Deletion of the gene Pip4k2c, a novel phosphatidylinositol kinase, results in hyperactivation of the immune system

By Hyeseok Shim, Chuan Wu, Shivan Ramsamooj, Kaitlyn N. Bosch, Zuojia Chen, B. Emerling, Jihye Yun, Hui Liu, R. Choo-wing, Zhiwei Yang and 3 more. 2016

62 citations recorded by the source corpus.

Subfields: Cell Biology, Immunology, Molecular Biology

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. J. Clarke
2. Lewis C. Cantley
3. Alec C. Kimmelman
4. D. Krainc
5. N. Divecha

In Immunology

1. Lewis C. Cantley
2. J. Asara
3. Alec C. Kimmelman

In Molecular Biology

1. Alec C. Kimmelman
2. J. Asara
3. Lewis C. Cantley
4. Mark A. Rubin
5. Olivier Elemento
6. J. Clarke
7. Nathanael S. Gray
8. D. Krainc

Citations in the corpus

• PIP4Ks Suppress Insulin Signaling through a Catalytic-Independent Mechanism (2018, unknown): “Homozygous germline deletion of Pip4k2b−/− in mice causes reduced adiposity and increased insulin sensitivity in muscle (Lamia et al., 2004), and Pip4k2c−/− mice have enhanced TORC1 signaling (Shim et al., 2016).”
• Phosphatidylinositol-5-phosphate 4-kinases regulate cellular lipid metabolism by facilitating autophagy (2018, background): “We have generated mice with each of these genes deleted in the germline (Emerling et al., 2013; Lamia et al., 2004; Shim et al., 2016).”
• Inhibition of PIP4Kγ ameliorates the pathological effects of mutant huntingtin protein (2017, background): “In a recent report, a homozygous mouse knock- out displayed no growth or behavioral abnormalities (Shim et al., 2016).”
• Targeting the PI5P4K lipid kinase family in cancer using covalent inhibitors (2020, background): “Deletion of PIP4K2C in mice resulted in an increase of proinflammatory cytokines and T-helper-cells, as well as a decrease in regulatory T-cells via hyperactivation of mTORC1 signaling (Shim et al., 2016).”