Identification of MΦ specific POTEE expression: Its role in mTORC2 activation via protein-protein interaction in TAMs.

Autor: Vekariya U; Toxicology and Experimental Medicine Division, CSIR-Central Drug Research Institute, Sector-10, Janakipuram Extension, Sitapur Road, Lucknow 226031, U.P., India., Rawat K; Toxicology and Experimental Medicine Division, CSIR-Central Drug Research Institute, Sector-10, Janakipuram Extension, Sitapur Road, Lucknow 226031, U.P., India., Saxena R; Toxicology and Experimental Medicine Division, CSIR-Central Drug Research Institute, Sector-10, Janakipuram Extension, Sitapur Road, Lucknow 226031, U.P., India., Tripathi RK; Toxicology and Experimental Medicine Division, CSIR-Central Drug Research Institute, Sector-10, Janakipuram Extension, Sitapur Road, Lucknow 226031, U.P., India. Electronic address: rk_tripathi@cdri.res.in.
Jazyk: angličtina
Zdroj: Cellular immunology [Cell Immunol] 2019 Jan; Vol. 335, pp. 30-40. Date of Electronic Publication: 2018 Nov 03.
DOI: 10.1016/j.cellimm.2018.10.010
Abstrakt: POTE is known as cancer antigen, expressed in many cancers, along with very few normal tissues like prostate, ovary, testes and embryo. Till date, POTEE identified as majorly expressed POTE paralog. Functionally, POTEF regulates TLR signaling which play important role in innate immunity provided clue about expression of POTE in immune cells. We have chosen three Thp1monocytes, Jurkat T1 and MΦ cells as a model. Here, first time we report expression of POTEE in immune cells specifically only in MΦ but not in monocytes or T-cells. In addition, expression level remains unaltered in MΦ subtypes M1 and M2 and MΦ subjected to various stresses, except MΦs treated with Hyp-CM where MΦs acquires properties of TAMs. In TAMs, POTEE was involved differential protein-protein interaction with mTOR, RICTOR, and Rad51 indicating its biological role in cell invasion through mTORC2 activation. siRNA mediated knockdown of POTEE suggests its importance in cell survival of MΦs as well as TAMs.
(Copyright © 2018 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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