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Article ; Online: Autophagy and Noroviruses.

Furlong, Kevin / Hwang, Seungmin

2019 Volume 11, Issue 3

Abstract: Autophagy is an essential cellular process by which a cell degrades materials within its cytoplasm. Intracellular pathogens like viruses must deal with autophagy, either positively or negatively, for their own survival and replication. For some viruses, ... ...

Abstract	Autophagy is an essential cellular process by which a cell degrades materials within its cytoplasm. Intracellular pathogens like viruses must deal with autophagy, either positively or negatively, for their own survival and replication. For some viruses, autophagy can even play proviral roles, helping their replication or dissemination. For other viruses, including noroviruses, the exact role of autophagy is more complex. This short review seeks to summarize the known interactions between autophagy, autophagy proteins and norovirus, and to address remaining questions relevant to these interactions.
MeSH term(s)	Animals ; Autophagy ; Cell Line ; GTP Phosphohydrolases/metabolism ; Host Microbial Interactions ; Host-Pathogen Interactions ; Humans ; Interferons/metabolism ; Mice ; Norovirus/physiology ; Virus Replication
Chemical Substances	Interferons (9008-11-1) ; GTP Phosphohydrolases (EC 3.6.1.-)
Language	English
Publishing date	2019-03-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v11030244
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: CAPRIN1 Is Required for Control of Viral Replication Complexes by Interferon Gamma.

Kurhade, Chaitanya / Kang, Soowon / Biering, Scott B / Hwang, Seungmin / Randall, Glenn

mBio

2023 Volume 14, Issue 3, Page(s) e0017223

Abstract: Replication complexes (RCs), formed by positive-strand (+) RNA viruses through rearrangements of host endomembranes, protect their replicating RNA from host innate immune defenses. We have shown that two evolutionarily conserved defense systems, ... ...

Abstract	Replication complexes (RCs), formed by positive-strand (+) RNA viruses through rearrangements of host endomembranes, protect their replicating RNA from host innate immune defenses. We have shown that two evolutionarily conserved defense systems, autophagy and interferon (IFN), target viral RCs and inhibit viral replication collaboratively. However, the mechanism by which autophagy proteins target viral RCs and the role of IFN-inducible GTPases in the disruption of RCs remains poorly understood. Here, using murine norovirus (MNV) as a model (+) RNA virus, we show that the guanylate binding protein 1 (GBP1) is the human GTPase responsible for inhibiting RCs. Furthermore, we found that ATG16L1 mediates the LC3 targeting of MNV RC by binding to WIPI2B and CAPRIN1, and that IFN gamma-mediated control of MNV replication was dependent on CAPRIN1. Collectively, this study identifies a novel mechanism for the autophagy machinery-mediated recognition and inhibition of viral RCs, a hallmark of (+) RNA virus replication.
MeSH term(s)	Humans ; Animals ; Mice ; Interferon-gamma ; Interferons ; GTP Phosphohydrolases/metabolism ; Virus Replication ; RNA ; Cell Cycle Proteins
Chemical Substances	Interferon-gamma (82115-62-6) ; Interferons (9008-11-1) ; GTP Phosphohydrolases (EC 3.6.1.-) ; RNA (63231-63-0) ; CAPRIN1 protein, human ; Cell Cycle Proteins
Language	English
Publishing date	2023-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.00172-23
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Article: Autophagy regulates tumor growth and metastasis.

Qiang, Lei / Zhao, Baozhong / Ming, Mei / Wang, Ning / He, Tong-Chuan / Hwang, Seungmin / Thorburn, Andrew / He, Yu-Ying

bioRxiv : the preprint server for biology

2023

Abstract: The role of autophagy in tumorigenesis and tumor metastasis remains poorly understood. Here we show that inhibition of autophagy stabilizes the transcription factor Twist1 through Sequestosome-1 (SQSTM1, also known as p62) and thus increases cell ... ...

Abstract	The role of autophagy in tumorigenesis and tumor metastasis remains poorly understood. Here we show that inhibition of autophagy stabilizes the transcription factor Twist1 through Sequestosome-1 (SQSTM1, also known as p62) and thus increases cell proliferation, migration, and epithelial-mesenchymal transition (EMT) in tumor development and metastasis. Inhibition of autophagy or p62 overexpression blocks Twist1 protein degradation in the proteasomes, while p62 inhibition enhances it. SQSTM1/p62 interacts with Twist1 via the UBA domain of p62, in a Twist1-ubiquitination-dependent manner. Lysine 175 in Twist1 is critical for Twist1 ubiquitination, degradation, and SQSTM1/p62 interaction. For squamous skin cancer and melanoma cells that express Twist1, SQSTM1/p62 increases tumor growth and metastasis in mice. Together, our results identified Twist1 as a key downstream protein for autophagy and suggest a critical role of the autophagy/p62/Twist1 axis in cancer development and metastasis.
Language	English
Publishing date	2023-11-03
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.31.564991
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Article: Direct Antiviral Mechanisms of Interferon-Gamma.

Kang, Soowon / Brown, Hailey M / Hwang, Seungmin

Immune network

2018 Volume 18, Issue 5, Page(s) e33

Abstract: Interferon-gamma (IFNG) is a pleiotropic cytokine that modulates both innate and adaptive immune networks; it is the most potent activator of macrophages and a signature cytokine of activated T lymphocytes. Though IFNG is now appreciated to have a ... ...

Abstract	Interferon-gamma (IFNG) is a pleiotropic cytokine that modulates both innate and adaptive immune networks; it is the most potent activator of macrophages and a signature cytokine of activated T lymphocytes. Though IFNG is now appreciated to have a multitude of roles in immune modulation and broad-spectrum pathogen defense, it was originally discovered, and named, as a secretory factor that interferes with viral replication. In contrast to the prototypical type I interferons produced by any cells upon viral infection, only specific subsets of immune cells can produce IFNG upon infection or stimulation with antigen or mitogen. Still, virtually all cells can respond to both types of interferons. This makes IFNG a versatile anti-microbial cytokine and also gives it a unique position in the antiviral defense system. The goal of this review is to highlight the direct antiviral mechanisms of IFNG, thereby clarifying its antiviral function in the effective control of viral infections.
Language	English
Publishing date	2018-10-17
Publishing country	Korea (South)
Document type	Journal Article ; Review
ZDB-ID	2536191-0
ISSN	2092-6685 ; 1598-2629
ISSN (online)	2092-6685
ISSN	1598-2629
DOI	10.4110/in.2018.18.e33
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Article ; Online: Preventive and Therapeutic Effects of Krill Oil on Obesity and Obesity-Induced Metabolic Syndromes in High-Fat Diet-Fed Mice.

Hwang, Seung-Min / Kim, Yeong Uk / Kim, Jong-Kyu / Chun, Yoon-Seok / Kwon, Young-Sam / Ku, Sae-Kwang / Song, Chang-Hyun

Marine drugs

2022 Volume 20, Issue 8

Abstract: Obesity increases the risks of metabolic syndromes including nonalcoholic fatty liver disease (NAFLD), diabetic dyslipidemia, and chronic kidney disease. Dietary krill oil (KO) has shown antioxidant and anti-inflammatory properties, thereby being a ... ...

Abstract	Obesity increases the risks of metabolic syndromes including nonalcoholic fatty liver disease (NAFLD), diabetic dyslipidemia, and chronic kidney disease. Dietary krill oil (KO) has shown antioxidant and anti-inflammatory properties, thereby being a therapeutic potential for obesity-induced metabolic syndromes. Thus, the effects of KO on lipid metabolic alteration were examined in a high-fat diet (HFD)-fed mice model. The HFD model (
MeSH term(s)	Animals ; Antioxidants/metabolism ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Diabetes Mellitus, Type 2/metabolism ; Diet, High-Fat/adverse effects ; Euphausiacea ; Glucose/metabolism ; Insulin Resistance ; Liver ; Metabolic Syndrome/metabolism ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease/drug therapy ; Obesity/complications ; Obesity/drug therapy ; Obesity/metabolism ; Triglycerides/metabolism
Chemical Substances	Antioxidants ; Triglycerides ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-07-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2175190-0
ISSN	1660-3397 ; 1660-3397
ISSN (online)	1660-3397
ISSN	1660-3397
DOI	10.3390/md20080483
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Article: Preventive and Therapeutic Effects of Krill Oil on Obesity and Obesity-Induced Metabolic Syndromes in High-Fat Diet-Fed Mice

Hwang, Seung-Min / Kim, Yeong Uk / Kim, Jong-Kyu / Chun, Yoon-Seok / Kwon, Young-Sam / Ku, Sae-Kwang / Song, Chang-Hyun

Marine drugs. 2022 July 27, v. 20, no. 8

2022

Abstract	Obesity increases the risks of metabolic syndromes including nonalcoholic fatty liver disease (NAFLD), diabetic dyslipidemia, and chronic kidney disease. Dietary krill oil (KO) has shown antioxidant and anti-inflammatory properties, thereby being a therapeutic potential for obesity-induced metabolic syndromes. Thus, the effects of KO on lipid metabolic alteration were examined in a high-fat diet (HFD)-fed mice model. The HFD model (n = 10 per group) received an oral gavage with distilled water as a control, metformin at 250 mg/kg, and KO at 400, 200, and 100 mg/kg for 12 weeks. The HFD-induced weight gain and fat deposition were significantly reduced in the KO treatments compared with the control. Blood levels were lower in parameters for NAFLD (e.g., alanine aminotransferase, and triglyceride), type 2 diabetes (e.g., glucose and insulin), and renal dysfunction (e.g., blood urea nitrogen and creatinine) by the KO treatments. The KO inhibited lipid synthesis through the modification of gene expressions in the liver and adipose tissues and adipokine-mediated pathways. Furthermore, KO showed hepatic antioxidant activities and glucose lowering effects. Histopathological analyses revealed that the KO ameliorated the hepatic steatosis, pancreatic endocrine/exocrine alteration, adipose tissue hypertrophy, and renal steatosis. These analyses suggest that KO may be promising for inhibiting obesity and metabolic syndromes.
Keywords	adipose tissue ; alanine transaminase ; antioxidants ; blood ; creatinine ; fatty liver ; genes ; glucose ; high fat diet ; histopathology ; hyperlipidemia ; hypertrophy ; insulin ; kidney diseases ; krill ; liver ; metformin ; models ; noninsulin-dependent diabetes mellitus ; obesity ; oils ; therapeutics ; triacylglycerols ; urea nitrogen ; weight gain
Language	English
Dates of publication	2022-0727
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2175190-0
ISSN	1660-3397
ISSN	1660-3397
DOI	10.3390/md20080483
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Autophagy gene-dependent intracellular immunity triggered by interferon-γ.

McAllaster, Michael R / Bhushan, Jaya / Balce, Dale R / Orvedahl, Anthony / Park, Arnold / Hwang, Seungmin / Sullender, Meagan E / Sibley, L David / Virgin, Herbert W

mBio

2023 , Page(s) e0233223

Abstract: Genes required for the lysosomal degradation pathway of autophagy play key roles in topologically distinct and physiologically important cellular processes. Some functions ... ...

Abstract	Genes required for the lysosomal degradation pathway of autophagy play key roles in topologically distinct and physiologically important cellular processes. Some functions of
Language	English
Publishing date	2023-10-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.02332-23
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Article ; Online: Quo vadis? Interferon-inducible GTPases go to their target membranes via the LC3-conjugation system of autophagy.

Choi, Jayoung / Biering, Scott B / Hwang, Seungmin

Small GTPases

2017 Volume 8, Issue 4, Page(s) 199–207

Abstract: Many intracellular pathogens survive and replicate within vacuole-like structures in the cytoplasm. It has been unclear how the host immune system controls such pathogen-containing vacuoles. Interferon-inducible GTPases are dynamin-like GTPases that ... ...

Abstract	Many intracellular pathogens survive and replicate within vacuole-like structures in the cytoplasm. It has been unclear how the host immune system controls such pathogen-containing vacuoles. Interferon-inducible GTPases are dynamin-like GTPases that target the membranes of pathogen-containing vacuoles. Upon their oligomerization on the membrane, the vacuole structure disintegrates and the pathogen gets exposed to the hostile cytoplasm. What has been obscure is how the immune system detects and directs the GTPases to these pathogen shelters. Using a common protist parasite of mice, Toxoplasma gondii, we found that the LC3 conjugation system of autophagy is necessary and sufficient for targeting the interferon-inducible GTPases to membranes. We dubbed this process Targeting by AutophaGy proteins (TAG). In canonical autophagy, the LC3 conjugation system is required to form membrane-bound autophagosomes, which encircle and deliver cytosolic materials to lysosomes for degradation. In TAG, however, the conjugation system is required to mark the membranes of pathogen-containing vacuoles with ubiquitin-like LC3 homologs, which function as molecular beacons to recruit the GTPases to their target membranes. Our data suggest that the LC3 conjugation system of autophagy plays an essential role in detecting and marking pathogen-containing vacuoles for immune effector targeting by the host immune system.
MeSH term(s)	Animals ; Autophagy ; Cell Membrane/metabolism ; GTP Phosphohydrolases/metabolism ; Humans ; Interferons/metabolism ; Microtubule-Associated Proteins/metabolism ; Toxoplasma/physiology
Chemical Substances	Microtubule-Associated Proteins ; Interferons (9008-11-1) ; GTP Phosphohydrolases (EC 3.6.1.-)
Language	English
Publishing date	2017--02
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2682247-7
ISSN	2154-1256 ; 2154-1248
ISSN (online)	2154-1256
ISSN	2154-1248
DOI	10.1080/21541248.2016.1213090
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Article ; Online: Autophagy and Inflammation.

Matsuzawa-Ishimoto, Yu / Hwang, Seungmin / Cadwell, Ken

Annual review of immunology

2017 Volume 36, Page(s) 73–101

Abstract: The cellular degradative pathway of autophagy has a fundamental role in immunity. Here, we review the function of autophagy and autophagy proteins in inflammation. We discuss how the autophagy machinery controls the burden of infectious agents while ... ...

Abstract	The cellular degradative pathway of autophagy has a fundamental role in immunity. Here, we review the function of autophagy and autophagy proteins in inflammation. We discuss how the autophagy machinery controls the burden of infectious agents while simultaneously limiting inflammatory pathologies, which often involves processes that are distinct from conventional autophagy. Among the newly emerging processes we describe are LC3-associated phagocytosis and targeting by autophagy proteins, both of which require many of the same proteins that mediate conventional autophagy. We also discuss how autophagy contributes to differentiation of myeloid and lymphoid cell types, coordinates multicellular immunity, and facilitates memory responses. Together, these functions establish an intimate link between autophagy, mucosal immunity, and chronic inflammatory diseases. Finally, we offer our perspective on current challenges and barriers to translation.
MeSH term(s)	Animals ; Autophagy ; Biomarkers ; Disease Susceptibility ; Gene Expression Regulation ; Host-Pathogen Interactions/genetics ; Host-Pathogen Interactions/immunology ; Humans ; Immune System/cytology ; Immune System/immunology ; Immune System/metabolism ; Immunomodulation ; Inflammation/diagnosis ; Inflammation/etiology ; Inflammation/metabolism ; Signal Transduction
Chemical Substances	Biomarkers
Language	English
Publishing date	2017-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604953-9
ISSN	1545-3278 ; 0732-0582
ISSN (online)	1545-3278
ISSN	0732-0582
DOI	10.1146/annurev-immunol-042617-053253
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Article ; Online: Partners in anti-crime: how interferon-inducible GTPases and autophagy proteins team up in cell-intrinsic host defense.

Coers, Jörn / Brown, Hailey M / Hwang, Seungmin / Taylor, Gregory A

Current opinion in immunology

2018 Volume 54, Page(s) 93–101

Abstract: Once pathogens have breached the mechanical barriers to infection, survived extracellular immunity and successfully invaded host cells, cell-intrinsic immunity becomes the last line of defense to protect the mammalian host against viruses, bacteria, ... ...

Abstract	Once pathogens have breached the mechanical barriers to infection, survived extracellular immunity and successfully invaded host cells, cell-intrinsic immunity becomes the last line of defense to protect the mammalian host against viruses, bacteria, fungi and protozoa. Many cell-intrinsic defense programs act as high-precision weapons that specifically target intracellular microbes or cytoplasmic sites of microbial replication while leaving endogenous organelles unharmed. Critical executioners of cell-autonomous immunity include interferon-inducible dynamin-like GTPases and autophagy proteins, which often act cooperatively in locating and antagonizing intracellular pathogens. Here, we discuss possible mechanistic models to account for the functional interactions that occur between these two distinct classes of host defense proteins.
MeSH term(s)	Animals ; Autophagy-Related Proteins/immunology ; Autophagy-Related Proteins/metabolism ; GTP Phosphohydrolases/immunology ; GTP Phosphohydrolases/metabolism ; Humans ; Interferons/immunology
Chemical Substances	Autophagy-Related Proteins ; Interferons (9008-11-1) ; GTP Phosphohydrolases (EC 3.6.1.-)
Language	English
Publishing date	2018-07-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2018.06.008
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