GRIM-19 associates with the serine protease HtrA2 for promoting cell death

X. Ma; S. Kalakonda; S. M. Srinivasula; S. P. Reddy; L. C. Platanias; D. V. Kalvakolanu

doi:10.1038/sj.onc.1210287

GRIM-19 associates with the serine protease HtrA2 for promoting cell death

X. Ma, S. Kalakonda, S. M. Srinivasula, S. P. Reddy, L. C. Platanias, D. V. Kalvakolanu^*

^*Corresponding author for this work

Medicine, Hematology Oncology Division

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

33 Scopus citations

Abstract

We have isolated a novel interferon (IFN)-retinoid regulated cell death regulatory protein genes associated with retinoid-IFN-induced mortality (GRIM)-19 earlier. To understand its mechanism of action, we have employed a yeast-two-hybrid screen and identified serine protease HtrA2 as its binding partner. GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner. In the presence of GRIM-19, the HtrA2-driven destruction of the antiapoptotic protein X-linked inhibitor of apoptosis (XIAP) is augmented. These interactions were disrupted by an human herpes virus-8 (HHV-8)-coded oncoprotein, vIRF1, and conferred resistance to IFN/RA-induced cell death. These data show a critical role of HtrA2 in a cytokine-induced cell death response for the first time and its inhibition by a viral protein.

Original language	English (US)
Pages (from-to)	4842-4849
Number of pages	8
Journal	Oncogene
Volume	26
Issue number	33
DOIs	https://doi.org/10.1038/sj.onc.1210287
State	Published - Jul 19 2007

Keywords

Cancer
Cell death
Cytokines
Growth suppression
Vitamins

ASJC Scopus subject areas

Molecular Biology
Genetics
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/sj.onc.1210287

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title = "GRIM-19 associates with the serine protease HtrA2 for promoting cell death",

abstract = "We have isolated a novel interferon (IFN)-retinoid regulated cell death regulatory protein genes associated with retinoid-IFN-induced mortality (GRIM)-19 earlier. To understand its mechanism of action, we have employed a yeast-two-hybrid screen and identified serine protease HtrA2 as its binding partner. GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner. In the presence of GRIM-19, the HtrA2-driven destruction of the antiapoptotic protein X-linked inhibitor of apoptosis (XIAP) is augmented. These interactions were disrupted by an human herpes virus-8 (HHV-8)-coded oncoprotein, vIRF1, and conferred resistance to IFN/RA-induced cell death. These data show a critical role of HtrA2 in a cytokine-induced cell death response for the first time and its inhibition by a viral protein.",

keywords = "Cancer, Cell death, Cytokines, Growth suppression, Vitamins",

author = "X. Ma and S. Kalakonda and Srinivasula, {S. M.} and Reddy, {S. P.} and Platanias, {L. C.} and Kalvakolanu, {D. V.}",

note = "Funding Information: DVK thanks National Cancer Institute for grant support CA105005. We also thank Patrick Moore, Emad Alnemri and Margaret Offerman for providing the reagents used in this study.",

year = "2007",

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doi = "10.1038/sj.onc.1210287",

language = "English (US)",

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AU - Ma, X.

AU - Kalakonda, S.

AU - Srinivasula, S. M.

AU - Reddy, S. P.

AU - Platanias, L. C.

AU - Kalvakolanu, D. V.

N1 - Funding Information: DVK thanks National Cancer Institute for grant support CA105005. We also thank Patrick Moore, Emad Alnemri and Margaret Offerman for providing the reagents used in this study.

PY - 2007/7/19

Y1 - 2007/7/19

N2 - We have isolated a novel interferon (IFN)-retinoid regulated cell death regulatory protein genes associated with retinoid-IFN-induced mortality (GRIM)-19 earlier. To understand its mechanism of action, we have employed a yeast-two-hybrid screen and identified serine protease HtrA2 as its binding partner. GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner. In the presence of GRIM-19, the HtrA2-driven destruction of the antiapoptotic protein X-linked inhibitor of apoptosis (XIAP) is augmented. These interactions were disrupted by an human herpes virus-8 (HHV-8)-coded oncoprotein, vIRF1, and conferred resistance to IFN/RA-induced cell death. These data show a critical role of HtrA2 in a cytokine-induced cell death response for the first time and its inhibition by a viral protein.

AB - We have isolated a novel interferon (IFN)-retinoid regulated cell death regulatory protein genes associated with retinoid-IFN-induced mortality (GRIM)-19 earlier. To understand its mechanism of action, we have employed a yeast-two-hybrid screen and identified serine protease HtrA2 as its binding partner. GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner. In the presence of GRIM-19, the HtrA2-driven destruction of the antiapoptotic protein X-linked inhibitor of apoptosis (XIAP) is augmented. These interactions were disrupted by an human herpes virus-8 (HHV-8)-coded oncoprotein, vIRF1, and conferred resistance to IFN/RA-induced cell death. These data show a critical role of HtrA2 in a cytokine-induced cell death response for the first time and its inhibition by a viral protein.

KW - Cancer

KW - Cell death

KW - Cytokines

KW - Growth suppression

KW - Vitamins

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GRIM-19 associates with the serine protease HtrA2 for promoting cell death

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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