| Suppression of ITPKB degradation by Trim25 confers TMZ resistance in glioblastoma through ROS homeostasis. | Suppression of ITPKB degradation by Trim25 confers TMZ resistance in glioblastoma through ROS homeostasis.
Yan Y, Zhou S, Chen X, Yi Q, Feng S, Zhao Z, Liu Y, Liang Q, Xu Z, Li Z, Sun L., Free PMC Article | 03/6/2024 |
| Genome-Wide Meta-Analysis Identifies Multiple Novel Rare Variants to Predict Common Human Infectious Diseases Risk. | Genome-Wide Meta-Analysis Identifies Multiple Novel Rare Variants to Predict Common Human Infectious Diseases Risk.
Gelemanović A, Ćatipović Ardalić T, Pribisalić A, Hayward C, Kolčić I, Polašek O., Free PMC Article | 05/12/2023 |
| Increased Levels of the Parkinson's Disease-Associated Gene ITPKB Correlate with Higher Expression Levels of alpha-Synuclein, Independent of Mutation Status. | Increased Levels of the Parkinson's Disease-Associated Gene ITPKB Correlate with Higher Expression Levels of α-Synuclein, Independent of Mutation Status.
Di Leva F, Filosi M, Oyston L, Silvestri E, Picard A, Lavdas AA, Lobbestael E, Baekelandt V, Neely GG, Pramstaller PP, Hicks AA, Corti C., Free PMC Article | 03/1/2023 |
| Association of ITPKB, IL1R2 and COQ7 with Parkinson's disease in Taiwan. | Association of ITPKB, IL1R2 and COQ7 with Parkinson's disease in Taiwan.
Fang HS, Wang CC, Chao CY, Fan WL, Su SC, Wu YR. | 03/5/2022 |
| Severe combined immunodeficiency caused by inositol-trisphosphate 3-kinase B (ITPKB) deficiency. | Severe combined immunodeficiency caused by inositol-trisphosphate 3-kinase B (ITPKB) deficiency.
Almutairi A, Wallace JG, Jaber F, Alosaimi MF, Jones J, Sallam MTH, Elnagdy MH, Chou J, Sobh A, Geha RS. | 02/20/2021 |
| study also suggests a distinctive signaling function of IP4 that regulates NOX4. Furthermore, pharmaceutical inhibition of ITPKB displayed synergistic attenuation of tumor growth with cisplatin, suggesting ITPKB as a promising synthetic lethal target for cancer therapeutic intervention to overcome cisplatin resistance. | Inositol-triphosphate 3-kinase B confers cisplatin resistance by regulating NOX4-dependent redox balance.
Pan C, Jin L, Wang X, Li Y, Chun J, Boese AC, Li D, Kang HB, Zhang G, Zhou L, Chen GZ, Saba NF, Shin DM, Magliocca KR, Owonikoko TK, Mao H, Lonial S, Kang S., Free PMC Article | 04/18/2020 |
| ITPKB does not affect the cellular actin structure and does not suppress dissemination of human lung cancer cells in mice. | Effect of the actin- and calcium-regulating activities of ITPKB on the metastatic potential of lung cancer cells.
Bäder S, Glaubke E, Grüb S, Muhs S, Wellbrock J, Nalaskowski M, Lange T, Windhorst S. | 04/6/2019 |
| miR-140-5p regulates this context-specific autophagy through its target, inositol 1,4,5-trisphosphate kinase 2 (IP3k2). Therefore, the results of the present study demonstrated that miR-140-5p mediated drug-resistance in osteosarcoma cells by inducing autophagy. | miR-140-5p attenuates chemotherapeutic drug-induced cell death by regulating autophagy through inositol 1,4,5-trisphosphate kinase 2 (IP3k2) in human osteosarcoma cells.
Wei R, Cao G, Deng Z, Su J, Cai L., Free PMC Article | 12/2/2017 |
| The authors confirm downregulation of miR-132 and upregulation of ITPKB in three distinct human Alzheimer's disease patient cohorts. | miR-132 loss de-represses ITPKB and aggravates amyloid and TAU pathology in Alzheimer's brain.
Salta E, Sierksma A, Vanden Eynden E, De Strooper B., Free PMC Article | 09/30/2017 |
| ITPKB is increased in Alzheimer's brain three-fold in the cerebral cortex of most patients with Alzheimer's disease compared with control subjects and accumulates in dystrophic neurites associated with amyloid plaques. | Inositol trisphosphate 3-kinase B is increased in human Alzheimer brain and exacerbates mouse Alzheimer pathology.
Stygelbout V, Leroy K, Pouillon V, Ando K, D'Amico E, Jia Y, Luo HR, Duyckaerts C, Erneux C, Schurmans S, Brion JP. | 04/12/2014 |
| a specific increase in inositol 1,4,5-trisphosphate 3-kinase A and B (ITPKA and ITPKB) was observed upon hESCs spontaneous differentiation. | A specific increase in inositol 1,4,5-trisphosphate 3-kinase B expression upon differentiation of human embryonic stem cells.
Hoofd C, Devreker F, Deneubourg L, Deleu S, Nguyen TM, Sermon K, Englert Y, Erneux C. | 09/29/2012 |
| IP3KB not only regulates cytoplasmic Ca(2+) signals by phosphorylation of subplasmalemmal and cytoplasmic Ins(1,4,5)P(3) but may also be involved in modulating nuclear Ca(2+) signals generated from these nuclear envelope invaginations. | Human inositol 1,4,5-trisphosphate 3-kinase isoform B (IP3KB) is a nucleocytoplasmic shuttling protein specifically enriched at cortical actin filaments and at invaginations of the nuclear envelope.
Nalaskowski MM, Fliegert R, Ernst O, Brehm MA, Fanick W, Windhorst S, Lin H, Giehler S, Hein J, Lin YN, Mayr GW., Free PMC Article | 03/26/2011 |
| Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator) | Variation at the NFATC2 locus increases the risk of thiazolidinedione-induced edema in the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) study.
Bailey SD, Xie C, Do R, Montpetit A, Diaz R, Mohan V, Keavney B, Yusuf S, Gerstein HC, Engert JC, Anand S, DREAM investigators., Free PMC Article | 09/15/2010 |
| Observational study of gene-disease association. (HuGE Navigator) | Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip.
Talmud PJ, Drenos F, Shah S, Shah T, Palmen J, Verzilli C, Gaunt TR, Pallas J, Lovering R, Li K, Casas JP, Sofat R, Kumari M, Rodriguez S, Johnson T, Newhouse SJ, Dominiczak A, Samani NJ, Caulfield M, Sever P, Stanton A, Shields DC, Padmanabhan S, Melander O, Hastie C, Delles C, Ebrahim S, Marmot MG, Smith GD, Lawlor DA, Munroe PB, Day IN, Kivimaki M, Whittaker J, Humphries SE, Hingorani AD, ASCOT investigators, NORDIL investigators, BRIGHT Consortium., Free PMC Article | 09/15/2010 |
| Clinical trial of gene-disease association and gene-environment interaction. (HuGE Navigator) | Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score.
Rose JE, Behm FM, Drgon T, Johnson C, Uhl GR., Free PMC Article | 06/30/2010 |
| In each of the three isoforms a nuclear export signal has evolved in the catalytic domain either de novo (IP3K-A) or as a substitute for an earlier evolved corresponding N-terminal signal (IP3K-B and IP3K-C). | Subcellular localisation of human inositol 1,4,5-trisphosphate 3-kinase C: species-specific use of alternative export sites for nucleo-cytoplasmic shuttling indicates divergent roles of the catalytic and N-terminal domains.
Nalaskowski MM, Windhorst S, Stockebrand MC, Mayr GW. | 01/21/2010 |
| results highlight the potential role of the three isoforms of InsP3 3-kinase as direct InsP3 metabolizing enzymes and direct regulators of Ca2+ responses to extracellular signals | The three isoenzymes of human inositol-1,4,5-trisphosphate 3-kinase show specific intracellular localization but comparable Ca2+ responses on transfection in COS-7 cells.
Dewaste V, Moreau C, De Smedt F, Bex F, De Smedt H, Wuytack F, Missiaen L, Erneux C., Free PMC Article | 01/21/2010 |
| We aim to summarize the existing information about functionally uncoupled IP(3)R and RyR channels, and to discuss the concept that those channels can participate in Ca(2+)-leak pathways. | Uncoupled IP3 receptor can function as a Ca2+-leak channel: cell biological and pathological consequences.
Szlufcik K, Missiaen L, Parys JB, Callewaert G, De Smedt H. | 01/21/2010 |