If-2α/ITPR1 axis: A new saboteur of NK-mediated lysis

Yosra Messai; Muhammad Zaeem Noman; Meriem Hasmim; Bernard Escudier; Salem Chouaib

doi:10.4161/2162402X.2014.985951

If-2α/ITPR1 axis: A new saboteur of NK-mediated lysis

Yosra Messai, Muhammad Zaeem Noman, Meriem Hasmim, Bernard Escudier, Salem Chouaib^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Research › peer-review

17 Citations (Scopus)

Abstract

We recently investigated the role of von Hippel-Lindau (VHL) mutation and the subsequent induction of hypoxia-inducible factor 2α (HIF-2α) in the regulation of renal cell carcinoma (RCC) susceptibility to natural killer (NK) cell- mediated killing. We demonstrated that the resistance of VHL-mutated RCC cell line 786-0 to NK-mediated lysis requires HIF-2 α and ITPR1, a direct novel target of HIF-2α, through the activation of autophagy in target cells by NK-derived signals.

Original language	English
Pages (from-to)	1-3
Number of pages	3
Journal	OncoImmunology
Volume	4
Issue number	2
DOIs	https://doi.org/10.4161/2162402X.2014.985951
Publication status	Published - 2015
Externally published	Yes

Keywords

Autophagy
Clear cell renal cell carcinoma
HIF-2α
ITPR1
NK cell
PVHL

Access to Document

10.4161/2162402X.2014.985951

Cite this

@article{b7423923de454c8d93bab910694d567c,

title = "If-2α/ITPR1 axis: A new saboteur of NK-mediated lysis",

abstract = "We recently investigated the role of von Hippel-Lindau (VHL) mutation and the subsequent induction of hypoxia-inducible factor 2α (HIF-2α) in the regulation of renal cell carcinoma (RCC) susceptibility to natural killer (NK) cell- mediated killing. We demonstrated that the resistance of VHL-mutated RCC cell line 786-0 to NK-mediated lysis requires HIF-2 α and ITPR1, a direct novel target of HIF-2α, through the activation of autophagy in target cells by NK-derived signals.",

keywords = "Autophagy, Clear cell renal cell carcinoma, HIF-2α, ITPR1, NK cell, PVHL",

author = "Yosra Messai and Noman, {Muhammad Zaeem} and Meriem Hasmim and Bernard Escudier and Salem Chouaib",

note = "Publisher Copyright: {\textcopyright} 2015 Taylor & Francis Group, LLC.",

year = "2015",

doi = "10.4161/2162402X.2014.985951",

language = "English",

volume = "4",

pages = "1--3",

journal = "OncoImmunology",

issn = "2162-4011",

publisher = "Landes Bioscience",

number = "2",

}

TY - JOUR

T1 - If-2α/ITPR1 axis

T2 - A new saboteur of NK-mediated lysis

AU - Messai, Yosra

AU - Noman, Muhammad Zaeem

AU - Hasmim, Meriem

AU - Escudier, Bernard

AU - Chouaib, Salem

PY - 2015

Y1 - 2015

N2 - We recently investigated the role of von Hippel-Lindau (VHL) mutation and the subsequent induction of hypoxia-inducible factor 2α (HIF-2α) in the regulation of renal cell carcinoma (RCC) susceptibility to natural killer (NK) cell- mediated killing. We demonstrated that the resistance of VHL-mutated RCC cell line 786-0 to NK-mediated lysis requires HIF-2 α and ITPR1, a direct novel target of HIF-2α, through the activation of autophagy in target cells by NK-derived signals.

AB - We recently investigated the role of von Hippel-Lindau (VHL) mutation and the subsequent induction of hypoxia-inducible factor 2α (HIF-2α) in the regulation of renal cell carcinoma (RCC) susceptibility to natural killer (NK) cell- mediated killing. We demonstrated that the resistance of VHL-mutated RCC cell line 786-0 to NK-mediated lysis requires HIF-2 α and ITPR1, a direct novel target of HIF-2α, through the activation of autophagy in target cells by NK-derived signals.

KW - Autophagy

KW - Clear cell renal cell carcinoma

KW - HIF-2α

KW - ITPR1

KW - NK cell

KW - PVHL

UR - http://www.scopus.com/inward/record.url?scp=84946072264&partnerID=8YFLogxK

U2 - 10.4161/2162402X.2014.985951

DO - 10.4161/2162402X.2014.985951

M3 - Article

AN - SCOPUS:84946072264

SN - 2162-4011

VL - 4

SP - 1

EP - 3

JO - OncoImmunology

JF - OncoImmunology

IS - 2

ER -

If-2α/ITPR1 axis: A new saboteur of NK-mediated lysis

Abstract

Keywords

Access to Document

Other files and links

Fingerprint

Cite this