ArticleProceedings of the National Academy of Sciences of the United States of America2008
Inositol trisphosphate 3-kinase B (InsP3KB) as a physiological modulator of myelopoiesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.Clinical science (London, England : 1979) · 2025Review
- Differentiation and homeostasis of effector Treg cells are regulated by inositol polyphosphates modulating CaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Inositol 1,4,5-trisphosphate 3-kinase B promotes CaScience signaling · 2021Article
- Article
- Neutrophils Derived from Genetically Modified Human Induced Pluripotent Stem Cells Circulate and Phagocytose Bacteria In Vivo.Stem cells translational medicine · 2019Article
- Conformational sampling of membranes by Akt controls its activation and inactivation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Regulation of Hematopoietic Cell Development and Function Through Phosphoinositides.Frontiers in immunology · 2018Review
- Article
- Common variable immunodeficiency associated with microdeletion of chromosome 1q42.1-q42.3 and inositol 1,4,5-trisphosphate kinase B (ITPKB) deficiency.Clinical & translational immunology · 2016Article
- Article
- Molecular control of PtdIns(3,4,5)P3 signaling in neutrophils.EMBO reports · 2015Review
- hCD2-iCre and Vav-iCre mediated gene recombination patterns in murine hematopoietic cells.PloS one · 2015Article
- Kinase AKT controls innate immune cell development and function.Immunology · 2013Review
- Inositol tetrakisphosphate limits NK cell effector functions by controlling PI3K signaling.Blood · 2013Article
- Article
- IP3 3-kinase opposes NGF driven neurite outgrowth.PloS one · 2012Article
- Defining signal transduction by inositol phosphates.Sub-cellular biochemistry · 2012Review
- 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.The Journal of biological chemistry · 2011Article
- Lipid signaling in T-cell development and function.Cold Spring Harbor perspectives in biology · 2010Review
- Inositol trisphosphate 3-kinases: focus on immune and neuronal signaling.Cellular and molecular life sciences : CMLS · 2010Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Inositol trisphosphate 3-kinase B (InsP3KB) belongs to a family of kinases that convert inositol 1,4,5-trisphosphate (Ins(1,4,5)P3 or IP3) to inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4). Previous studies have shown that disruption of InsP3KB leads to impaired T cell and B cell development as well as hyperactivation of neutrophils. Here, we demonstrate that InsP3KB is also a physiological modulator of myelopoiesis. The InsP3KB gene is expressed in all hematopoietic stem/progenitor cell populations. In InsP3KB null mice, the bone marrow granulocyte monocyte progenitor (GMP) population was expanded, and GMP cells proliferated significantly faster. Consequently, neutrophil production in the bone marrow was enhanced, and the peripheral blood neutrophil count was also substantially elevated in these mice. These effects might be due to enhancement of PtdIns(3,4,5)P3/Akt signaling in the InsP3KB null cells. Phosphorylation of cell cycle-inhibitory protein p21(cip1), one of the downstream targets of Akt, was augmented, which can lead to the suppression of the cell cycle-inhibitory effect of p21.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.