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Article ; Online: Cytosolic DNA sensor IFI16 proteins: Potential molecular integrators of interactions among the aging hallmarks.

Choubey, Divaker

2022 Volume 82, Page(s) 101765

Abstract: Cellular changes that are linked to aging in humans include genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, cellular senescence, and altered intercellular communications. The extent of the changes in these ... ...

Abstract	Cellular changes that are linked to aging in humans include genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, cellular senescence, and altered intercellular communications. The extent of the changes in these aging hallmarks and their interactions with each other are part of the human aging. However, the molecular mechanisms through which the aging hallmarks interact with each other remain unclear. Studies have indicated a potential role for the type I interferon (IFN) and p53-inducible IFI16 proteins in interactions with the aging hallmarks. The IFI16 proteins are members of the PYHIN protein family. Proteins in the family share a DNA-binding domain (the HIN domain) and a protein-protein interaction pyrin domain (PYD). IFI16 proteins are needed for cytosolic DNA-induced activation of the cGAS-STING pathway for type I IFN (IFN-β) expression. The pathway plays an important role in aging-related inflammation (inflammaging). Further, increased levels of the IFI16 proteins potentiate the cell growth inhibitory functions of the p53 and pRb tumor suppressors proteins. Moreover, IFI16 proteins are needed for most aging hallmarks. Therefore, here we discuss how an improved understanding of the role of the IFI16 proteins in integration of the aging hallmarks has potential to improve the human health and lifespan.
MeSH term(s)	Humans ; Tumor Suppressor Protein p53/metabolism ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Cellular Senescence/genetics ; Aging/genetics ; DNA/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism
Chemical Substances	Tumor Suppressor Protein p53 ; Phosphoproteins ; DNA (9007-49-2) ; IFI16 protein, human (148998-64-5) ; Nuclear Proteins
Language	English
Publishing date	2022-10-19
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2075672-0
ISSN	1872-9649 ; 1568-1637
ISSN (online)	1872-9649
ISSN	1568-1637
DOI	10.1016/j.arr.2022.101765
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Article ; Online: Type I interferon (IFN)-inducible Absent in Melanoma 2 proteins in neuroinflammation: implications for Alzheimer's disease.

Choubey, Divaker

Journal of neuroinflammation

2019 Volume 16, Issue 1, Page(s) 236

Abstract: Cumulative evidence indicates that activation of innate immune responses in the central nervous system (CNS) induces the expression of type 1 interferons (T1 IFNs), a family of cytokines. The T1 IFNs (IFN-α/β), through activation of the JAK/STAT- ... ...

Abstract	Cumulative evidence indicates that activation of innate immune responses in the central nervous system (CNS) induces the expression of type 1 interferons (T1 IFNs), a family of cytokines. The T1 IFNs (IFN-α/β), through activation of the JAK/STAT-signaling in microglia, astrocytes, and neurons, induce the expression of IFN-inducible proteins, which mediate the pro- and anti-inflammatory functions of IFNs. Accordingly, T1 IFN-inducible Absent in Melanoma 2 proteins (murine Aim2 and human AIM2) negatively regulate the expression of TI IFNs and, upon sensing higher levels of cytosolic DNA, assemble the Aim2/AIM2 inflammasome, resulting in activation of caspase-1, pyroptosis, and the secretion of pro-inflammatory cytokines (e.g., IL-1β and IL-18). Of interest, studies have indicated a role for the Aim2/AIM2 proteins in neuroinflammation and neurodegenerative diseases, including Alzheimer's disease (AD). The ability of Aim2/AIM2 proteins to exert pro- and anti-inflammatory effects in CNS may depend upon age, sex hormones, cell-types, and the expression of species-specific negative regulators of the Aim2/AIM2 inflammasome. Therefore, we discuss the role of Aim2/AIM2 proteins in the development of AD. An improved understanding of the role of Absent in Melanoma 2 proteins in AD could identify new approaches to treat patients.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Animals ; Brain/metabolism ; Cytokines/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Humans ; Inflammasomes/metabolism ; Inflammation/genetics ; Inflammation/metabolism ; Neuroglia/metabolism ; Neurons/metabolism ; Signal Transduction/physiology
Chemical Substances	AIM2 protein, human ; Cytokines ; DNA-Binding Proteins ; Inflammasomes
Language	English
Publishing date	2019-11-26
Publishing country	England
Document type	Journal Article ; Review
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-019-1639-5
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Article ; Online: Absent in melanoma 2 proteins in the development of cancer.

Choubey, Divaker

Cellular and molecular life sciences : CMLS

2016 Volume 73, Issue 23, Page(s) 4383–4395

Abstract: Recent studies utilizing chemical-induced colitis-associated and sporadic colon cancer in mouse models indicated a protective role for absent in melanoma 2 (Aim2) in colon epithelial cells. Accordingly, mutations in the human AIM2 gene have been found in ...

Abstract	Recent studies utilizing chemical-induced colitis-associated and sporadic colon cancer in mouse models indicated a protective role for absent in melanoma 2 (Aim2) in colon epithelial cells. Accordingly, mutations in the human AIM2 gene have been found in colorectal cancer (CRC), and reduced expression of AIM2 in CRC is associated with its progression. Furthermore, the overexpression of AIM2 protein in human cancer cell lines inhibits cell proliferation. Interferon-inducible Aim2 and AIM2 are members of the PYHIN (PYRIN and HIN domain-containing) protein family and share ~57 % amino acid identity. The family also includes murine p202, human PYRIN-only protein 3, and IFI16, which negatively regulate Aim2/AIM2 functions. Because the CRC incidence and mortality rates are higher among men compared with women and the expression of Aim2/AIM2 proteins and their regulators is dependent upon age, gender, and sex hormones, we discuss the potential roles of Aim2/AIM2 in the development of cancer. An improved understanding of the biological functions of the AIM2 in the development of CRC will likely identify new therapeutic approaches to treat patients.
MeSH term(s)	Animals ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Cell Proliferation ; Colitis/pathology ; DNA-Binding Proteins/metabolism ; Humans ; Neoplasms/metabolism ; Neoplasms/pathology ; Protein Multimerization
Chemical Substances	DNA-Binding Proteins
Language	English
Publishing date	2016-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-016-2296-9
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Article: Human Prostate Epithelial Cells Activate the AIM2 Inflammasome upon Cellular Senescence: Role of POP3 Protein in Aging-Related Prostatic Inflammation.

Panchanathan, Ravichandran / Ramalingam, Vaikundamoorthy / Liu, Hongzhu / Choubey, Divaker

Life (Basel, Switzerland)

2021 Volume 11, Issue 4

Abstract: Increased levels of type I (T1) interferon (IFN)-inducible POP3 protein in myeloid cells inhibit activation of the AIM2 inflammasome and production of IL-1β and IL-18 proinflammatory cytokines. ... ...

Abstract	Increased levels of type I (T1) interferon (IFN)-inducible POP3 protein in myeloid cells inhibit activation of the AIM2 inflammasome and production of IL-1β and IL-18 proinflammatory cytokines. The
Language	English
Publishing date	2021-04-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life11040366
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Article ; Online: Human Prostate Epithelial Cells Activate the AIM2 Inflammasome upon Cellular Senescence

Ravichandran Panchanathan / Vaikundamoorthy Ramalingam / Hongzhu Liu / Divaker Choubey

Life, Vol 11, Iss 366, p

Role of POP3 Protein in Aging-Related Prostatic Inflammation

2021 Volume 366

Abstract	Increased levels of type I (T1) interferon (IFN)-inducible POP3 protein in myeloid cells inhibit activation of the AIM2 inflammasome and production of IL-1β and IL-18 proinflammatory cytokines. The AIM2 mRNA levels were significantly higher in benign prostate hyperplasia (BPH) than the normal prostate. Further, human normal prostate epithelial cells (PrECs), upon becoming senescent, activated an inflammasome. Because in aging related BPH senescent PrECs accumulate, we investigated the role of POP3 and AIM2 proteins in pre-senescent and senescent PrECs. Here we report that the basal levels of the POP3 mRNA and protein were lower in senescent ( versus young or old) PrECs that exhibited activation of the T1 IFN response. Further, treatment of PrECs and a BPH cell line (BPH-1) that expresses the androgen receptor (AR) with the male sex hormone dihydrotestosterone (DHT) increased the basal levels of POP3 mRNA and protein, but not AIM2, and inhibited activation of the AIM2 inflammasome. Of interest, a stable knockdown of POP3 protein expression in the BPH-1 cell line increased cytosolic DNA-induced activation of AIM2 inflammasome. These observations suggest a potential role of POP3 protein in aging-related prostatic inflammation.
Keywords	prostate ; senescence ; inflammation ; AIM2 inflammasome ; POP3 ; Science ; Q
Subject code	570
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Interferon (IFN)-inducible Absent in Melanoma 2 proteins in the negative regulation of the type I IFN response: Implications for lupus nephritis.

Choubey, Divaker / Panchanathan, Ravichandran

Cytokine

2019 Volume 132, Page(s) 154682

Abstract: Systemic lupus erythematosus (SLE) is a complex autoimmune disease that exhibits a strong female bias (female-to-male ratio 9:1) in patients. Further, 40-60% SLE patients develop lupus nephritis (LN), which significantly increases the mortality rates. ... ...

Abstract	Systemic lupus erythematosus (SLE) is a complex autoimmune disease that exhibits a strong female bias (female-to-male ratio 9:1) in patients. Further, 40-60% SLE patients develop lupus nephritis (LN), which significantly increases the mortality rates. The failure of current therapies to adequately treat LN in patients reflects an incomplete understanding of the disease pathogenesis. Notably, a chronic increase in serum interferon-α (IFN-α) activity is a heritable risk factor to develop SLE. Accordingly, blood cells from most SLE patients with an active disease exhibit an increase in the expression of the type I IFN (IFN-α/β)-stimulated genes (ISGs, also referred to as "IFN-signature"), a type I IFN response. Further, LN patients during renal flares also exhibit an "IFN-signature" in renal biopsies. Therefore, an improved understanding of the regulation of type I IFNs expression is needed. Basal levels of the IFN-β through "priming" of IFN-α producing cells augment the expression of the IFN-α genes. Of interest, recent studies have indicated a role for the type I IFN-inducible Absent in Melanoma 2 proteins (the murine Aim2 and human AIM2) in the negative regulation of the type I IFN response through inflammasome-dependent and independent mechanisms. Further, an increase in the expression of Aim2 and AIM2 proteins in kidney and renal macrophages associated with the development of nephritis. Therefore, we discuss the role of Aim2/AIM2 proteins in the regulation of type I IFNs and LN. An improved understanding of the mechanisms by which the Absent in Melanoma 2 proteins suppress the type I IFN response and modulate nephritis is key to identify novel therapeutic targets to treat a group of LN patients.
Language	English
Publishing date	2019-03-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1018055-2
ISSN	1096-0023 ; 1043-4666
ISSN (online)	1096-0023
ISSN	1043-4666
DOI	10.1016/j.cyto.2019.03.008
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Article: Absent in melanoma 2 proteins in the development of cancer

Choubey, Divaker

Cellular and molecular life sciences. 2016 Dec., v. 73, no. 23

2016

Abstract	Recent studies utilizing chemical-induced colitis-associated and sporadic colon cancer in mouse models indicated a protective role for absent in melanoma 2 (Aim2) in colon epithelial cells. Accordingly, mutations in the human AIM2 gene have been found in colorectal cancer (CRC), and reduced expression of AIM2 in CRC is associated with its progression. Furthermore, the overexpression of AIM2 protein in human cancer cell lines inhibits cell proliferation. Interferon-inducible Aim2 and AIM2 are members of the PYHIN (PYRIN and HIN domain-containing) protein family and share ~57Â % amino acid identity. The family also includes murine p202, human PYRIN-only protein 3, and IFI16, which negatively regulate Aim2/AIM2 functions. Because the CRC incidence and mortality rates are higher among men compared with women and the expression of Aim2/AIM2 proteins and their regulators is dependent upon age, gender, and sex hormones, we discuss the potential roles of Aim2/AIM2 in the development of cancer. An improved understanding of the biological functions of the AIM2 in the development of CRC will likely identify new therapeutic approaches to treat patients.
Keywords	amino acids ; animal models ; carcinogenesis ; cell proliferation ; colon ; colorectal neoplasms ; epithelial cells ; gender ; genes ; humans ; melanoma ; men ; mice ; mortality ; mutation ; patients ; protective effect ; proteins ; sex hormones ; women
Language	English
Dates of publication	2016-12
Size	p. 4383-4395.
Publishing place	Springer International Publishing
Document type	Article
Note	Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-016-2296-9
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Interferon-inducible Ifi200-family genes as modifiers of lupus susceptibility.

Choubey, Divaker

Immunology letters

2012 Volume 147, Issue 1-2, Page(s) 10–17

Abstract: Both genetic and environmental factors contribute to the development and progression of systemic lupus erythematosus (SLE), a complex autoimmune disease. The disease exhibits a strong gender bias and develops predominantly in females. Additionally, most ... ...

Abstract	Both genetic and environmental factors contribute to the development and progression of systemic lupus erythematosus (SLE), a complex autoimmune disease. The disease exhibits a strong gender bias and develops predominantly in females. Additionally, most SLE patients exhibit increased serum levels of interferon-α (IFN-α) and the "IFN signature". Studies using the mouse models of lupus have identified several lupus susceptibility loci, including the New Zealand Black (NZB)-derived autoimmunity 2 (Nba2) interval on the chromosome 1. The interval, which is syntenic to the human chromosome 1q region, harbors the FcγR family, SLAM/CD2-family, and the IFN-inducible Ifi200-family genes (encoding for the p200-family proteins). Studies involving the B6.Nba2 congenic mice revealed that the development of antinuclear autoantibodies (ANAs) depends on the age, gender, and activation of type I IFN-signaling. Interestingly, recent studies involving the generation of Nba2 subcongenic mouse lines and generation of mice deficient for the Fcgr2b or Aim2 gene within the interval have provided evidence that epistatic interactions among the Nba2 genes contribute to increased lupus susceptibility. Given that the expression of some of the p200-family proteins is differentially regulated by sex hormones and these proteins differentially regulate cytosolic DNA-induced production of type I IFN and proinflammatory cytokines (IL-1β and IL-18), the major known contributors of SLE-associated inflammation, we discuss the recent advancements in our understanding of the role of p200-family proteins in lupus susceptibility modification. An improved understanding of the role of p200-family proteins in the development of autoimmunity is likely to identify new approaches to treat SLE patients.
MeSH term(s)	Animals ; Antigens, CD/genetics ; Autoimmunity/genetics ; Epistasis, Genetic ; Gene Expression Regulation ; Genes, Modifier ; Genetic Predisposition to Disease ; Humans ; Immunologic Factors/genetics ; Interferon Regulatory Factors/metabolism ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/metabolism ; Nuclear Proteins/genetics ; Receptors, Cell Surface/genetics ; Receptors, IgG/genetics ; Signaling Lymphocytic Activation Molecule Family Member 1
Chemical Substances	Antigens, CD ; Fc gamma receptor IIB ; HIN-200 protein, human ; Immunologic Factors ; Interferon Regulatory Factors ; Nuclear Proteins ; Receptors, Cell Surface ; Receptors, IgG ; Signaling Lymphocytic Activation Molecule Family Member 1 (169535-43-7)
Language	English
Publishing date	2012-07-24
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	445150-8
ISSN	1879-0542 ; 0165-2478
ISSN (online)	1879-0542
ISSN	0165-2478
DOI	10.1016/j.imlet.2012.07.003
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Zs.A 1512: Show issues

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Article ; Online: DNA-responsive inflammasomes and their regulators in autoimmunity.

Choubey, Divaker

Clinical immunology (Orlando, Fla.)

2011 Volume 142, Issue 3, Page(s) 223–231

Abstract: Upon sensing microbial and self-derived DNA, DNA sensors initiate innate immune responses. These sensors include the interferon (IFN)-inducible Toll-like receptor 9 (TLR9) and PYHIN proteins. Upon sensing DNA, cytosolic (murine Aim2 and human AIM2) and ... ...

Abstract	Upon sensing microbial and self-derived DNA, DNA sensors initiate innate immune responses. These sensors include the interferon (IFN)-inducible Toll-like receptor 9 (TLR9) and PYHIN proteins. Upon sensing DNA, cytosolic (murine Aim2 and human AIM2) and nuclear (IFI16) PYHIN proteins recruit an adaptor protein (ASC) and pro-caspase-1 to form an inflammasome, which activates caspase-1. The activated caspase-1 cleaves pro-IL-1β and pro-IL-18 to generate active forms. However, upon sensing cytosolic DNA, the IFI16 protein recruits STING to induce the expression of type I IFN. Recognition of self DNA by innate immune cells contributes to the production of increased levels of type I IFN. Given that the type I IFNs modulate the expression of inflammasome proteins and that the IFN-inducible proteins inhibit the activity of DNA-responsive inflammasomes, an improved understanding of the molecular mechanisms that regulate the activity of DNA-responsive inflammasomes is likely to identify new therapeutic targets to treat autoimmune diseases.
MeSH term(s)	Animals ; Autoimmune Diseases/genetics ; Autoimmune Diseases/immunology ; Autoimmunity ; DNA/immunology ; Humans ; Immunity, Innate ; Inflammasomes/immunology
Chemical Substances	Inflammasomes ; DNA (9007-49-2)
Language	English
Publishing date	2011-12-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2011.12.007
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Article ; Online: Absent in Melanoma 2 proteins in SLE.

Choubey, Divaker / Panchanathan, Ravichandran

Clinical immunology (Orlando, Fla.)

2017 Volume 176, Page(s) 42–48

Abstract: Type I interferons (IFN-α/β)-inducible PYRIN and HIN domain-containing protein family includes Absent in Melanoma 2 (murine Aim2 and human AIM2), murine p202, and human PYRIN-only protein 3 (POP3). The generation of Aim2-deficient mice indicated that the ...

Abstract	Type I interferons (IFN-α/β)-inducible PYRIN and HIN domain-containing protein family includes Absent in Melanoma 2 (murine Aim2 and human AIM2), murine p202, and human PYRIN-only protein 3 (POP3). The generation of Aim2-deficient mice indicated that the Aim2 protein is essential for inflammasome activation, resulting in the secretion of interleukin-1β (IL-1β) and IL-18 and cell death by pyroptosis. Further, Aim2-deficiency also increased constitutive expression of the IFN-β and expression of the p202 protein. Notably, an increased expression of p202 protein in female mice associated with the development of systemic lupus erythematosus (SLE). SLE in patients is characterized by a constitutive increase in serum levels of IFN-α and an increase in the expression IFN-stimulated genes. Recent studies indicate that p202 and POP3 proteins inhibit activation of the Aim2/AIM2 inflammasome and promote IFN-β expression. Therefore, we discuss the role of Aim2/AIM2 proteins in the suppression of type I IFNs production and lupus susceptibility.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; DNA-Binding Proteins/metabolism ; Humans ; Interferon Type I/metabolism ; Interleukin-18/metabolism ; Interleukin-1beta/metabolism ; Lupus Erythematosus, Systemic/metabolism ; Melanoma/metabolism ; Tumor Suppressor p53-Binding Protein 1/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; DNA-Binding Proteins ; Interferon Type I ; Interleukin-18 ; Interleukin-1beta ; Tumor Suppressor p53-Binding Protein 1
Language	English
Publishing date	2017-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2016.12.011
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