The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes

10.1371/journal.pone.0035924

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Main Authors:	Renga B., Francisci D., D'Amore C., Schiaroli E., Mencarelli A., Cipriani S., Baldelli F., Fiorucci S.
Other Authors:	DUKE-NUS MEDICAL SCHOOL
Format:	Article
Published:	2019
Subjects:	CD36 antigen CD40 antigen CD86 antigen cell nucleus receptor farnesoid X receptor intercellular adhesion molecule 1 Janus kinase 1 monocyte chemotactic protein 1 peptide vaccine peroxisome proliferator activated receptor gamma protein p17 receptor for activated C kinase 1 recombinant protein STAT1 protein 2,4 thiazolidinedione derivative 3 [2 [2 chloro 4 [3 (2,6 dichlorophenyl) 5 isopropyl 4 isoxazolylmethoxy]phenyl]vinyl]benzoic acid CD14 antigen cell receptor cell surface receptor drug derivative farnesoid X-activated receptor fludarabine Gag protein GNB2L1 protein, human guanine nucleotide binding protein Human immunodeficiency virus antigen isoxazole derivative Janus kinase p17 protein, Human Immunodeficiency Virus Type 1 rosiglitazone STAT1 protein, human tumor protein vidarabine article controlled study down regulation gene control gene expression human human cell Human immunodeficiency virus 1 Human immunodeficiency virus infected patient Human immunodeficiency virus infection inflammation lipid metabolism macrophage monocyte promoter region protein expression signal transduction vaccination atherosclerosis cell line cell separation drug effect drug potentiation enzymology gene expression regulation genetics immunology metabolism pathology phenotype phosphorylation serodiagnosis Antigens, CD14 Atherosclerosis Cell Line Cell Separation gag Gene Products, Human Immunodeficiency Virus Gene Expression Regulation GTP-Binding Proteins HIV Antigens HIV Infections HIV-1 Humans Inflammation Isoxazoles Janus Kinases Lipid Metabolism Macrophages Monocytes Neoplasm Proteins Neutralization Tests Phenotype Phosphorylation PPAR gamma Receptors, Cell Surface Receptors, Cytoplasmic and Nuclear Signal Transduction STAT1 Transcription Factor Thiazolidinediones Vaccination Vidarabine
Online Access:	https://scholarbank.nus.edu.sg/handle/10635/161986
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Institution:	National University of Singapore

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spelling	sg-nus-scholar.10635-1619862023-10-31T21:20:43Z The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes Renga B. Francisci D. D'Amore C. Schiaroli E. Mencarelli A. Cipriani S. Baldelli F. Fiorucci S. DUKE-NUS MEDICAL SCHOOL NUSHS PROJECT CD36 antigen CD40 antigen CD86 antigen cell nucleus receptor farnesoid X receptor intercellular adhesion molecule 1 Janus kinase 1 monocyte chemotactic protein 1 peptide vaccine peroxisome proliferator activated receptor gamma protein p17 receptor for activated C kinase 1 recombinant protein STAT1 protein 2,4 thiazolidinedione derivative 3 [2 [2 chloro 4 [3 (2,6 dichlorophenyl) 5 isopropyl 4 isoxazolylmethoxy]phenyl]vinyl]benzoic acid CD14 antigen cell receptor cell surface receptor drug derivative farnesoid X receptor farnesoid X-activated receptor fludarabine Gag protein GNB2L1 protein, human guanine nucleotide binding protein Human immunodeficiency virus antigen isoxazole derivative Janus kinase p17 protein, Human Immunodeficiency Virus Type 1 peroxisome proliferator activated receptor gamma rosiglitazone STAT1 protein STAT1 protein, human tumor protein vidarabine article controlled study down regulation gene control gene expression human human cell Human immunodeficiency virus 1 Human immunodeficiency virus infected patient Human immunodeficiency virus infection inflammation lipid metabolism macrophage monocyte promoter region protein expression signal transduction vaccination atherosclerosis cell line cell separation drug effect drug potentiation enzymology gene expression regulation genetics Human immunodeficiency virus infection immunology inflammation metabolism pathology phenotype phosphorylation serodiagnosis Human immunodeficiency virus 1 Antigens, CD14 Atherosclerosis Cell Line Cell Separation gag Gene Products, Human Immunodeficiency Virus Gene Expression Regulation GTP-Binding Proteins HIV Antigens HIV Infections HIV-1 Humans Inflammation Isoxazoles Janus Kinases Lipid Metabolism Macrophages Monocytes Neoplasm Proteins Neutralization Tests Phenotype Phosphorylation PPAR gamma Receptors, Cell Surface Receptors, Cytoplasmic and Nuclear Signal Transduction STAT1 Transcription Factor Thiazolidinediones Vaccination Vidarabine 10.1371/journal.pone.0035924 PLoS ONE 7 4 e35924 2019-11-11T06:40:07Z 2019-11-11T06:40:07Z 2012 Article Renga B., Francisci D., D'Amore C., Schiaroli E., Mencarelli A., Cipriani S., Baldelli F., Fiorucci S. (2012). The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes. PLoS ONE 7 (4) : e35924. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0035924 19326203 https://scholarbank.nus.edu.sg/handle/10635/161986 Attribution 4.0 International http://creativecommons.org/licenses/by/4.0/ Unpaywall 20191101
institution	National University of Singapore
building	NUS Library
continent	Asia
country	Singapore Singapore
content_provider	NUS Library
collection	ScholarBank@NUS
topic	CD36 antigen CD40 antigen CD86 antigen cell nucleus receptor farnesoid X receptor intercellular adhesion molecule 1 Janus kinase 1 monocyte chemotactic protein 1 peptide vaccine peroxisome proliferator activated receptor gamma protein p17 receptor for activated C kinase 1 recombinant protein STAT1 protein 2,4 thiazolidinedione derivative 3 [2 [2 chloro 4 [3 (2,6 dichlorophenyl) 5 isopropyl 4 isoxazolylmethoxy]phenyl]vinyl]benzoic acid CD14 antigen cell receptor cell surface receptor drug derivative farnesoid X receptor farnesoid X-activated receptor fludarabine Gag protein GNB2L1 protein, human guanine nucleotide binding protein Human immunodeficiency virus antigen isoxazole derivative Janus kinase p17 protein, Human Immunodeficiency Virus Type 1 peroxisome proliferator activated receptor gamma rosiglitazone STAT1 protein STAT1 protein, human tumor protein vidarabine article controlled study down regulation gene control gene expression human human cell Human immunodeficiency virus 1 Human immunodeficiency virus infected patient Human immunodeficiency virus infection inflammation lipid metabolism macrophage monocyte promoter region protein expression signal transduction vaccination atherosclerosis cell line cell separation drug effect drug potentiation enzymology gene expression regulation genetics Human immunodeficiency virus infection immunology inflammation metabolism pathology phenotype phosphorylation serodiagnosis Human immunodeficiency virus 1 Antigens, CD14 Atherosclerosis Cell Line Cell Separation gag Gene Products, Human Immunodeficiency Virus Gene Expression Regulation GTP-Binding Proteins HIV Antigens HIV Infections HIV-1 Humans Inflammation Isoxazoles Janus Kinases Lipid Metabolism Macrophages Monocytes Neoplasm Proteins Neutralization Tests Phenotype Phosphorylation PPAR gamma Receptors, Cell Surface Receptors, Cytoplasmic and Nuclear Signal Transduction STAT1 Transcription Factor Thiazolidinediones Vaccination Vidarabine
spellingShingle	CD36 antigen CD40 antigen CD86 antigen cell nucleus receptor farnesoid X receptor intercellular adhesion molecule 1 Janus kinase 1 monocyte chemotactic protein 1 peptide vaccine peroxisome proliferator activated receptor gamma protein p17 receptor for activated C kinase 1 recombinant protein STAT1 protein 2,4 thiazolidinedione derivative 3 [2 [2 chloro 4 [3 (2,6 dichlorophenyl) 5 isopropyl 4 isoxazolylmethoxy]phenyl]vinyl]benzoic acid CD14 antigen cell receptor cell surface receptor drug derivative farnesoid X receptor farnesoid X-activated receptor fludarabine Gag protein GNB2L1 protein, human guanine nucleotide binding protein Human immunodeficiency virus antigen isoxazole derivative Janus kinase p17 protein, Human Immunodeficiency Virus Type 1 peroxisome proliferator activated receptor gamma rosiglitazone STAT1 protein STAT1 protein, human tumor protein vidarabine article controlled study down regulation gene control gene expression human human cell Human immunodeficiency virus 1 Human immunodeficiency virus infected patient Human immunodeficiency virus infection inflammation lipid metabolism macrophage monocyte promoter region protein expression signal transduction vaccination atherosclerosis cell line cell separation drug effect drug potentiation enzymology gene expression regulation genetics Human immunodeficiency virus infection immunology inflammation metabolism pathology phenotype phosphorylation serodiagnosis Human immunodeficiency virus 1 Antigens, CD14 Atherosclerosis Cell Line Cell Separation gag Gene Products, Human Immunodeficiency Virus Gene Expression Regulation GTP-Binding Proteins HIV Antigens HIV Infections HIV-1 Humans Inflammation Isoxazoles Janus Kinases Lipid Metabolism Macrophages Monocytes Neoplasm Proteins Neutralization Tests Phenotype Phosphorylation PPAR gamma Receptors, Cell Surface Receptors, Cytoplasmic and Nuclear Signal Transduction STAT1 Transcription Factor Thiazolidinediones Vaccination Vidarabine Renga B. Francisci D. D'Amore C. Schiaroli E. Mencarelli A. Cipriani S. Baldelli F. Fiorucci S. The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes
description	10.1371/journal.pone.0035924
author2	DUKE-NUS MEDICAL SCHOOL
author_facet	DUKE-NUS MEDICAL SCHOOL Renga B. Francisci D. D'Amore C. Schiaroli E. Mencarelli A. Cipriani S. Baldelli F. Fiorucci S.
format	Article
author	Renga B. Francisci D. D'Amore C. Schiaroli E. Mencarelli A. Cipriani S. Baldelli F. Fiorucci S.
author_sort	Renga B.
title	The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes
title_short	The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes
title_full	The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes
title_fullStr	The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes
title_full_unstemmed	The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes
title_sort	hiv matrix protein p17 subverts nuclear receptors expression and induces a stat1-dependent proinflammatory phenotype in monocytes
publishDate	2019
url	https://scholarbank.nus.edu.sg/handle/10635/161986
_version_	1781791873315110912

The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes

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