Increased Insulin Sensitivity and Reduced Adiposity in Phosphatidylinositol 5-Phosphate 4-Kinase β−/− Mice

By Katja A. Lamia, O. Peroni, Young-Bum Kim, L. Rameh, B. Kahn, Lewis C. Cantley. 2004

124 citations recorded by the source corpus.

Subfields: Cell Biology, Physiology, Surgery

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Citations in the corpus

In B cells, phosphatidylinositol 5-phosphate 4-kinase–α synthesizes PI(4,5)P2 to impact mTORC2 and Akt signaling (2016, background): “No Akt phenotype was found in PIP4K2A knockout mice (21), but as far as we are aware, cells of the hematopoietic lineage were not studied there; another study from the same group elegantly showed the tissue variability of gene knockouts, with PIP4K2B knockout mice having enhanced insulininduced Akt ”
The lipid kinase PI5P4Kβ is an intracellular GTP sensor for metabolism and tumorigenesis (2016, unknown): “In line with this notion, it is intriguing that the PI5P4Kb knockout mice display the phenotypic link to tumorigenesis as well as wholebodymetabolism (Emerling et al., 2013; Lamia et al., 2004).”
PIP4Ks Suppress Insulin Signaling through a Catalytic-Independent Mechanism (2018, background): “Loss of PIP4Ks results in increased PI(5)P levels, increased PI3K activation, and defects in autophagy PIP4K2A/B/C triple knockout 293T cells (hereafter TKO) and triple knockdown HeLa cells (hereafter TKD) recapitulated previously reported phenotypes observed when one or more of these genes were del”
Phosphoinositides: tiny lipids with giant impact on cell regulation. (2013, background): “Deletion of PIPKII in mice increases insulin sensitivity by enhancing Akt activation in muscle (848), and overexpression studies suggest that the enzyme attenuates insulin signaling (218).”
Phosphatidylinositol-5-phosphate 4-kinases regulate cellular lipid metabolism by facilitating autophagy (2018, methodology): “MEF DNA was prepared from the head using DNeasy (Qiagen) and genotyped using the primer pairs as previously described (Emerling et al., 2013; Lamia et al., 2004).”
Phosphatidylinositol 5-phosphate 4-kinase (PIP4K) regulates TOR signaling and cell growth during Drosophila development (2013, background): “This phenotype is reminiscent of that seen in a mouse knockout of PIP4Kβ (18); these mice are reported to be smaller than wild-type controls and together with our findings suggest an evolutionarily conserved role for PIP4K in regulating growth in metazoans.”
Deletion of the gene Pip4k2c, a novel phosphatidylinositol kinase, results in hyperactivation of the immune system (2016, background): “Deletion of Pip4k2b enhances Akt activation but, surprisingly, does not result in enhanced mTORC1 signaling (4, 5).”
Targeting the PI5P4K lipid kinase family in cancer using covalent inhibitors (2020, background): “PIP4K2B-null mice were found to have increased insulin sensitivity and reduced adiposity (Lamia et al., 2004).”
Depletion of a Putatively Druggable Class of Phosphatidylinositol Kinases Inhibits Growth of p53-Null Tumors (2013, background): “In other contexts, activation of the PI3K/AKT pathway enhances glucose uptake and metabolism, and, in the context of wild-type p53, deletion of PIP4K2B in mice activates the PI3K/AKT pathway and enhances glucose uptake into muscle (Lamia et al., 2004).”