Yasinska, Inna M., Gibbs, Bernhard F, Lall, Gurprit S., Sumbayev, Vadim V. (2013) The HIF-1 transcription complex is essential for translational control of myeloid hematopoietic cell function. Cellular and Molecular Life Sciences, 71 (4). pp. 699-710. ISSN 1420-682X. E-ISSN 1420-9071. (doi:10.1007/s00018-013-1421-2) (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided) (KAR id:59444)
The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided. | |
Official URL: http://dx.doi.org/10.1007/s00018-013-1421-2 |
Abstract
Mammalian myeloid cells are crucial effectors of host innate immune defense. Normal and pathological responses of these cells require adaptation to signaling stress through the hypoxia-inducible factor 1 (HIF-1) transcription complex. Adapted cells activate the mammalian target of rapamycin (mTOR), via S2448 phosphorylation, which induces de novo translation of vital signaling proteins. However, the molecular mechanisms underlying this signaling dogma remain unclear. Here, we demonstrate for the first time that inactivation of HIF-1, by silencing its inducible alpha subunit, significantly decreases mTOR S2448 phosphorylation caused by ligand-dependent activation of human myeloid leukemia cells. This shows that HIF-1 is essential for the activation of mTOR and serves at a crucial juncture of myeloid cell function in both in vitro and in vivo systems.
Item Type: | Article |
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DOI/Identification number: | 10.1007/s00018-013-1421-2 |
Subjects: |
Q Science > QP Physiology (Living systems) > QP506 Molecular biology Q Science > QP Physiology (Living systems) > QP517 Biochemistry Q Science > QR Microbiology > QR180 Immunology R Medicine > RC Internal medicine > RC254 Neoplasms. Tumors. Oncology |
Divisions: | Divisions > Division of Natural Sciences > Medway School of Pharmacy |
Depositing User: | Bernhard F. Gibbs |
Date Deposited: | 05 Dec 2016 10:58 UTC |
Last Modified: | 16 Nov 2021 10:24 UTC |
Resource URI: | https://kar.kent.ac.uk/id/eprint/59444 (The current URI for this page, for reference purposes) |
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