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Journal articles on the topic 'Phosphatidylinositol-4-phosphate 5-kinase de type 1'

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Published: 7 October 2023

Last updated: 31 July 2025

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1

van Horck, Francis P. G., Emmanuelle Lavazais, Britta J. Eickholt, Wouter H. Moolenaar та Nullin Divecha. "Essential Role of Type Iα Phosphatidylinositol 4-Phosphate 5-Kinase in Neurite Remodeling". Current Biology 12, № 3 (2002): 241–45. http://dx.doi.org/10.1016/s0960-9822(01)00660-1.

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Shim, Hyeseok, Chuan Wu, Shivan Ramsamooj, et al. "Deletion of the gene Pip4k2c, a novel phosphatidylinositol kinase, results in hyperactivation of the immune system." Proceedings of the National Academy of Sciences 113, no. 27 (2016): 7596–601. http://dx.doi.org/10.1073/pnas.1600934113.

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Type 2 phosphatidylinositol-5-phosphate 4-kinase (PI5P4K) converts phosphatidylinositol-5-phosphate to phosphatidylinositol-4,5-bisphosphate. Mammals have three enzymes PI5P4Kα, PI5P4Kβ, and PI5P4Kγ, and these enzymes have been implicated in metabolic control, growth control, and a variety of stress responses. Here, we show that mice with germline deletion of type 2 phosphatidylinositol-5-phosphate 4-kinase gamma (Pip4k2c), the gene encoding PI5P4Kγ, appear normal in regard to growth and viability but have increased inflammation and T-cell activation as they age. Immune cell infiltrates increa

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Bridges, Dave, Jing-Tyan Ma, Sujin Park, Ken Inoki, Lois S. Weisman, and Alan R. Saltiel. "Phosphatidylinositol 3,5-bisphosphate plays a role in the activation and subcellular localization of mechanistic target of rapamycin 1." Molecular Biology of the Cell 23, no. 15 (2012): 2955–62. http://dx.doi.org/10.1091/mbc.e11-12-1034.

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The kinase complex mechanistic target of rapamycin 1 (mTORC1) plays an important role in controlling growth and metabolism. We report here that the stepwise formation of phosphatidylinositol 3-phosphate (PI(3)P) and phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2) regulates the cell type–specific activation and localization of mTORC1. PI(3)P formation depends on the class II phosphatidylinositol 3-kinase (PI3K) PI3K-C2α, as well as the class III PI3K Vps34, while PI(3,5)P2 requires the phosphatidylinositol-3-phosphate-5-kinase PIKFYVE. In this paper, we show that PIKFYVE and PI3K-C2α are nece

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Prasad, K. V., R. Kapeller, O. Janssen, et al. "Phosphatidylinositol (PI) 3-kinase and PI 4-kinase binding to the CD4-p56lck complex: the p56lck SH3 domain binds to PI 3-kinase but not PI 4-kinase." Molecular and Cellular Biology 13, no. 12 (1993): 7708–17. http://dx.doi.org/10.1128/mcb.13.12.7708-7717.1993.

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CD4 serves as a receptor for major histocompatibility complex class II antigens and as a receptor for the human immunodeficiency virus type 1 (HIV-1) viral coat protein gp120. It is coupled to the protein-tyrosine kinase p56lck, an interaction necessary for an optimal response of certain T cells to antigen. In addition to the protein-tyrosine kinase domain, p56lck possesses Src homology 2 and 3 (SH2 and SH3) domains as well as a unique N-terminal region. The mechanism by which p56lck generates intracellular signals is unclear, although it has the potential to interact with various downstream m

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Prasad, K. V., R. Kapeller, O. Janssen, et al. "Phosphatidylinositol (PI) 3-kinase and PI 4-kinase binding to the CD4-p56lck complex: the p56lck SH3 domain binds to PI 3-kinase but not PI 4-kinase." Molecular and Cellular Biology 13, no. 12 (1993): 7708–17. http://dx.doi.org/10.1128/mcb.13.12.7708.

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CD4 serves as a receptor for major histocompatibility complex class II antigens and as a receptor for the human immunodeficiency virus type 1 (HIV-1) viral coat protein gp120. It is coupled to the protein-tyrosine kinase p56lck, an interaction necessary for an optimal response of certain T cells to antigen. In addition to the protein-tyrosine kinase domain, p56lck possesses Src homology 2 and 3 (SH2 and SH3) domains as well as a unique N-terminal region. The mechanism by which p56lck generates intracellular signals is unclear, although it has the potential to interact with various downstream m

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Davis, J. N., C. O. Rock, M. Cheng, et al. "Complementation of growth factor receptor-dependent mitogenic signaling by a truncated type I phosphatidylinositol 4-phosphate 5-kinase." Molecular and Cellular Biology 17, no. 12 (1997): 7398–406. http://dx.doi.org/10.1128/mcb.17.12.7398.

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Substitution of phenylalanine for tyrosine at codon 809 (Y809F) of the human colony-stimulating factor 1 (CSF-1) receptor (CSF-1R) impairs ligand-stimulated tyrosine kinase activity, prevents induction of c-MYC and cyclin D1 genes, and blocks CSF-1-dependent progression through the G1 phase of the cell cycle. We devised an unbiased genetic screen to isolate genes that restore the ability of CSF-1 to stimulate growth in cells that express mutant CSF-1R (Y809F). This screen led us to identify a truncated form of the murine type Ibeta phosphatidylinositol 4-phosphate 5-kinase (mPIP5K-Ibeta). This

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Demian, Douglas J., Susan L. Clugston, Meta M. Foster, et al. "High-Throughput, Cell-Free, Liposome-Based Approach for Assessing In Vitro Activity of Lipid Kinases." Journal of Biomolecular Screening 14, no. 7 (2009): 838–44. http://dx.doi.org/10.1177/1087057109339205.

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Lipid kinases are central players in lipid signaling pathways involved in inflammation, tumorigenesis, and metabolic syndrome. A number of these kinase targets have proven difficult to investigate in higher throughput cell-free assay systems. This challenge is partially due to specific substrate interaction requirements for several of the lipid kinase family members and the resulting incompatibility of these substrates with most established, homogeneous assay formats. Traditional, cell-free in vitro investigational methods for members of the lipid kinase family typically involve substrate inco

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Huang, Luofei, Han Li, and Quanzhi Lin. "Identification of key genes and diagnostic biomarkers for peripheral atherosclerosis: A multi-omics approach." Medicine 104, no. 21 (2025): e42437. https://doi.org/10.1097/md.0000000000042437.

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Peripheral atherosclerosis (PAS), characterized by lipid plaque accumulation in arterial walls, significantly increases cardiovascular risk. This study aimed to identify molecular biomarkers and elucidate underlying mechanisms of PAS progression. We analyzed 2 gene expression omnibus datasets (GSE28829, GSE100927) to identify differentially expressed genes (P < .05, |log2FC| ≥ 0.585). Functional enrichment (Gene Ontology/Kyoto Encyclopedia of Genes and Genomes) and Mendelian randomization analyses were performed using genome-wide association study and expression quantitative trait loci data

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9

Yamamoto, Masaya, Mark Z. Chen, Ying-Jie Wang та ін. "Hypertonic Stress Increases Phosphatidylinositol 4,5-Bisphosphate Levels by Activating PIP5KIβ". Journal of Biological Chemistry 281, № 43 (2006): 32630–38. http://dx.doi.org/10.1074/jbc.m605928200.

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Hyperosmotic stress increases phosphoinositide levels, reorganizes the actin cytoskeleton, and induces multiple acute and adaptive physiological responses. Here we showed that phosphatidylinositol 4,5-bisphosphate (PIP2) level increased rapidly in HeLa cells during hypertonic treatment. Depletion of the human type I phosphatidylinositol 4-phosphate 5-kinase β isoform (PIP5KIβ) by RNA interference impaired both the PIP2 and actin cytoskeletal responses. PIP5KIβ was recruited to membranes and was activated by hypertonic stress through Ser/Thr dephosphorylation. Calyculin A, a protein phosphatase

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Gerber, Pehuén Pereyra, Mercedes Cabrini, Carolina Jancic, et al. "Rab27a controls HIV-1 assembly by regulating plasma membrane levels of phosphatidylinositol 4,5-bisphosphate." Journal of Cell Biology 209, no. 3 (2015): 435–52. http://dx.doi.org/10.1083/jcb.201409082.

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During the late stages of the HIV-1 replication cycle, the viral polyprotein Pr55Gag is recruited to the plasma membrane (PM), where it binds phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) and directs HIV-1 assembly. We show that Rab27a controls the trafficking of late endosomes carrying phosphatidylinositol 4-kinase type 2 α (PI4KIIα) toward the PM of CD4+ T cells. Hence, Rab27a promotes high levels of PM phosphatidylinositol 4-phosphate and the localized production of PI(4,5)P2, therefore controlling Pr55Gag membrane association. Rab27a also controls PI(4,5)P2 levels at the virus-containi

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Kunii, Yasuto, Junya Matsumoto, Ryuta Izumi, et al. "Evidence for Altered Phosphoinositide Signaling-Associated Molecules in the Postmortem Prefrontal Cortex of Patients with Schizophrenia." International Journal of Molecular Sciences 22, no. 15 (2021): 8280. http://dx.doi.org/10.3390/ijms22158280.

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Phosphoinositides (PIs) play important roles in the structure and function of the brain. Associations between PIs and the pathophysiology of schizophrenia have been studied. However, the significance of the PI metabolic pathway in the pathology of schizophrenia is unknown. We examined the expression of PI signaling-associated proteins in the postmortem brain of schizophrenia patients. Protein expression levels of phosphatidylinositol 4-phosphate 5-kinase type-1 gamma (PIP5K1C), phosphatidylinositol 4-kinase alpha (PIK4CA, also known as PIK4A), phosphatase and tensin homolog deleted from chromo

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Zhang, Jiping, Ruihua Luo, Heqing Wu, Shunhui Wei, Weiping Han та GuoDong Li. "Role of Type Iα Phosphatidylinositol-4-Phosphate 5-Kinase in Insulin Secretion, Glucose Metabolism, and Membrane Potential in INS-1 β-Cells". Endocrinology 150, № 5 (2008): 2127–35. http://dx.doi.org/10.1210/en.2008-0516.

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Insulin secretion from β-cells is regulated by a complex signaling network. Our earlier study has reported that Rac1 participates in glucose- and cAMP-induced insulin secretion probably via maintaining a functional actin structure for recruitment of insulin granules. Type Iα phosphatidylinositol-4-phosphate 5-kinase (PIP5K-Iα) is a downstream effector of Rac1 and a critical enzyme for synthesis of phosphatidylinositol-4,5-bisphosphate (PIP2). By using an RNA interference technique, PIP5K-Iα in INS-1 β-cells could be specifically knocked down by 70–75%. PIP5K-Iα knockdown disrupted filamentous

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PANARETOU, Christina, and Sharon A. TOOZE. "Regulation and recruitment of phosphatidylinositol 4-kinase on immature secretory granules is independent of ADP-ribosylation factor 1." Biochemical Journal 363, no. 2 (2002): 289–95. http://dx.doi.org/10.1042/bj3630289.

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Heterotrimeric G-proteins, as well as small GTPases of the Rho and ADP-ribosylation factor (ARF) family, are implicated in the regulation of lipid kinases, including PtdIns 4-kinases and PtdIns(4)P 5-kinases. Here, we describe a PtdIns 4-kinase activity on immature secretory granules (ISGs), regulated secretory organelles formed from the trans-Golgi network (TGN), and investigate the regulation of PtdIns4P levels on these membranes. Over 50% of the PtdIns 4-kinase activity on ISGs is inhibited by both a low concentration of adenosine and the monoclonal antibody 4C5G, a specific inhibitor of th

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Jones, David H., James B. Morris, Clive P. Morgan, Hisatake Kondo, Robin F. Irvine, and Shamshad Cockcroft. "Type I Phosphatidylinositol 4-Phosphate 5-Kinase Directly Interacts with ADP-ribosylation Factor 1 and Is Responsible for Phosphatidylinositol 4,5-Bisphosphate Synthesis in the Golgi Compartment." Journal of Biological Chemistry 275, no. 18 (2000): 13962–66. http://dx.doi.org/10.1074/jbc.c901019199.

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15

Yan, Qinnan, Huanqing Gao, Qing Yao, Kun Ling, and Guozhi Xiao. "Loss of phosphatidylinositol-4-phosphate 5-kinase type-1 gamma (Pip5k1c) in mesenchymal stem cells leads to osteopenia by impairing bone remodeling." Journal of Biological Chemistry 298, no. 3 (2022): 101639. http://dx.doi.org/10.1016/j.jbc.2022.101639.

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Mace, Emily M., Jinyi Zhang, Katherine A. Siminovitch, and Fumio Takei. "Elucidation of the integrin LFA-1–mediated signaling pathway of actin polarization in natural killer cells." Blood 116, no. 8 (2010): 1272–79. http://dx.doi.org/10.1182/blood-2009-12-261487.

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Abstract The leukocyte integrin LFA-1 is critical for natural killer (NK) cell cytotoxicity as it mediates NK-cell adhesion to target cells and generates activating signals that lead to polarization of the actin cytoskeleton. However, the LFA-1–mediated signaling pathway is not fully understood. Here, we examined the subcellular localization of actin-associated proteins in wild-type, talin-deficient, and Wiskott-Aldrich Syndrome protein (WASP)–deficient NK cells bound to beads coated with the LFA-1 ligand intercellular adhesion molecule-1 (ICAM-1). In addition, we carried out coimmunoprecipita

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Mikhalitskaya, E. V., O. V. Roshchina, S. A. Ivanova, and N. A. Bokhan. "Study of the polymorphic variants of the PIP5K2A gene association with the comorbidity of alcoholism and affective disorders." V.M. BEKHTEREV REVIEW OF PSYCHIATRY AND MEDICAL PSYCHOLOGY, no. 4-1 (December 9, 2019): 124–26. http://dx.doi.org/10.31363/2313-7053-2019-4-1-124-126.

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One of the common pathogenetic mechanisms of the formation of alcohol dependence and depressive disorders can be a violation of the neurotransmitter systems, in particular — dopamine. Phosphatidylinositol-4-phosphate-5-kinase type 2 alpha (PIP5K2A) plays an important role in the regulation of neuronal excitability and synaptic dopamine neurotransmission. The aim of this study was to assess the presence of associations of the PIP5K2A gene polymorphic variants with the comorbid course of alcohol dependence and depressive disorders. This study showed differences in the frequency of the genotype d

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Papasotiriou, Ioannis, Panagiotis Apostolou, Dimitrios-Athanasios Ntanovasilis, Panagiotis Parsonidis, Daniar Osmonov, and Klaus-Peter Jünemann. "Study and detection of potential markers for predicting metastasis into lymph nodes in prostate cancer." Biomarkers in Medicine 14, no. 14 (2020): 1317–27. http://dx.doi.org/10.2217/bmm-2020-0372.

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Hormone-refractory prostate carcinoma has a different cell surface protein profile than hormone-sensitive prostate carcinoma, which provides migration ability and interactions with organs/tissues. Detection and association of these proteins with lymph node metastasis via lymphadenectomy might be beneficial for patients. Gene expression analysis in hormone-refractory and hormone-sensitive commercial cancer cell lines was performed and, after co-cultivation with osteoblasts or endothelial cells, knockdown experiments followed to validate potential biomarkers. “ Myeloid-associated differentiation

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Xie, Y., L. Zhu, and G. Zhao. "Assignment¹ of type I phosphatidylinositol-4-phosphate 5-kinase (PIP5K1A) to human chromosome bands 1q22→ q24 by in situ hybridization." Cytogenetic and Genome Research 88, no. 3-4 (2000): 197–99. http://dx.doi.org/10.1159/000015545.

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Kawase, Atsushi, Yuta Inoue, Miho Hirosoko, Yuka Sugihara, Hiroaki Shimada, and Masahiro Iwaki. "Decrease in Multidrug Resistance-associated Protein 2 Activities by Knockdown of Phosphatidylinositol 4-phosphate 5-kinase in Hepatocytes and Cancer Cells." Journal of Pharmacy & Pharmaceutical Sciences 22 (November 19, 2019): 576–84. http://dx.doi.org/10.18433/jpps30444.

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Purpose: The plasma membrane localization and transport activity of multidrug resistance-associated protein 2 (MRP2/ABCC2) and P-glycoprotein (P-gp/ABCB1) efflux transporters are governed by transporter-associated proteins. Phosphatidylinositol 4,5-bisphosphate (PIP2) formed by phosphatidylinositol 4-phosphate 5-kinase type 1 (PIP5K1) activates the linker function of radixin for efflux transporters. Radixin is involved in the plasma membrane localization of efflux transporters. We examined whether PIP5K1 could be a target for the modulation of transporter activities in hepatocytes and cancer c

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Jakobsen, Søren N., D. Grahame Hardie, Nick Morrice, and Hans E. Tornqvist. "5′-AMP-activated Protein Kinase Phosphorylates IRS-1 on Ser-789 in Mouse C2C12 Myotubes in Response to 5-Aminoimidazole-4-carboxamide Riboside." Journal of Biological Chemistry 276, no. 50 (2001): 46912–16. http://dx.doi.org/10.1074/jbc.c100483200.

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Exercise is known to increase insulin sensitivity and is an effective form of treatment for the hyperglycemia observed in type 2 diabetes. Activation of 5′-AMP-activated protein kinase (AMPK) by 5-aminoimidazole-4-carboxamide riboside (AICAR), exercise, or electrically stimulated contraction leads to increased glucose transport in skeletal muscle. Here we report the first evidence of a direct interaction between AMPK and the most upstream component of the insulin-signaling cascade, insulin receptor substrate-1 (IRS-1). We find that AMPK rapidly phosphorylates IRS-1 on Ser-789 in cell-free assa

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Le, Duong Duy Thai, Truc Phan Hoang Le та Sang Yoon Lee. "PIP5Kγ Mediates PI(4,5)P2/Merlin/LATS1 Signaling Activation and Interplays with Hsc70 in Hippo–YAP Pathway Regulation". International Journal of Molecular Sciences 24, № 19 (2023): 14786. http://dx.doi.org/10.3390/ijms241914786.

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The type I phosphatidylinositol 4-phosphate 5-kinase (PIP5K) family produces the critical lipid regulator phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) in the plasma membrane (PM). Here, we investigated the potential role of PIP5Kγ, a PIP5K isoform, in the Hippo pathway. The ectopic expression of PIP5Kγ87 or PIP5Kγ90, two major PIP5Kγ splice variants, activated large tumor suppressor kinase 1 (LATS1) and inhibited Yes-associated protein (YAP), whereas PIP5Kγ knockdown yielded opposite effects. The regulatory effects of PIP5Kγ were dependent on its catalytic activity and the presence of Mer

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Park, S., W. Lee, KH You, et al. "Regulation of phosphatidylinositol-phosphate kinase IIgamma gene transcription by thyroid-stimulating hormone in thyroid cells." Journal of Molecular Endocrinology 26, no. 2 (2001): 127–33. http://dx.doi.org/10.1677/jme.0.0260127.

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This study was performed to evaluate the effects of thyroid-stimulating hormone (TSH) on phosphatidylinositol-4-phosphate 5-kinase type IIgamma (PIPKIIgamma) gene expression in the thyrocytes of FRTL-5 cells. Although PIPKIIgamma mRNA was expressed constantly in the absence of added TSH, its expression increased remarkably in the presence of 10(-9) M TSH. This increase started within 6 h of the addition of TSH, and reached a maximum at 8 h. The mRNA expression properties of PIPKIIgamma in the cells were identified using inhibitors. Actinomycin D blocked PIPKIIgamma transcription strongly, whil

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Jones, Carol A., Suzanne E. Greer-Phillips, and Katherine A. Borkovich. "The Response Regulator RRG-1 Functions Upstream of a Mitogen-activated Protein Kinase Pathway Impacting Asexual Development, Female Fertility, Osmotic Stress, and Fungicide Resistance inNeurospora crassa." Molecular Biology of the Cell 18, no. 6 (2007): 2123–36. http://dx.doi.org/10.1091/mbc.e06-03-0226.

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Two-component systems, consisting of proteins with histidine kinase and/or response regulator domains, regulate environmental responses in bacteria, Archaea, fungi, slime molds, and plants. Here, we characterize RRG-1, a response regulator protein from the filamentous fungus Neurospora crassa. The cell lysis phenotype of Δrrg-1 mutants is reminiscent of osmotic-sensitive (os) mutants, including nik-1/os-1 (a histidine kinase) and strains defective in components of a mitogen-activated protein kinase (MAPK) pathway: os-4 (MAPK kinase kinase), os-5 (MAPK kinase), and os-2 (MAPK). Similar to os mu

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Grey, Andrew, Qi Chen, Karen Callon, Xin Xu, Ian R. Reid, and Jill Cornish. "The Phospholipids Sphingosine-1-Phosphate and Lysophosphatidic Acid Prevent Apoptosis in Osteoblastic Cells via a Signaling Pathway Involving Gi Proteins and Phosphatidylinositol-3 Kinase." Endocrinology 143, no. 12 (2002): 4755–63. http://dx.doi.org/10.1210/en.2002-220347.

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Abstract The naturally occurring phospholipids lysophosphatidic acid (LPA) and sphingosine-1-phosphate (S1P) have recently emerged as bioactive compounds that exert mitogenic effects in many cell types, including osteoblasts. In the current study, we examined the ability of each of these compounds to influence osteoblast survival. Using terminal deoxynucleotidyl transferase-mediated deoxyuridine 5′-triphosphate nick-end labeling and DNA fragmentation assays, we found that both LPA and S1P dose-dependently inhibited (by at least 50% and 40%, respectively) the apoptosis induced by serum withdraw

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Tan, Xiaojun, Narendra Thapa, Yihan Liao, Suyong Choi, and Richard A. Anderson. "PtdIns(4,5)P2 signaling regulates ATG14 and autophagy." Proceedings of the National Academy of Sciences 113, no. 39 (2016): 10896–901. http://dx.doi.org/10.1073/pnas.1523145113.

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Autophagy is a regulated self-digestion pathway with fundamental roles in cell homeostasis and diseases. Autophagy is regulated by coordinated actions of a series of autophagy-related (ATG) proteins. The Barkor/ATG14(L)–VPS34 (a class III phosphatidylinositol 3-kinase) complex and its product phosphatidylinositol 3-phosphate [PtdIns(3)P] play key roles in autophagy initiation. ATG14 contains a C-terminal Barkor/ATG14(L) autophagosome-targeting sequence (BATS) domain that senses the curvature of PtdIns(3)P-containing membrane. The BATS domain also strongly binds PtdIns(4,5)P2, but the functiona

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Jessen, Niels, Rasmus Pold, Esben S. Buhl, Lasse S. Jensen, Ole Schmitz, and Sten Lund. "Effects of AICAR and exercise on insulin-stimulated glucose uptake, signaling, and GLUT-4 content in rat muscles." Journal of Applied Physiology 94, no. 4 (2003): 1373–79. http://dx.doi.org/10.1152/japplphysiol.00250.2002.

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Physical activity is known to increase insulin action in skeletal muscle, and data have indicated that 5′-AMP-activated protein kinase (AMPK) is involved in the molecular mechanisms behind this beneficial effect. 5-Aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) can be used as a pharmacological tool to repetitively activate AMPK, and the objective of this study was to explore whether the increase in insulin-stimulated glucose uptake after either long-term exercise or chronic AICAR administration was followed by fiber-type-specific changes in insulin signaling and/or changes in GLUT-4

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Heled, Yuval, Yair Shapiro, Yoav Shani, et al. "Physical exercise prevents the development of type 2 diabetes mellitus in Psammomys obesus." American Journal of Physiology-Endocrinology and Metabolism 282, no. 2 (2002): E370—E375. http://dx.doi.org/10.1152/ajpendo.00296.2001.

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We hypothesized that exercise training might prevent diabetes mellitus in Psammomys obesus. Animals were assigned to three groups: high-energy diet (CH), high-energy diet and exercise (EH), and low-energy diet (CL). The EH group ran on a treadmill 5 days/wk, twice a day. After 4 wk, 93% of the CH group were diabetic compared with only 20% of the EH group. There was no difference in weight gain among the groups. Both EH and CH groups were hyperinsulinemic. Epididymal fat (% of body weight) was higher in the CH group than in either the EH and or the CL group. Protein kinase C (PKC)-δ activity an

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Ono, Hiraku, Hideki Katagiri, Makoto Funaki, et al. "Regulation of Phosphoinositide Metabolism, Akt Phosphorylation, and Glucose Transport by PTEN (Phosphatase and Tensin Homolog Deleted on Chromosome 10) in 3T3-L1 Adipocytes." Molecular Endocrinology 15, no. 8 (2001): 1411–22. http://dx.doi.org/10.1210/mend.15.8.0684.

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Abstract To investigate the roles of PTEN (phosphatase and tensin homolog deleted on chromosome 10) in the regulation of 3-position phosphorylated phosphoinositide metabolism as well as insulin-induced Akt phosphorylation and glucose metabolism, wild-type PTEN and its phosphatase-dead mutant (C124S) with or without an N-terminal myristoylation tag were overexpressed in Sf-9 cells and 3T3-L1 adipocytes using baculovirus and adenovirus systems, respectively. When expressed in Sf-9 cells together with the p110α catalytic subunit of phosphoinositide 3-kinase, myristoylated PTEN markedly reduced th

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Shi, Min, Michael L. Mathai, Guoqin Xu, Xiao Q. Su та Andrew J. McAinch. "The effect of dietary supplementation with blueberry, cyanidin-3-O-β-glucoside, yoghurt and its peptides on gene expression associated with glucose metabolism in skeletal muscle obtained from a high-fat-high-carbohydrate diet induced obesity model". PLOS ONE 17, № 9 (2022): e0270306. http://dx.doi.org/10.1371/journal.pone.0270306.

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Obesity is a leading global health problem contributing to various chronic diseases, including type II diabetes mellitus (T2DM). The aim of this study was to investigate whether blueberries, yoghurt, and their respective bioactive components, Cyanidin-3-O-β-glucoside (C3G) and peptides alone or in combinations, alter the expression of genes related to glucose metabolism in skeletal muscles from diet-induced obese mice. In extensor digitorum longus (EDL), yoghurt up-regulated the expression of activation of 5’adenosine monophosphate-activated protein kinase (AMPK), insulin receptor substrate-1

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Dantas, Ana Paula V., Junsuke Igarashi, and Thomas Michel. "Sphingosine 1-phosphate and control of vascular tone." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (2003): H2045—H2052. http://dx.doi.org/10.1152/ajpheart.01089.2002.

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Sphingosine-1-phosphate (S1P) is a platelet-derived lipid mediator that activates the endothelial isoform of nitric oxide synthase (eNOS) in endothelial cells. However, the role of S1P in endothelium-dependent vasodilation and the signaling pathways elicited by S1P in intact vessels are largely unknown. We found that S1P induces dose-dependent transient relaxation of isolated pressurized mesenteric arterioles (EC5010 ± 3 nM); maximal vasodilation (55 ± 8%) is seen ∼2 min after S1P addition and returns to baseline by 5 min. S1P promotes comparable responses in arterioles from wild-type but not

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Farese, Robert V., Mini P. Sajan, and Mary L. Standaert. "Insulin-Sensitive Protein Kinases (Atypical Protein Kinase C and Protein Kinase B/Akt): Actions and Defects in Obesity and Type II Diabetes." Experimental Biology and Medicine 230, no. 9 (2005): 593–605. http://dx.doi.org/10.1177/153537020523000901.

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Glucose transport into muscle is the initial process in glucose clearance and is uniformly defective in insulin-resistant conditions of obesity, metabolic syndrome, and Type II diabetes mellitus. Insulin regulates glucose transport by activating insulin receptor substrate-1 (IRS-1)-dependent phosphatidylinositol 3-kinase (PI3K) which, via increases in PI-3, 4, 5-triphosphate (PIP3), activates atypical protein kinase C (aPKC) and protein kinase B (PKB/Akt). Here, we review (i) the evidence that both aPKC and PKB are required for insulin-stimulated glucose transport, (ii) abnormalities in muscle

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Javaux, F., M. F. Vincent, D. R. Wagner, and G. van den Berghe. "Cell-type specificity of inhibition of glycolysis by 5-amino-4-imidazolecarboxamide riboside. Lack of effect in rabbit cardiomyocytes and human erythrocytes, and inhibition in FTO-2B rat hepatoma cells." Biochemical Journal 305, no. 3 (1995): 913–19. http://dx.doi.org/10.1042/bj3050913.

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The nucleoside AICAriboside (5-amino-4-imidazolecarboxamide riboside) has been shown to inhibit glycolysis in isolated rat hepatocytes [Vincent, Bontemps and Van den Berghe (1992) Biochem. J. 281, 267-272]. The effect is mediated by AICA-ribotide (ZMP), the product of the phosphorylation of AICA-riboside by adenosine kinase. To assess the cell-type specificity of the effect, studies were conducted in rabbit cardiomyocytes, human erythrocytes and rat hepatoma FTO-2B cells. AICA-riboside had no effect on glycolysis in cardiomyocytes, and a slight stimulatory effect in erythrocytes, but inhibited

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Bonangelino, C. J., N. L. Catlett, and L. S. Weisman. "Vac7p, a novel vacuolar protein, is required for normal vacuole inheritance and morphology." Molecular and Cellular Biology 17, no. 12 (1997): 6847–58. http://dx.doi.org/10.1128/mcb.17.12.6847.

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During cell division, the vacuole of Saccharomyces cerevisiae partitions between mother and daughter cells. A portion of the parental vacuole membrane moves into the bud, and ultimately membrane scission divides the vacuole into two separate structures. Here we characterize two yeast mutations causing defects in vacuole membrane scission, vac7-1 and vac14-1. A third mutant, afab1-2 strain, isolated in a nonrelated screen (A. Yamamoto et al., Mol. Biol. Cell 6:525-539, 1995) shares the vacuolar phenotypes of the vac7-1 and vac14-1 strains. Unlike the wild type, mutant vacuoles are not multilobe

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Corse, Emily, Krista Goodman, Morgan O'Shea, et al. "Abstract 5574: Degradation of PIP4K2C by novel bivalent functional degrader LRK-A induces tumor regression in CRC." Cancer Research 84, no. 6_Supplement (2024): 5574. http://dx.doi.org/10.1158/1538-7445.am2024-5574.

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Abstract Phosphatidylinositol 5-phosphate 4-kinase, type II, gamma (PIP4K2C) is a lipid kinase with critical roles in vesicular trafficking, autophagy-dependent catabolism, and modulation of the immune system. Family members PIP4K2A and PIP4K2B are implicated in regulation of autophagy, cancer cell proliferation, and response to insulin, whereas PIP4K2C has a unique function in the immune response to cancer. Beyond the ability to convert PI5P to PI45P2, PIP4K2 kinases regulate membrane localization and clustering of PI45P2 and thus govern multiple aspects of membrane trafficking. These activit

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Lee, Myung-Ja, Denis Feliers, Meenalakshmi M. Mariappan, et al. "A role for AMP-activated protein kinase in diabetes-induced renal hypertrophy." American Journal of Physiology-Renal Physiology 292, no. 2 (2007): F617—F627. http://dx.doi.org/10.1152/ajprenal.00278.2006.

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We tested the hypothesis that AMP-activated protein kinase (AMPK), an energy sensor, regulates diabetes-induced renal hypertrophy. In kidney glomerular epithelial cells, high glucose (30 mM), but not equimolar mannitol, stimulated de novo protein synthesis and induced hypertrophy in association with increased phosphorylation of eukaryotic initiation factor 4E binding protein 1 and decreased phosphorylation of eukaryotic elongation factor 2, regulatory events in mRNA translation. These high-glucose-induced changes in protein synthesis were phosphatidylinositol 3-kinase, Akt, and mammalian targe

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Canabal, Debra D., Joseph G. Potian, Ricardo G. Duran, Joseph J. McArdle, and Vanessa H. Routh. "Hyperglycemia impairs glucose and insulin regulation of nitric oxide production in glucose-inhibited neurons in the ventromedial hypothalamus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 2 (2007): R592—R600. http://dx.doi.org/10.1152/ajpregu.00207.2007.

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Physiological changes in extracellular glucose, insulin, and leptin regulate glucose-excited (GE) and glucose-inhibited (GI) neurons in the ventromedial hypothalamus (VMH). Nitric oxide (NO) signaling, which is involved in the regulation of food intake and insulin signaling, is altered in obesity and diabetes. We previously showed that glucose and leptin inhibit NO production via the AMP-activated protein kinase (AMPK) pathway, while insulin stimulates NO production via the phosphatidylinositol-3-OH kinase (PI3K) pathway in VMH GI neurons. Hyperglycemia-induced inhibition of AMPK reduces PI3K

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McEwen, Scott T., Sarah F. Balus, Matthew J. Durand, and Julian H. Lombard. "Angiotensin II maintains cerebral vascular relaxation via EGF receptor transactivation and ERK1/2." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 4 (2009): H1296—H1303. http://dx.doi.org/10.1152/ajpheart.01325.2008.

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This study identified, on the integrative level, two components of the ANG II signaling pathway that lay downstream from the ANG II type 1 (AT1) receptor and are critically involved in maintaining vascular relaxation in cerebral resistance arteries. In these experiments, the relaxation of isolated middle cerebral arteries (MCA) in response to ACh (10−9-10−5 M), iloprost (10−16-10−11 g/ml), and reduced PO2 was lost and the ratio of phospho-ERK/ERK1/2 was significantly reduced in aortas of male Sprague-Dawley rats fed a high-salt (HS; 4% NaCl) diet to suppress plasma ANG II levels. In salt-fed r

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Egom, Emmanuel Eroume A., Tamer M. A. Mohamed, Mamas A. Mamas, et al. "Activation of Pak1/Akt/eNOS signaling following sphingosine-1-phosphate release as part of a mechanism protecting cardiomyocytes against ischemic cell injury." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 4 (2011): H1487—H1495. http://dx.doi.org/10.1152/ajpheart.01003.2010.

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We investigated whether plasma long-chain sphingoid base (LCSB) concentrations are altered by transient cardiac ischemia during percutaneous coronary intervention (PCI) in humans and examined the signaling through the sphingosine-1-phosphate (S1P) cascade as a mechanism underlying the S1P cardioprotective effect in cardiac myocytes. Venous samples were collected from either the coronary sinus ( n = 7) or femoral vein ( n = 24) of 31 patients at 1 and 5 min and 12 h, following induction of transient myocardial ischemia during elective PCI. Coronary sinus levels of LCSB were increased by 1,072%

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Kushnir, O. Yu, and I. M. Yaremii. "AGE-RELATED CHANGES OF GLYCOLYTIC ACTIVITY AND ANTIOXIDANT CAPACITY IN THE BLOOD OF ALLOXAN DIABETIC RATS." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 20, no. 3 (2020): 169–73. http://dx.doi.org/10.31718/2077-1096.20.3.169.

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The increasing incidence of type 1 diabetes coupled with advances in treatment of type 1 diabetes has resulted in an unprecedented number of older adults living with and controllable type 1 diabetes. The objective of this experimental study was to assess the impact of aging on the level of basal glycaemia and activities of glucose-6-phosphate dehydrogenase [EC1.1.1.49], pyruvate kinase [EC 2.7.1.40] and glutathione reductase [EC1.6.4.2] in erythrocytes of alloxan-diabetic rats. Methods: We used 100 male Wistar rats, divided into two age groups: I group included- 2-month (adult) animals, and II

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Chavakis, Triantafyllos, Antje Willuweit, Florea Lupu, Klaus Preissner, and Sandip Kanse. "Release of Soluble Urokinase Receptor from Vascular Cells*." Thrombosis and Haemostasis 86, no. 08 (2001): 686–93. http://dx.doi.org/10.1055/s-0037-1616105.

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SummaryUrokinase-type plasminogen activator (uPA) and its cell surface-receptor (uPAR) regulate cellular functions linked to adhesion and migration and contribute to pericellular proteolysis in tissue remodelling processes. Soluble uPAR (suPAR) is present in the circulation, peritoneal and ascitic fluid and in the cystic fluid from ovarian cancer. We have investigated the origin and the vascular distribution of the soluble receptor, which accounts for 10-20% of the total receptor in vascular endothelial and smooth muscle cells. Phase separation analysis of the cell conditioned media with Trito

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Munnik, T., R. F. Irvine, and A. Musgrave. "Rapid turnover of phosphatidylinositol 3-phosphate in the green alga Chlamydomonas eugametos: signs of a phosphatidylinositide 3-kinase signalling pathway in lower plants?" Biochemical Journal 298, no. 2 (1994): 269–73. http://dx.doi.org/10.1042/bj2980269.

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When Chlamydomonas eugametos gametes were incubated in carrier-free [32P]P1, the label was rapidly incorporated into PtdInsP and PtdInsP2 and, after reaching a maximum within minutes, was chased out by recirculating unlabelled P1 in the cell. This pulse-chase labelling pattern reflects their rapid turnover. In contrast, 32P incorporation into the structural lipids was slow and continued for hours. Of the radioactivity in the PtdInsP spot, 15% was in PtdIns3P and the rest in PtdIns4P, and of that in the PtdInsP2 spot, 1% was in PtdIns(3,4)P2 and the rest in PtdIns(4,5)P2, confirming the finding

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Lamia, Katja A., Odile D. Peroni, Young-Bum Kim, Lucia E. Rameh, Barbara B. Kahn та Lewis C. Cantley. "Increased Insulin Sensitivity and Reduced Adiposity in Phosphatidylinositol 5-Phosphate 4-Kinase β−/− Mice". Molecular and Cellular Biology 24, № 11 (2004): 5080–87. http://dx.doi.org/10.1128/mcb.24.11.5080-5087.2004.

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ABSTRACT Phosphorylated derivatives of the lipid phosphatidylinositol are known to play critical roles in insulin response. Phosphatidylinositol 5-phosphate 4-kinases convert phosphatidylinositol 5-phosphate to phosphatidylinositol 4,5-bis-phosphate. To understand the physiological role of these kinases, we generated mice that do not express phosphatidylinositol 5-phosphate 4-kinase β. These mice are hypersensitive to insulin and have reduced body weights compared to wild-type littermates. While adult male mice lacking phosphatidylinositol 5-phosphate 4-kinase β have significantly less body fa

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Friedlaender, M. M., D. Jain, Z. Ahmed, D. Hart, R. L. Barnett, and E. P. Nord. "Endothelin activation of phospholipase D: dual modulation by protein kinase C and Ca2+." American Journal of Physiology-Renal Physiology 264, no. 5 (1993): F845—F853. http://dx.doi.org/10.1152/ajprenal.1993.264.5.f845.

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Previous work from this laboratory has identified an endothelin (ET) type A (ETA) receptor on cultured rat renal medullary interstitial cells (RMIC), coupled to phosphatidylinositol-specific phospholipase C (PI-PLC), dihydropyridine-insensitive receptor-operated Ca2+ channels, and phospholipase A2. The current studies explored a role for ET stimulation of phosphatidylcholine-specific phospholipase D (PC-PLD) in intracellular signaling of this cell type. ET stimulated PLD activation, as measured by phosphatidic acid (PA) or phosphatidylethanol (PEt) accumulation, in a time- and concentration-de

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Ford, Christopher P., Kenneth V. Wong, Van B. Lu, Elena Posse de Chaves, and Peter A. Smith. "Differential Neurotrophic Regulation of Sodium and Calcium Channels in an Adult Sympathetic Neuron." Journal of Neurophysiology 99, no. 3 (2008): 1319–32. http://dx.doi.org/10.1152/jn.00966.2007.

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Adult neuronal phenotype is maintained, at least in part, by the sensitivity of individual neurons to a specific selection of neurotrophic factors and the availability of such factors in the neurons' environment. Nerve growth factor (NGF) increases the functional expression of Na+ channel currents ( INa) and both N- and L-type Ca2+ currents ( ICa,N and ICa,L) in adult bullfrog sympathetic ganglion (BFSG) B-neurons. The effects of NGF on ICa involve the mitogen-activated protein kinase (MAPK) pathway. Prolonged exposure to the ganglionic neurotransmitter luteinizing hormone releasing hormone (L

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Bulhak, Aliaksandr A., Christian Jung, Claes-Göran Östenson, Jon O. Lundberg, Per-Ove Sjöquist та John Pernow. "PPAR-α activation protects the type 2 diabetic myocardium against ischemia-reperfusion injury: involvement of the PI3-Kinase/Akt and NO pathway". American Journal of Physiology-Heart and Circulatory Physiology 296, № 3 (2009): H719—H727. http://dx.doi.org/10.1152/ajpheart.00394.2008.

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Several clinical studies have shown the beneficial cardiovascular effects of fibrates in patients with diabetes and insulin resistance. The ligands of peroxisome proliferator-activated receptor-α (PPAR-α) reduce ischemia-reperfusion injury in nondiabetic animals. We hypothesized that the activation of PPAR-α would exert cardioprotection in type 2 diabetic Goto-Kakizaki (GK) rats, involving mechanisms related to nitric oxide (NO) production via the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. GK rats and age-matched Wistar rats (n ≥ 7) were given either 1) the PPAR-α agonist WY-14643 (WY),

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GHELLI, Anna, Anna M. PORCELLI, Annalisa FACCHINI, Silvana HRELIA, Flavio FLAMIGNI та Michela RUGOLO. "Phospholipase D1 is threonine-phosphorylated in human-airway epithelial cells stimulated by sphingosine-1-phosphate by a mechanism involving Src tyrosine kinase and protein kinase Cδ". Biochemical Journal 366, № 1 (2002): 187–93. http://dx.doi.org/10.1042/bj20020264.

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The regulatory role of protein kinase C (PKC) δ isoform in the stimulation of phospholipase D (PLD) by sphingosine-1-phosphate (SPP) in a human-airway epithelial cell line (CFNPE9o−) was revealed by using antisense oligodeoxynucleotide to PKCδ, in combination with the specific inhibitor rottlerin. Cell treatment with antisense oligodeoxynucleotide, but not with sense oligodeoxynucleotide, completely eliminated PKCδ expression and resulted in the strong inhibition of SPP-stimulated phosphatidic acid formation. Indeed, among the PKCα, β, δ, ∊ and ζ isoforms expressed in these cells, only PKCδ wa

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Arai, N., H. Masuzaki, T. Tanaka та ін. "Ceramide and Adenosine 5′-Monophosphate-Activated Protein Kinase Are Two Novel Regulators of 11β-Hydroxysteroid Dehydrogenase Type 1 Expression and Activity in Cultured Preadipocytes". Endocrinology 148, № 11 (2007): 5268–77. http://dx.doi.org/10.1210/en.2007-0349.

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Increased activity of intracellular glucocorticoid reactivating enzyme, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in obese adipose tissue contributes to adipose dysfunction. As recent studies have highlighted a potential role of preadipocytes in adipose dysfunction, we tested the hypothesis that a variety of metabolic stress mediated by ceramide or AMP-activated protein kinase (AMPK) would regulate 11β-HSD1 in preadipocytes. The present study is the first to show that 1) expression of 11β-HSD1 in 3T3-L1 preadipocytes was robustly induced when cells were treated with cell-permeable cer

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YAMADA, Kazuya, and Tamio NOGUCHI. "Nutrient and hormonal regulation of pyruvate kinase gene expression." Biochemical Journal 337, no. 1 (1998): 1–11. http://dx.doi.org/10.1042/bj3370001.

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Mammalian pyruvate kinase (PK), a key glycolytic enzyme, has two genes named PKL and PKM, which produce the L- and R-type isoenzymes by means of alternative promoters, and the M1-and M2-types by mutually exclusive alternative splicing respectively. The expression of these genes is tissue-specific and under developmental, dietary and hormonal control. The L-type isoenzyme (L-PK) gene contains multiple regulatory elements necessary for regulation in the 5´ flanking region, up to position -170. Both L-II and L-III elements are required for stimulation of L-PK gene transcription by carbohydrates s

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Luo, Jian-Dong, Tai-Ping Hu, Li Wang, Min-Sheng Chen, Shi-Ming Liu, and Alex F. Chen. "Sonic hedgehog improves delayed wound healing via enhancing cutaneous nitric oxide function in diabetes." American Journal of Physiology-Endocrinology and Metabolism 297, no. 2 (2009): E525—E531. http://dx.doi.org/10.1152/ajpendo.00308.2009.

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Sonic hedgehog (SHH) plays an important role in postnatal tissue repair. The present study tested the hypothesis that impaired SHH pathway results in delayed wound healing by suppressing cutaneous nitric oxide (NO) function in type 1 diabetes. Adult male C57/B6 mice and streptozotocin (STZ)-induced type 1 diabetic mice were used. Although cutaneous SHH and Patched-1 (Ptc-1 encoded by PTCH, PTCH 1) proteins were increased significantly on day 4 after wounding compared with day 0 in normal mice, both were decreased significantly in STZ-induced diabetic mice. Topical application of SHH restored w

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