4:28doi: 10.1186/1750-1326-4-28.
Tamayev, R., Zhou, D., & D'Adamio, L. (2009). The interactome of the amyloid beta precursor protein family members is shaped by phosphorylation of their intracellular domains. Molecular neurodegeneration, 428. https://doi.org/10.1186/1750-1326-4-28
Tamayev, Robert, et al. "The interactome of the amyloid beta precursor protein family members is shaped by phosphorylation of their intracellular domains." Molecular neurodegeneration vol. 4 (2009): 28. doi: https://doi.org/10.1186/1750-1326-4-28
Tamayev R, Zhou D, D'Adamio L. The interactome of the amyloid beta precursor protein family members is shaped by phosphorylation of their intracellular domains. Mol Neurodegener. 2009 Jul 14;4:28. doi: 10.1186/1750-1326-4-28. PMID: 19602287; PMCID: PMC2723102.
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UPLC-QTOF/MS-Based Lipidomic Profiling of Liver Qi-Stagnation and Spleen-Deficiency Syndrome in Patients with Hyperlipidemia.

Evidence-based complementary and alternative medicine : eCAM

Shenghua P, Shuyu T, Kunping L, Huixia Z, Xue X, Jiao G.
PMID: 30245731
Evid Based Complement Alternat Med. 2018 Aug 30;2018:4530849. doi: 10.1155/2018/4530849. eCollection 2018.

Hyperlipidemia is a common disease caused by abnormal plasma lipid metabolism. Lipidomics is a powerful and efficient technology to study the integration of disease and syndrome of Chinese medicine. This study investigated specific changes in lipid metabolites from hyperlipidemia...

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Shenghua P, Shuyu T, Kunping L, et al. UPLC-QTOF/MS-Based Lipidomic Profiling of Liver Qi-Stagnation and Spleen-Deficiency Syndrome in Patients with Hyperlipidemia. Evid Based Complement Alternat Med. 2018;2018:4530849doi: 10.1155/2018/4530849.
Shenghua, P., Shuyu, T., Kunping, L., Huixia, Z., Xue, X., & Jiao, G. (2018). UPLC-QTOF/MS-Based Lipidomic Profiling of Liver Qi-Stagnation and Spleen-Deficiency Syndrome in Patients with Hyperlipidemia. Evidence-based complementary and alternative medicine : eCAM, 20184530849. https://doi.org/10.1155/2018/4530849
Shenghua, Piao, et al. "UPLC-QTOF/MS-Based Lipidomic Profiling of Liver Qi-Stagnation and Spleen-Deficiency Syndrome in Patients with Hyperlipidemia." Evidence-based complementary and alternative medicine : eCAM vol. 2018 (2018): 4530849. doi: https://doi.org/10.1155/2018/4530849
Shenghua P, Shuyu T, Kunping L, Huixia Z, Xue X, Jiao G. UPLC-QTOF/MS-Based Lipidomic Profiling of Liver Qi-Stagnation and Spleen-Deficiency Syndrome in Patients with Hyperlipidemia. Evid Based Complement Alternat Med. 2018 Aug 30;2018:4530849. doi: 10.1155/2018/4530849. eCollection 2018. PMID: 30245731; PMCID: PMC6136559.
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Lipid metabolism of phenol-tolerant .

Biotechnology for biofuels

Henson WR, Hsu FF, Dantas G, Moon TS, Foston M.
PMID: 30607174
Biotechnol Biofuels. 2018 Dec 28;11:339. doi: 10.1186/s13068-018-1337-z. eCollection 2018.

BACKGROUND: Lignin is a recalcitrant aromatic polymer that is a potential feedstock for renewable fuel and chemical production. RESULTS: We hypothesize that the composition of lipids plays an important role in phenol tolerance. To test this hypothesis, we applied...

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Henson WR, Hsu FF, Dantas G, et al. Lipid metabolism of phenol-tolerant . Biotechnol Biofuels. 2018;11:339doi: 10.1186/s13068-018-1337-z.
Henson, W. R., Hsu, F. F., Dantas, G., Moon, T. S., & Foston, M. (2018). Lipid metabolism of phenol-tolerant . Biotechnology for biofuels, 11339. https://doi.org/10.1186/s13068-018-1337-z
Henson, William R, et al. "Lipid metabolism of phenol-tolerant ." Biotechnology for biofuels vol. 11 (2018): 339. doi: https://doi.org/10.1186/s13068-018-1337-z
Henson WR, Hsu FF, Dantas G, Moon TS, Foston M. Lipid metabolism of phenol-tolerant . Biotechnol Biofuels. 2018 Dec 28;11:339. doi: 10.1186/s13068-018-1337-z. eCollection 2018. PMID: 30607174; PMCID: PMC6309088.
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In situ probing changes in fatty-acyl chain length and desaturation of lipids in cancerous areas using mass spectrometry imaging.

Journal of mass spectrometry : JMS

Guo L, Lai Z, Wang Y, Li Z.
PMID: 32776652
J Mass Spectrom. 2020 Jul 11;56(4):e4621. doi: 10.1002/jms.4621. Epub 2020 Jul 11.

Aberrant changes in the expression levels and structure of lipids may shape tumor microenvironment. In this study, we have performed mass spectrometry imaging and profiling analysis of 63 tissues of five types of cancer, namely, breast, colorectal, esophageal, lung,...

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Guo L, Lai Z, Wang Y, et al. In situ probing changes in fatty-acyl chain length and desaturation of lipids in cancerous areas using mass spectrometry imaging. J Mass Spectrom. 2020;56(4):e4621doi: 10.1002/jms.4621.
Guo, L., Lai, Z., Wang, Y., & Li, Z. (2020). In situ probing changes in fatty-acyl chain length and desaturation of lipids in cancerous areas using mass spectrometry imaging. Journal of mass spectrometry : JMS, 56(4), e4621. https://doi.org/10.1002/jms.4621
Guo, Lei, et al. "In situ probing changes in fatty-acyl chain length and desaturation of lipids in cancerous areas using mass spectrometry imaging." Journal of mass spectrometry : JMS vol. 56,4 (2020): e4621. doi: https://doi.org/10.1002/jms.4621
Guo L, Lai Z, Wang Y, Li Z. In situ probing changes in fatty-acyl chain length and desaturation of lipids in cancerous areas using mass spectrometry imaging. J Mass Spectrom. 2020 Jul 11;56(4):e4621. doi: 10.1002/jms.4621. Epub 2020 Jul 11. PMID: 32776652.
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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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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. 2022 Jan 22;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. (2022). 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 (2022): 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. 2022 Jan 22;589:71-77. doi: 10.1016/j.bbrc.2021.11.106. Epub 2021 Dec 03. PMID: 34894559.
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Lipidomics analysis of human follicular fluid form normal-weight patients with polycystic ovary syndrome: a pilot study.

Journal of ovarian research

Ban Y, Ran H, Chen Y, Ma L.
PMID: 34645507
J Ovarian Res. 2021 Oct 13;14(1):135. doi: 10.1186/s13048-021-00885-y.

BACKGROUND: The polycystic ovary syndrome (PCOS) is the most common endocrine associated with insulin resistance, even in the absence of overweight. The global lipid profile of the follicular fluid in PCOS with normal weight as yet has not been...

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Ban Y, Ran H, Chen Y, et al. Lipidomics analysis of human follicular fluid form normal-weight patients with polycystic ovary syndrome: a pilot study. J Ovarian Res. 2021;14(1):135doi: 10.1186/s13048-021-00885-y.
Ban, Y., Ran, H., Chen, Y., & Ma, L. (2021). Lipidomics analysis of human follicular fluid form normal-weight patients with polycystic ovary syndrome: a pilot study. Journal of ovarian research, 14(1), 135. https://doi.org/10.1186/s13048-021-00885-y
Ban, Yanna, et al. "Lipidomics analysis of human follicular fluid form normal-weight patients with polycystic ovary syndrome: a pilot study." Journal of ovarian research vol. 14,1 (2021): 135. doi: https://doi.org/10.1186/s13048-021-00885-y
Ban Y, Ran H, Chen Y, Ma L. Lipidomics analysis of human follicular fluid form normal-weight patients with polycystic ovary syndrome: a pilot study. J Ovarian Res. 2021 Oct 13;14(1):135. doi: 10.1186/s13048-021-00885-y. PMID: 34645507; PMCID: PMC8515674.
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The Hob proteins are novel and conserved lipid-binding proteins at ER-PM contact sites.

Journal of cell science

Neuman SD, Jorgensen JR, Cavanagh AT, Smyth JT, Selegue JE, Emr SD, Bashirullah A.
PMID: 34415038
J Cell Sci. 2022 Mar 01;135(5). doi: 10.1242/jcs.259086. Epub 2021 Aug 20.

Membrane contact sites are critical junctures for organelle signaling and communication. Endoplasmic reticulum-plasma membrane (ER-PM) contact sites were the first membrane contact sites to be described; however, the protein composition and molecular function of these sites is still emerging....

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Neuman SD, Jorgensen JR, Cavanagh AT, et al. The Hob proteins are novel and conserved lipid-binding proteins at ER-PM contact sites. J Cell Sci. 2021;135(5)doi: 10.1242/jcs.259086.
Neuman, S. D., Jorgensen, J. R., Cavanagh, A. T., Smyth, J. T., Selegue, J. E., Emr, S. D., & Bashirullah, A. (2022). The Hob proteins are novel and conserved lipid-binding proteins at ER-PM contact sites. Journal of cell science, 135(5), . https://doi.org/10.1242/jcs.259086
Neuman, Sarah D, et al. "The Hob proteins are novel and conserved lipid-binding proteins at ER-PM contact sites." Journal of cell science vol. 135,5 (2022). doi: https://doi.org/10.1242/jcs.259086
Neuman SD, Jorgensen JR, Cavanagh AT, Smyth JT, Selegue JE, Emr SD, Bashirullah A. The Hob proteins are novel and conserved lipid-binding proteins at ER-PM contact sites. J Cell Sci. 2022 Mar 01;135(5). doi: 10.1242/jcs.259086. Epub 2021 Aug 20. PMID: 34415038; PMCID: PMC8403981.
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Untargeted lipidomic analysis of primary human epidermal melanocytes acutely and chronically exposed to UV radiation.

Molecular omics

Dalmau N, Andrieu-Abadie N, Tauler R, Bedia C.
PMID: 29748690
Mol Omics. 2018 Jun 12;14(3):170-180. doi: 10.1039/c8mo00060c.

Ultraviolet (UV) radiation present in sunlight has been related to harmful effects on skin such as premature aging and skin cancer. In order to study the effects of UV radiation on skin, many investigations have been carried out at...

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Dalmau N, Andrieu-Abadie N, Tauler R, et al. Untargeted lipidomic analysis of primary human epidermal melanocytes acutely and chronically exposed to UV radiation. Mol Omics. 2018;14(3):170-180doi: 10.1039/c8mo00060c.
Dalmau, N., Andrieu-Abadie, N., Tauler, R., & Bedia, C. (2018). Untargeted lipidomic analysis of primary human epidermal melanocytes acutely and chronically exposed to UV radiation. Molecular omics, 14(3), 170-180. https://doi.org/10.1039/c8mo00060c
Dalmau, Núria, et al. "Untargeted lipidomic analysis of primary human epidermal melanocytes acutely and chronically exposed to UV radiation." Molecular omics vol. 14,3 (2018): 170-180. doi: https://doi.org/10.1039/c8mo00060c
Dalmau N, Andrieu-Abadie N, Tauler R, Bedia C. Untargeted lipidomic analysis of primary human epidermal melanocytes acutely and chronically exposed to UV radiation. Mol Omics. 2018 Jun 12;14(3):170-180. doi: 10.1039/c8mo00060c. PMID: 29748690.
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Tissue protein and lipid alterations in response to metallic impaction.

Journal of cellular biochemistry

Seidman SA, Johnson NA, Arbelo U, Aribindi K, Bhattacharya SK.
PMID: 30277616
J Cell Biochem. 2018 Sep 11; doi: 10.1002/jcb.27563. Epub 2018 Sep 11.

Tissue response to metallic contact and injury remains poorly understood at the level of proteins and lipid changes. We used corneas as a model system (bovine, porcine [n = 300 each], and human corneas [n = 6]) to characterize...

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Seidman SA, Johnson NA, Arbelo U, et al. Tissue protein and lipid alterations in response to metallic impaction. J Cell Biochem. 2018;doi: 10.1002/jcb.27563.
Seidman, S. A., Johnson, N. A., Arbelo, U., Aribindi, K., & Bhattacharya, S. K. (2018). Tissue protein and lipid alterations in response to metallic impaction. Journal of cellular biochemistry, . https://doi.org/10.1002/jcb.27563
Seidman, Shari A, et al. "Tissue protein and lipid alterations in response to metallic impaction." Journal of cellular biochemistry vol. (2018). doi: https://doi.org/10.1002/jcb.27563
Seidman SA, Johnson NA, Arbelo U, Aribindi K, Bhattacharya SK. Tissue protein and lipid alterations in response to metallic impaction. J Cell Biochem. 2018 Sep 11; doi: 10.1002/jcb.27563. Epub 2018 Sep 11. PMID: 30277616.
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Identification of mitogen-activated protein kinase docking sites in enzymes that metabolize phosphatidylinositols and inositol phosphates.

Cell communication and signaling : CCS

Caldwell KK, Sosa M, Buckley CT.
PMID: 16445858
Cell Commun Signal. 2006 Jan 30;4:2. doi: 10.1186/1478-811X-4-2.

BACKGROUND: Reversible interactions between the components of cellular signaling pathways allow for the formation and dissociation of multimolecular complexes with spatial and temporal resolution and, thus, are an important means of integrating multiple signals into a coordinated cellular response....

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Caldwell KK, Sosa M, Buckley CT. Identification of mitogen-activated protein kinase docking sites in enzymes that metabolize phosphatidylinositols and inositol phosphates. Cell Commun Signal. 2006;4:2doi: 10.1186/1478-811X-4-2.
Caldwell, K. K., Sosa, M., & Buckley, C. T. (2006). Identification of mitogen-activated protein kinase docking sites in enzymes that metabolize phosphatidylinositols and inositol phosphates. Cell communication and signaling : CCS, 42. https://doi.org/10.1186/1478-811X-4-2
Caldwell, Kevin K, et al. "Identification of mitogen-activated protein kinase docking sites in enzymes that metabolize phosphatidylinositols and inositol phosphates." Cell communication and signaling : CCS vol. 4 (2006): 2. doi: https://doi.org/10.1186/1478-811X-4-2
Caldwell KK, Sosa M, Buckley CT. Identification of mitogen-activated protein kinase docking sites in enzymes that metabolize phosphatidylinositols and inositol phosphates. Cell Commun Signal. 2006 Jan 30;4:2. doi: 10.1186/1478-811X-4-2. PMID: 16445858; PMCID: PMC1379644.
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Showing 1 to 12 of 52 entries