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Journal articles on the topic 'PIP5K1'

Author: Grafiati

Published: 7 October 2023

Last updated: 31 July 2025

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1

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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2

Wright, Brittany D., Catherine Simpson, Michael Stashko, et al. "Development of a High-Throughput Screening Assay to Identify Inhibitors of the Lipid Kinase PIP5K1C." Journal of Biomolecular Screening 20, no. 5 (2014): 655–62. http://dx.doi.org/10.1177/1087057114564057.

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Phosphatidylinositol 4-phosphate 5-kinases (PIP5Ks) regulate a variety of cellular processes, including signaling through G protein-coupled receptors (GPCRs), endocytosis, exocytosis, and cell migration. These lipid kinases synthesize phosphatidylinositol 4,5-bisphosphate (PIP2) from phosphatidylinositol 4-phosphate [PI(4)P]. Because small-molecule inhibitors of these lipid kinases did not exist, molecular and genetic approaches were predominantly used to study PIP5K1 regulation of these cellular processes. Moreover, standard radioisotope-based lipid kinase assays cannot be easily adapted for

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3

Wang, Yanfeng, Lurong Lian, Aae Suzuki, et al. "Loss of Individual PIP5KI Isoforms Demonstrate That Spatial PIP2 Synthesis Is Required for Platelet Second Messenger Formation & Integrity of the Actin Cytoskeleton." Blood 112, no. 11 (2008): 109. http://dx.doi.org/10.1182/blood.v112.11.109.109.

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Abstract Following thrombin stimulation, platelet PIP5KI synthesizes phosphatidylinositol 4,5-bisphosphate (PIP2), which can be hydrolyzed by phospholipase C to generate second messengers such as IP3. PIP2 also regulates cytoskeletal dynamics by directly interacting with actin-binding proteins. Three isoforms of PIP5KI (α, β, and γ) are all capable of phosphorylating PI4P to synthesize PIP2. However, these isoforms have different primary structures, expression levels in various tissues, and intracellular localization. We have generated and characterized murine lines lacking PIP5KIβ or PIP5KIγ,

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4

Padrón, David, Ying Jie Wang, Masaya Yamamoto, Helen Yin та Michael G. Roth. "Phosphatidylinositol phosphate 5-kinase Iβ recruits AP-2 to the plasma membrane and regulates rates of constitutive endocytosis". Journal of Cell Biology 162, № 4 (2003): 693–701. http://dx.doi.org/10.1083/jcb.200302051.

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Overexpression of phosphatidylinositol phosphate 5-kinase (PIP5KI) isoforms α, β, or γ in CV-1 cells increased phosphatidylinositol 4,5-bisphosphate (PIP2) levels by 35, 180, and 0%, respectively. Endocytosis of transferrin receptors, association of AP-2 proteins with membranes, and the number of clathrin-coated pits at the plasma membrane increased when PIP2 increased. When expression of PIP5KIβ was inhibited with small interference RNA in HeLa cells, expression of PIP5KIα was also reduced slightly, but PIP5KIγ expression was increased. PIP2 levels and internalization of transferrin receptors

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5

Chen, Xinsheng, Yanfeng Wang, Tami L. Bach та ін. "Mice Lacking PIP5Kβ or PIP5Kγ Have Unique Cytoskeletal Changes within Their Megakaryocytes & Platelets." Blood 106, № 11 (2005): 380. http://dx.doi.org/10.1182/blood.v106.11.380.380.

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Abstract Phosphatidylinositol-4, 5-bisphosphate (PIP2) is vital for the signaling cascades that are critical for actin dynamics. Although all PIP5K isoforms (α , β , and γ ) synthesize PIP2 by phosphorylating PI4P, the isoforms have different primary structures, expression levels in various tissues, and intracellular localization. To test the hypothesis that the functions of these isoforms are also different, we have generated murine lines that contain null mutations in either of two platelet PIP5K isoforms, PIP5Kβ and PIP5Kγ . PIP5Kβ -null mice were born 42% less than anticipated by Mendelian

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6

Clarke, Jonathan H., Piers C. Emson та Robin F. Irvine. "Localization of phosphatidylinositol phosphate kinase IIγ in kidney to a membrane trafficking compartment within specialized cells of the nephron". American Journal of Physiology-Renal Physiology 295, № 5 (2008): F1422—F1430. http://dx.doi.org/10.1152/ajprenal.90310.2008.

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PIP4Ks (type II phosphatidylinositol 4-phosphate kinases) are phosphatidylinositol 5-phosphate (PtdIns5P) 4-kinases, believed primarily to regulate cellular PtdIns5P levels. In this study, we investigated the expression, localization, and associated biological activity of the least-studied PIP4K isoform, PIP4Kγ. Quantitative RT-PCR and in situ hybridization revealed that compared with PIP4Kα and PIP4Kβ, PIP4Kγ is expressed at exceptionally high levels in the kidney, especially the cortex and outer medulla. A specific antibody was raised to PIP4Kγ, and immunohistochemistry with this and with an

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7

Wang, Yanfeng, Aae Suzuki, Lurong Lian та ін. "Platelets Lacking PIP5KIγ Have Impaired Cytoskeletal Dynamics and Adhesion, but No Defect in Integrin Activation." Blood 114, № 22 (2009): 772. http://dx.doi.org/10.1182/blood.v114.22.772.772.

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Abstract Abstract 772 Following thrombin stimulation, platelet PIP5KI synthesizes phosphatidylinositol 4,5-bisphosphate (PIP2), which can be hydrolyzed by phospholipase C to generate second messengers such as IP3. PIP2 also regulates cytoskeletal dynamics by directly interacting with actin-binding proteins such as talin. Three isoforms of PIP5KI (α, β, and γ) are all capable of phosphorylating PI4P to synthesize PIP2. We have generated and characterized murine lines lacking individual PIP5KI isoforms. While mice lacking PIP5KIα and PIP5KIα have absent second messenger formation and partially i

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8

Khadka, Bijendra, and Radhey S. Gupta. "Novel Molecular Signatures in the PIP4K/PIP5K Family of Proteins Specific for Different Isozymes and Subfamilies Provide Important Insights into the Evolutionary Divergence of this Protein Family." Genes 10, no. 4 (2019): 312. http://dx.doi.org/10.3390/genes10040312.

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Members of the PIP4K/PIP5K family of proteins, which generate the highly important secondary messenger phosphatidylinositol-4,5-bisphosphate, play central roles in regulating diverse signaling pathways. In eukaryotic organisms, multiple isozymes and subfamilies of PIP4K/PIP5K proteins are found and it is of much interest to understand their evolution and species distribution and what unique molecular and biochemical characteristics distinguish specific isozymes and subfamilies of proteins. We report here the species distribution of different PIP4K/PIP5K family of proteins in eukaryotic organis

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9

Bultsma, Yvette, Willem-Jan Keune та Nullin Divecha. "PIP4Kβ interacts with and modulates nuclear localization of the high-activity PtdIns5P-4-kinase isoform PIP4Kα". Biochemical Journal 430, № 2 (2010): 223–35. http://dx.doi.org/10.1042/bj20100341.

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The β-isoform of PIP4K (PtdIns5P-4-kinase) regulates the levels of nuclear PtdIns5P, which in turn modulates the acetylation of the tumour suppressor p53. The crystal structure of PIP4Kβ demonstrated that it can form a homodimer with the two subunits arranged in opposite orientations. Using MS, isoform-specific antibodies against PIP4Ks, RNAi (RNA interference) suppression and overexpression studies, we show that PIP4Kβ interacts in vitro and in vivo with the PIP4Kα isoform. As the two isoforms phosphorylate the same substrate to generate the same product, the interaction could be considered t

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Drake, J. M., and J. Huang. "PIP5K1 inhibition as a therapeutic strategy for prostate cancer." Proceedings of the National Academy of Sciences 111, no. 35 (2014): 12578–79. http://dx.doi.org/10.1073/pnas.1413363111.

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Aikawa, Yoshikatsu, and Thomas F. J. Martin. "ARF6 regulates a plasma membrane pool of phosphatidylinositol(4,5)bisphosphate required for regulated exocytosis." Journal of Cell Biology 162, no. 4 (2003): 647–59. http://dx.doi.org/10.1083/jcb.200212142.

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ADP-ribosylation factor (ARF) 6 regulates endosomal plasma membrane trafficking in many cell types, but is also suggested to play a role in Ca2+-dependent dense-core vesicle (DCV) exocytosis in neuroendocrine cells. In the present work, expression of the constitutively active GTPase-defective ARF6Q67L mutant in PC12 cells was found to inhibit Ca2+-dependent DCV exocytosis. The inhibition of exocytosis was accompanied by accumulation of ARFQ67L, phosphatidylinositol 4,5-bisphosphate (PIP2), and the phosphatidylinositol 4-phosphate 5-kinase type I (PIP5KI) on endosomal membranes with their corre

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Fairn, Gregory D., Koji Ogata, Roberto J. Botelho, et al. "An electrostatic switch displaces phosphatidylinositol phosphate kinases from the membrane during phagocytosis." Journal of Cell Biology 187, no. 5 (2009): 701–14. http://dx.doi.org/10.1083/jcb.200909025.

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Plasmalemmal phosphatidylinositol (PI) 4,5-bisphosphate (PI4,5P2) synthesized by PI 4-phosphate (PI4P) 5-kinase (PIP5K) is key to the polymerization of actin that drives chemotaxis and phagocytosis. We investigated the means whereby PIP5K is targeted to the membrane and its fate during phagosome formation. Homology modeling revealed that all PIP5K isoforms feature a positively charged face. Together with the substrate-binding loop, this polycationic surface is proposed to constitute a coincidence detector that targets PIP5Ks to the plasmalemma. Accordingly, manipulation of the surface charge d

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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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Wang, Yanfeng, Rustem Litvinov, John W. Weisel, John H. Hartwig та Charles S. Abrams. "PIP5KIγ Knockout Megakaryocytes Have Defects in Their Cytoskeleton & Demarcation Membrane System, yet Form Proplatlets & Platelets." Blood 108, № 11 (2006): 1793. http://dx.doi.org/10.1182/blood.v108.11.1793.1793.

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Abstract Phosphatidylinositol-4,5-bisphosphate (PIP2) is a critical component of intracellular signaling cascades as well as actin dynamics. It is synthesized by the phosphorylation of PI4P by one of three isoforms of PIP5KI (α,β, or γ). We found that the targeted disruption of PIP5KIγ results in early prenatal mortality that prevented studies of bone marrow or liver hematopoietic cells. However, we were able to analyze yolk sac progenitor cells differentiated ex vivo into megakaryocytes. Imaging in the electron microscope showed that PIP5KIγ-null megakaryocytes have normal architectural appea

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15

Zeng, Xuankun, Arzu Uyar, Dexin Sui та ін. "Structural insights into lethal contractural syndrome type 3 (LCCS3) caused by a missense mutation of PIP5Kγ". Biochemical Journal 475, № 14 (2018): 2257–69. http://dx.doi.org/10.1042/bcj20180326.

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Signaling molecule phosphatidylinositol 4,5-bisphosphate is produced primarily by phosphatidylinositol 4-phosphate 5-kinase (PIP5K). PIP5K is essential for the development of the human neuronal system, which has been exemplified by a recessive genetic disorder, lethal congenital contractural syndrome type 3, caused by a single aspartate-to-asparagine mutation in the kinase domain of PIP5Kγ. So far, the exact role of this aspartate residue has yet to be elucidated. In this work, we conducted structural, functional and computational studies on a zebrafish PIP5Kα variant with a mutation at the sa

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Hassan, Bassem A., Sergei N. Prokopenko, Sebastian Breuer, Bing Zhang, Achim Paululat, and Hugo J. Bellen. "skittles, a Drosophila Phosphatidylinositol 4-Phosphate 5-Kinase, Is Required for Cell Viability, Germline Development and Bristle Morphology, But Not for Neurotransmitter Release." Genetics 150, no. 4 (1998): 1527–37. http://dx.doi.org/10.1093/genetics/150.4.1527.

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Abstract The phosphatidylinositol pathway is implicated in the regulation of numerous cellular functions and responses to extracellular signals. An important branching point in the pathway is the phosphorylation of phosphatidylinositol 4-phosphate by the phosphatidylinositol 4-phosphate 5-kinase (PIP5K) to generate the second messenger phosphatidylinositol 4,5-bis-phosphate (PIP2). PIP5K and PIP2 have been implicated in signal transduction, cytoskeletal regulation, DNA synthesis, and vesicular trafficking. We have cloned and generated mutations in a Drosophila PIP5K type I (skittles). Our anal

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Kuroda, Ryo, Mariko Kato, Tomohiko Tsuge, and Takashi Aoyama. "Arabidopsis phosphatidylinositol 4‐phosphate 5‐kinase genes PIP5K7 , PIP5K8 , and PIP5K9 are redundantly involved in root growth adaptation to osmotic stress." Plant Journal 106, no. 4 (2021): 913–27. http://dx.doi.org/10.1111/tpj.15207.

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18

Parkhitko, Andrey A., Arashdeep Singh, Sharon Hsieh, et al. "Cross-species identification of PIP5K1-, splicing- and ubiquitin-related pathways as potential targets for RB1-deficient cells." PLOS Genetics 17, no. 2 (2021): e1009354. http://dx.doi.org/10.1371/journal.pgen.1009354.

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The RB1 tumor suppressor is recurrently mutated in a variety of cancers including retinoblastomas, small cell lung cancers, triple-negative breast cancers, prostate cancers, and osteosarcomas. Finding new synthetic lethal (SL) interactions with RB1 could lead to new approaches to treating cancers with inactivated RB1. We identified 95 SL partners of RB1 based on a Drosophila screen for genetic modifiers of the eye phenotype caused by defects in the RB1 ortholog, Rbf1. We validated 38 mammalian orthologs of Rbf1 modifiers as RB1 SL partners in human cancer cell lines with defective RB1 alleles.

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Ling, King-Hwa, Shu-San Loo, Rozita Rosli, Mariana Nor Shamsudin, Rahmah Mohamed, and Kiew-Lian Wan. "In Silico Identification and Characterization of a Putative Phosphatidylinositol 4-Phosphate 5-Kinase (PIP5K) Gene in Eimeria Tenella." In Silico Biology: Journal of Biological Systems Modeling and Multi-Scale Simulation 7, no. 1 (2007): 115–21. https://doi.org/10.3233/isb-00281.

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Phosphatidylinositol 4-phosphate 5-kinases (PIP5Ks) play diverse roles in the cellular biology of many organisms, including signal transduction, secretion and vesicular trafficking, and regulation of cytoskeleton assembly. Discovery of the PIP5K gene in Eimeria tenella may shed light on its role in the biology of this avian protozoan, and afford further understanding of the cell-host interaction, particularly during the invasion process. In this study, we report the identification of the PIP5K coding region in the genome sequence of Eimeria tenella using in silico gene prediction approaches. P

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Wang, Yanfeng, Lurong Lian, Tami L. Bach, Xinsheng Chen, Qing-Min Chen та Charles S. Abrams. "PIP5Kγ-Null Mutation Induces Cytoskeletal Changes within Megakaryocytes." Blood 104, № 11 (2004): 629. http://dx.doi.org/10.1182/blood.v104.11.629.629.

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Abstract All eukaryotic cells contain the phospholipid phosphatidylinositol-4, 5-bisphosphate (PIP2) that serves multiple roles in signaling cascades critical for actin dynamics. Phosphatidylinositol-4-phosphate 5 kinase (PIP5K) catalyzes the synthesis of PIP2 by phosphorylating PI4P. Although the classical PIP5K isoforms (α, β, and γ) generate the same phospholipid product, the isoforms have different primary structures, are expressed at different levels in various tissues, and localize in different intracellular compartments. Therefore, it is likely that the functions of these isoforms are d

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Chen, Xinsheng, Yanfeng Wang, Edward K. Williamson та ін. "Loss of PIP5KIβ Causes a Defect in Lamellipodia Formation and Shear Resistant Adhesion." Blood 108, № 11 (2006): 141. http://dx.doi.org/10.1182/blood.v108.11.141.141.

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Abstract Phosphatidylinositol 4,5-bisphosphate (PIP2) is widely known for the production of lipid second messengers after its hydrolysis by phospholipase C or phosphorylation by phosphatidylinositol 3-kinase. PIP2 also regulates cytoskeletal dynamics by directly interacting with actin-binding proteins. Three isoforms of PIP5KI (α, β, and γ) are all capable of phosphorylating PI4P to synthesize PIP2. However, these isoforms have different primary structures, expression levels in various tissues, and intracellular localization. Our previous studies have demonstrated that PIP5KIβ and PIP5KIγ are

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Semenas, J., A. Hedblom, R. R. Miftakhova, et al. "The role of PI3K/AKT-related PIP5K1 and the discovery of its selective inhibitor for treatment of advanced prostate cancer." Proceedings of the National Academy of Sciences 111, no. 35 (2014): E3689—E3698. http://dx.doi.org/10.1073/pnas.1405801111.

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Liu, Aizhuo, Dexin Sui, Dianqing Wu, and Jian Hu. "The activation loop of PIP5K functions as a membrane sensor essential for lipid substrate processing." Science Advances 2, no. 11 (2016): e1600925. http://dx.doi.org/10.1126/sciadv.1600925.

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Phosphatidylinositol 4-phosphate 5-kinase (PIP5K), a representative member of the phosphatidylinositol phosphate kinase (PIPK) family, is a major enzyme that biosynthesizes the signaling molecule PI(4,5)P2 (phosphatidylinositol 4,5-bisphosphate) in eukaryotic cells. The stringent specificity toward lipid substrates and the high sensitivity to the membrane environment strongly suggest a membrane-sensing mechanism, but the underlying structural basis is still largely unknown. We present a nuclear magnetic resonance (NMR) study on a peptide commensurate with a PIP5K’s activation loop, which has b

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Carpenter, C. L. "Btk-dependent regulation of phosphoinositide synthesis." Biochemical Society Transactions 32, no. 2 (2004): 326–29. http://dx.doi.org/10.1042/bst0320326.

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Activation of the BCR (B cell antigen receptor) stimulates the production of both PtdIns(3,4,5)P3 and Ins(1,4,5)P3. PtdIns(3,4,5)P3 and Ins(1,4,5)P3 are generated from a common substrate, PtdIns(4,5)P2. In some systems, continuous PtdIns(4,5)P2 synthesis is necessary for maximal Ins(1,4,5)P3 production, but whether this is true for the BCR, and whether PtdIns(4,5)P2 synthesis is regulated following BCR activation, are not known. We found that Btk (Bruton's tyrosine kinase), a member of the Tec family of cytoplasmic protein tyrosine kinases, is constitutively associated with PIP5Ks (phosphatidy

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Di Meo, Danila, Trisha Kundu, Priyadarshini Ravindran, Bhavin Shah та Andreas W. Püschel. "Pip5k1γ regulates axon formation by limiting Rap1 activity". Life Science Alliance 7, № 5 (2024): e202302383. http://dx.doi.org/10.26508/lsa.202302383.

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During their differentiation, neurons establish a highly polarized morphology by forming axons and dendrites. Cortical and hippocampal neurons initially extend several short neurites that all have the potential to become an axon. One of these neurites is then selected as the axon by a combination of positive and negative feedback signals that promote axon formation and prevent the remaining neurites from developing into axons. Here, we show that Pip5k1γ is required for the formation of a single axon as a negative feedback signal that regulates C3G and Rap1 through the generation of phosphatidy

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Wang, Zepeng, Zhongyu Wang, Xianguo Li, et al. "Identification and Analysis of the Expression of the PIP5K Gene Family in Tomatoes." International Journal of Molecular Sciences 25, no. 1 (2023): 159. http://dx.doi.org/10.3390/ijms25010159.

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To explore the function of phosphatidylinositol 4-phosphate 5-kinase (PIP5K) in tomatoes, members of the tomato PIP5K family were identified and characterized using bioinformatic methods, and their expression patterns were also analyzed under salt stress and in different tissues. Twenty-one PIP5K members—namely, SlPIP5K1–SlPIP5K21—were identified from ten chromosomes, and these were divided into three groups according to a phylogenetic analysis. Further bioinformatic analysis showed four pairs of collinear relationships and fragment replication events among the SlPIP5K family members. To under

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El Sayegh, T. Y., P. D. Arora, K. Ling та ін. "Phosphatidylinositol-4,5 Bisphosphate Produced by PIP5KIγ Regulates Gelsolin, Actin Assembly, and Adhesion Strength of N-Cadherin Junctions". Molecular Biology of the Cell 18, № 8 (2007): 3026–38. http://dx.doi.org/10.1091/mbc.e06-12-1159.

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Phosphoinositides regulate several actin-binding proteins but their role at intercellular adhesions has not been defined. We found that phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) was generated at sites of N-cadherin–mediated intercellular adhesion and was a critical regulator of intercellular adhesion strength. Immunostaining for PI(4,5)P2 or transfection with GFP-PH-PLCδ showed that PI(4,5)P2 was enriched at sites of N-cadherin adhesions and this enrichment required activated Rac1. Isoform-specific immunostaining for type I phosphatidylinositol 4-phosphate 5 kinase (PIP5KI) showed that

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Zarza, Xavier, Ringo Van Wijk, Lana Shabala, et al. "Lipid kinases PIP5K7 and PIP5K9 are required for polyamine‐triggered K + efflux in Arabidopsis roots." Plant Journal 104, no. 2 (2020): 416–32. http://dx.doi.org/10.1111/tpj.14932.

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Wang, Ying Jie, Wen Hong Li, Jing Wang та ін. "Critical role of PIP5KIγ87 in InsP3-mediated Ca2+ signaling". Journal of Cell Biology 167, № 6 (2004): 1005–10. http://dx.doi.org/10.1083/jcb.200408008.

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Phosphatidylinositol 4,5-bisphosphate (PIP2) is the obligatory precursor of inositol 1,4,5-trisphosphate (InsP3 or IP3) and is therefore critical to intracellular Ca2+ signaling. Using RNA interference (RNAi), we identified the short splice variant of type I phosphatidylinositol 4-phosphate 5-kinase γ (PIP5KIγ87) as the major contributor of the PIP2 pool that supports G protein–coupled receptor (GPCR)-mediated IP3 generation. PIP5KIγ87 RNAi decreases the histamine-induced IP3 response and Ca2+ flux by 70%. Strikingly, RNAi of other PIP5KI isoforms has minimal effect, even though some of these

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Zhao, Xiaoying, Penglei Cui, Guoli Hu та ін. "PIP5k1β controls bone homeostasis through modulating both osteoclast and osteoblast differentiation". Journal of Molecular Cell Biology 12, № 1 (2019): 55–70. http://dx.doi.org/10.1093/jmcb/mjz028.

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Abstract PIP5k1β is crucial to the generation of phosphotidylinosotol (4, 5)P2. PIP5k1β participates in numerous cellular activities, such as B cell and platelet activation, cell phagocytosis and endocytosis, cell apoptosis, and cytoskeletal organization. In the present work, we aimed to examine the function of PIP5k1β in osteoclastogenesis and osteogenesis to provide promising strategies for osteoporosis prevention and treatment. We discovered that PIP5k1β deletion in mice resulted in obvious bone loss and that PIP5k1β was highly expressed during both osteoclast and osteoblast differentiation

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Ren, X. D., G. M. Bokoch, A. Traynor-Kaplan, G. H. Jenkins, R. A. Anderson, and M. A. Schwartz. "Physical association of the small GTPase Rho with a 68-kDa phosphatidylinositol 4-phosphate 5-kinase in Swiss 3T3 cells." Molecular Biology of the Cell 7, no. 3 (1996): 435–42. http://dx.doi.org/10.1091/mbc.7.3.435.

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Our previous work showed that post-translationally modified Rho in its GTP-bound state stimulated phosphatidylinositol 4-phosphate 5-kinase (PIP5K) activity in mouse fibroblast lysates. To investigate whether Rho physically interacts with PIP5K, we incubated immobilized Rho-GST with Swiss 3T3 cell lysates and tested for retained PIP5K activity. Rho-GST, but not Ras-GST or GST alone, bound significant PIP5K activity. The binding of PIP5K was independent of whether Rho was in a GTP- or GDP-bound state. An antibody against a 68-kDa human erythrocyte type I PIP5K recognized a single 68-kDa protein

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Abajy, Mohammad Y., Jolanta Kopeć, Katarzyna Schiwon, et al. "A Type IV-Secretion-Like System Is Required for Conjugative DNA Transport of Broad-Host-Range Plasmid pIP501 in Gram-Positive Bacteria." Journal of Bacteriology 189, no. 6 (2007): 2487–96. http://dx.doi.org/10.1128/jb.01491-06.

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ABSTRACT Plasmid pIP501 has a very broad host range for conjugative transfer among a wide variety of gram-positive bacteria and gram-negative Escherichia coli. Functionality of the pIP501 transfer (tra) genes in E. coli was proven by pIP501 retrotransfer to Enterococcus faecalis (B. Kurenbach, C. Bohn, J. Prabhu, M. Abudukerim, U. Szewzyk, and E. Grohmann, Plasmid 50:86-93, 2003). The 15 pIP501 tra genes are organized in a single operon (B. Kurenbach, J. Kopeć, M. Mägdefrau, K. Andreas, W. Keller, C. Bohn, M. Y. Abajy, and E. Grohmann, Microbiology 152:637-645, 2006). The pIP501 tra operon i

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Mao, Yuntao S., Masaki Yamaga, Xiaohui Zhu та ін. "Essential and unique roles of PIP5K-γ and -α in Fcγ receptor-mediated phagocytosis". Journal of Cell Biology 184, № 2 (2009): 281–96. http://dx.doi.org/10.1083/jcb.200806121.

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The actin cytoskeleton is dynamically remodeled during Fcγ receptor (FcγR)-mediated phagocytosis in a phosphatidylinositol (4,5)-bisphosphate (PIP2)-dependent manner. We investigated the role of type I phosphatidylinositol 4-phosphate 5-kinase (PIP5K) γ and α isoforms, which synthesize PIP2, during phagocytosis. PIP5K-γ−/− bone marrow–derived macrophages (BMM) have a highly polymerized actin cytoskeleton and are defective in attachment to IgG-opsonized particles and FcγR clustering. Delivery of exogenous PIP2 rescued these defects. PIP5K-γ knockout BMM also have more RhoA and less Rac1 activat

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Shimada, Takashi L., Shigeyuki Betsuyaku, Noriko Inada, et al. "Enrichment of Phosphatidylinositol 4,5-Bisphosphate in the Extra-Invasive Hyphal Membrane Promotes Colletotrichum Infection of Arabidopsis thaliana." Plant and Cell Physiology 60, no. 7 (2019): 1514–24. http://dx.doi.org/10.1093/pcp/pcz058.

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Abstract Pathogenic fungi from the genus Colletotrichum form invasive hyphae; the hyphae are surrounded by an extra-invasive hyphal membrane (EIHM), which is continuous with the plant plasma membrane. Although the EIHM plays a crucial role as the interface between plant and fungal cells, its precise function during Colletotrichum infection remains elusive. Here, we show that enrichment of phosphoinositides (PIs) has a crucial role in Colletotrichum infection. We observed the localization of PIs in Arabidopsis thaliana cells infected by A. thaliana-adapted Colletotrichum higginsianum (Ch), and

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Goessweiner-Mohr, Nikolaus, Markus Eder, Gerhard Hofer, et al. "Structure of the double-stranded DNA-binding type IV secretion protein TraN fromEnterococcus." Acta Crystallographica Section D Biological Crystallography 70, no. 9 (2014): 2376–89. http://dx.doi.org/10.1107/s1399004714014187.

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Conjugative transfer through type IV secretion multiprotein complexes is the most important means of spreading antimicrobial resistance. Plasmid pIP501, frequently found in clinicalEnterococcus faecalisandEnterococcus faeciumisolates, is the first Gram-positive (G+) conjugative plasmid for which self-transfer to Gram-negative (G−) bacteria has been demonstrated. The pIP501-encoded type IV secretion system (T4SS) protein TraN localizes to the cytoplasm and shows specific DNA binding. The specific DNA-binding site upstream of the pIP501 origin of transfer (oriT) was identified by a novel footpri

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Xie, Zhongjian, Sandra M. Chang, Sally D. Pennypacker, Er-Yuan Liao та Daniel D. Bikle. "Phosphatidylinositol-4-phosphate 5-kinase 1α Mediates Extracellular Calcium-induced Keratinocyte Differentiation". Molecular Biology of the Cell 20, № 6 (2009): 1695–704. http://dx.doi.org/10.1091/mbc.e08-07-0756.

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Extracellular calcium (Cao) is a major regulator of keratinocyte differentiation, but the mechanism is unclear. Phosphatidylinositol-4-phosphate 5-kinase 1α (PIP5K1α) is critical in synthesizing phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2]. In this study, we sought to determine whether PIP5K1α plays a role in mediating the ability of Cao to induce keratinocyte differentiation. We found that treatment of human keratinocytes in culture with Cao resulted in increased PIP5K1α level and activity, as well as PI(4,5)P2 level, binding of phosphatidylinositol 3,4,5-triphosphate [PI(3,4,5)P3] to an

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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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Chakrabarti, Rajarshi, Sulagna Sanyal, Amit Ghosh, Kaushik Bhar, Chandrima Das та Anirban Siddhanta. "Phosphatidylinositol-4-phosphate 5-Kinase 1α Modulates Ribosomal RNA Gene Silencing through Its Interaction with Histone H3 Lysine 9 Trimethylation and Heterochromatin Protein HP1-α". Journal of Biological Chemistry 290, № 34 (2015): 20893–903. http://dx.doi.org/10.1074/jbc.m114.633727.

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Phosphoinositide signaling has been implicated in the regulation of numerous cellular processes including cytoskeletal dynamics, cellular motility, vesicle trafficking, and gene transcription. Studies have also shown that nuclear phosphoinositide(s) regulates processes such as mRNA export, cell cycle progression, gene transcription, and DNA repair. We have shown previously that the nuclear form of phosphatidylinositol-4-phosphate 5-kinase 1α (PIP5K), the enzyme responsible for phosphatidylinositol 4,5-bisphosphate synthesis, is modified by small ubiquitin-like modifier (SUMO)-1. In this study,

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Serror, Pascale, Golnar Ilami, Hichem Chouayekh, S. Dusko Ehrlich, and Emmanuelle Maguin. "Transposition in Lactobacillus delbrueckii subsp. bulgaricus: identification of two thermosensitive replicons and two functional insertion sequences." Microbiology 149, no. 6 (2003): 1503–11. http://dx.doi.org/10.1099/mic.0.25827-0.

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In this report, it is shown that the rolling circle replicon pG+host and the theta replicon pIP501 are thermosensitive in Lactobacillus delbrueckii subsp. bulgaricus (Lactobacillus bulgaricus). Using a pIP501 derivative as a delivery vector for six insertion sequences originating from lactic acid bacteria, it is shown that IS1223 and IS1201 transpose in L. bulgaricus.

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Kurenbach, Brigitta, Jolanta Kopeć, Marion Mägdefrau, et al. "The TraA relaxase autoregulates the putative type IV secretion-like system encoded by the broad-host-range Streptococcus agalactiae plasmid pIP501." Microbiology 152, no. 3 (2006): 637–45. http://dx.doi.org/10.1099/mic.0.28468-0.

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The conjugative multiple antibiotic resistance plasmid pIP501 can be transferred and stably maintained in a variety of Gram-positive genera, including multicellular Streptomyces lividans, as well as in Gram-negative Escherichia coli. The 15 putative pIP501 transfer (tra) genes are organized in an operon-like structure terminating in a strong transcriptional terminator. This paper reports co-transcription of the pIP501 tra genes in exponentially growing Enterococcus faecalis JH2-2 cells, as shown by RT-PCR. The tra genes are expressed throughout the life cycle of Ent. faecalis, and the expressi

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Wong, Ka-Wing, та Ralph R. Isberg. "Arf6 and Phosphoinositol-4-Phosphate-5-Kinase Activities Permit Bypass of the Rac1 Requirement for β1 Integrin–mediated Bacterial Uptake". Journal of Experimental Medicine 198, № 4 (2003): 603–14. http://dx.doi.org/10.1084/jem.20021363.

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Efficient entry of the bacterium Yersinia pseudotuberculosis into mammalian cells requires the binding of the bacterial invasin protein to β1 integrin receptors and the activation of the small GTPase Rac1. We report here that this Rac1-dependent pathway involves recruitment of phosphoinositol-4-phosphate-5-kinase (PIP5K) to form phosphoinositol-4,5-bisphosphate (PIP2) at the phagocytic cup. Reducing the concentration of PIP2 in the target cell by using a membrane-targeted PIP2-specific phosphatase lowered bacterial uptake proportionately. PIP2 formation is regulated by Arf6. An Arf6 derivative

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SANTONI, Véronique, Joëlle VINH, Delphine PFLIEGER, Nicolas SOMMERER, and Christophe MAUREL. "A proteomic study reveals novel insights into the diversity of aquaporin forms expressed in the plasma membrane of plant roots." Biochemical Journal 373, no. 1 (2003): 289–96. http://dx.doi.org/10.1042/bj20030159.

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Aquaporins are channel proteins that facilitate the diffusion of water across cell membranes. The genome of Arabidopsis thaliana encodes 35 full-length aquaporin homologues. Thirteen of them belong to the plasma membrane intrinsic protein (PIP) subfamily and predominantly sit at the plasma membrane (PM). In the present work we combine separations of membrane proteins (by one- and two-dimensional gel electrophoresis) with identification by MS (matrix-assisted laser-desorption ionization–time-of-flight and electrospray-ionization tandem MS) to take an inventory of aquaporin isoforms expressed in

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Kumari, Aastha, Avishek Ghosh, Sourav Kolay, and Padinjat Raghu. "Septins tune lipid kinase activity and PI(4,5)P₂ turnover during G-protein–coupled PLC signalling in vivo." Life Science Alliance 5, no. 6 (2022): e202101293. http://dx.doi.org/10.26508/lsa.202101293.

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Phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] hydrolysis by phospholipase C (PLC) is a conserved mechanism of signalling. Given the low abundance of PI(4,5)P2, its hydrolysis needs to be coupled to resynthesis to ensure continued PLC activity; however, the mechanism by which depletion is coupled to resynthesis remains unknown. PI(4,5)P2 synthesis is catalyzed by the phosphorylation of phosphatidylinositol 4 phosphate (PI4P) by phosphatidylinositol 4 phosphate 5 kinase (PIP5K). In Drosophila photoreceptors, photon absorption is transduced into PLC activity and during this process, PI(4,5)P2

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Wang, Y., X. Chen, L. Lian, et al. "Loss of PIP5KI demonstrates that PIP5KI isoform-specific PIP2 synthesis is required for IP3 formation." Proceedings of the National Academy of Sciences 105, no. 37 (2008): 14064–69. http://dx.doi.org/10.1073/pnas.0804139105.

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Horaud, T., G. de Céspèdes, and P. Trieu-Cuot. "Chromosomal gentamicin resistance transposon Tn3706 in Streptococcus agalactiae B128." Antimicrobial Agents and Chemotherapy 40, no. 5 (1996): 1085–90. http://dx.doi.org/10.1128/aac.40.5.1085.

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Streptococcus agalactiae B128 is the only highly gentamicin-resistant group B streptococcal (GBS) strain described so far. This strain carries a chromosomal gentamicin resistance transposon, designated Tn3706, which is similar, if not identical, to the Tn4001 and Tn5281 transpons detected in Staphylococcus aureus and Enterococcus faecalis, respectively. Transposition of Tn3706 occurred onto the GBS plasmid pIP501 in two different loci of its 7.5-kb AvaII fragment carrying the genes for chloramphenicol and erythromycin resistance. Molecular analysis of pIP501 derivatives showed that Tn3706 is c

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Wang, Xiaoxiang, Lan Yu, Xing Xiong, Yao Chen, and Bo Men. "Bone Marrow Mesenchymal Stem Cells (BMSCs) Transplantation Alleviates Acute Pancreatitis Through Inhibiting Inflammation and Promoting Caspase-8 Apoptosis Pathway." Journal of Biomaterials and Tissue Engineering 12, no. 5 (2022): 1034–39. http://dx.doi.org/10.1166/jbt.2022.2969.

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Bone marrow mesenchymal stem cells (BMSCs) are capable of multipolar differentiation and repairing injured tissues. Herein, we aimed to investigate the mechanism by how BMSCs modulate the apoptotic pathway in the acute pancreatitis (AP). In this study, primary BMSCs were cultured and administrated into 10 AP mice while 10 healthy mice were taken as a blank group and 10 AP mice as a control group. The mouse pancreatic tissues were assessed by HE staining and evaluated by pancreatitis score and serum amylase detection. Level of inflammatory factors CRP and TNF-α was measured by ELISA and PIPK1,

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Yamamoto, Masaya, Donald H. Hilgemann, Siyi Feng, et al. "Phosphatidylinositol 4,5-Bisphosphate Induces Actin Stress-Fiber Formation and Inhibits Membrane Ruffling in Cv1 Cells." Journal of Cell Biology 152, no. 5 (2001): 867–76. http://dx.doi.org/10.1083/jcb.152.5.867.

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Phosphatidylinositol 4,5 bisphosphate (PIP2) is widely implicated in cytoskeleton regulation, but the mechanisms by which PIP2 effect cytoskeletal changes are not defined. We used recombinant adenovirus to infect CV1 cells with the mouse type I phosphatidylinositol phosphate 5-kinase α (PIP5KI), and identified the players that modulate the cytoskeleton in response to PIP2 signaling. PIP5KI overexpression increased PIP2 and reduced phosphatidylinositol 4 phosphate (PI4P) levels. It promoted robust stress-fiber formation in CV1 cells and blocked PDGF-induced membrane ruffling and nucleated actin

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van den Bout, Iman, David R. Jones, Zahid H. Shah, et al. "Collaboration of AMPK and PKC to induce phosphorylation of Ser413 on PIP5K1B resulting in decreased kinase activity and reduced PtdIns(4,5)P2 synthesis in response to oxidative stress and energy restriction." Biochemical Journal 455, no. 3 (2013): 347–58. http://dx.doi.org/10.1042/bj20130259.

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Karlsson, Richard, Per Larsson, Regina Miftakhova та ін. "Establishment of Prostate Tumor Growth and Metastasis Is Supported by Bone Marrow Cells and Is Mediated by PIP5K1α Lipid Kinase". Cancers 12, № 9 (2020): 2719. http://dx.doi.org/10.3390/cancers12092719.

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Cancer cells facilitate growth and metastasis by using multiple signals from the cancer-associated microenvironment. However, it remains poorly understood whether prostate cancer (PCa) cells may recruit and utilize bone marrow cells for their growth and survival. Furthermore, the regulatory mechanisms underlying interactions between PCa cells and bone marrow cells are obscure. In this study, we isolated bone marrow cells that mainly constituted populations that were positive for CD11b and Gr1 antigens from xenograft PC-3 tumor tissues from athymic nu/nu mice. We found that the tumor-infiltrate

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Yamamoto, A., D. B. DeWald, I. V. Boronenkov, R. A. Anderson, S. D. Emr, and D. Koshland. "Novel PI(4)P 5-kinase homologue, Fab1p, essential for normal vacuole function and morphology in yeast." Molecular Biology of the Cell 6, no. 5 (1995): 525–39. http://dx.doi.org/10.1091/mbc.6.5.525.

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The FAB1 gene of budding yeast is predicted to encode a protein of 257 kDa that exhibits significant sequence homology to a human type II PI(4)P 5-kinase (PIP5K-II). The recently cloned human PIP5K-II specifically converts PI(4)P to PI(4,5)P2 (Boronenkov and Anderson, 1995). The region of highest similarity between Fab1p and PIP5K-II includes a predicted nucleotide binding motif, which is likely to correspond to the catalytic domain of the protein. Interestingly, neither PIP5K-II nor Fab1p exhibit significant homology with cloned PI 3-kinases or PI 4-kinases. fab1 mutations result in the forma

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