Interferon-inducible protein 205 (p205) plays a role in adipogenic differentiation of mouse adipose-derived stem cells

Liu, Feihan; Jiao, Yang; Zhu, Zhiqian; Sun, Chaochen; Li, Haifang

doi:10.1016/j.mce.2014.05.009

Cited by 9 publications

(8 citation statements)

References 20 publications

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“…IFI205 was previously identified as a candidate cytosolic dsDNA sensor by proteomic screening for ISGs ( 53 ). IFI205 is also an inducer of adipogenic differentiation and localizes in the nuclei of osteosarcoma and adipose-tissue-derived stem cells, where it interacts with several transcription factors ( 54 , 55 ). We showed, however, that IFI205 is localized in the cytoplasm in fibroblasts and in macrophages, the latter of which is a cell type that is probably important for the sensing of both endogenous and exogenous cytosolic DNA.…”

Section: Discussionmentioning

confidence: 99%

“…This difference in localization between our studies and those of others may be due to cell type differences, different molecular tags (HA versus myc), or transient versus stable transfection. Moreover, the anti-IFI205 peptide antibodies used in one study would also recognize MNDA and MNDAL ( 54 ). Our finding of Ifi205’s cytosolic location in macrophages is consistent with its role in the sensing of endogenous reverse transcripts.…”

Section: Discussionmentioning

confidence: 99%

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AIM2-Like Receptors Positively and Negatively Regulate the Interferon Response Induced by Cytosolic DNA

Nakaya

Lilue

Stavrou

et al. 2017

mBio

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Cytosolic DNAs derived from retrotransposons serve as pathogen-associated molecular patterns for pattern recognition receptors (PRRs) that stimulate the induction of interferons (IFNs) and other cytokines, leading to autoimmune disease. Cyclic GMP-AMP synthase is one PRR that senses retrotransposon DNA, activating type I IFN responses through the stimulator of IFN genes (STING). Absent in melanoma 2 (AIM2)-like receptors (ALRs) have also been implicated in these pathways. Here we show that the mouse ALR IFI205 senses cytosolic retrotransposon DNA independently of cyclic GMP-AMP production. AIM2 antagonizes IFI205-mediated IFN induction activity by sequestering it from STING. We also found that the complement of genes located in the ALR locus in C57BL/6 and AIM2 knockout mice are different and unique, which has implications for interpretation of the sensing of pathogens in different mouse strains. Our data suggest that members of the ALR family are critical to the host IFN response to endogenous DNA.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

AIM2-Like Receptors Positively and Negatively Regulate the Interferon Response Induced by Cytosolic DNA

Nakaya

Lilue

Stavrou

et al. 2017

mBio

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“…Previously, Parsons et al had shown that TNFα treatment could enhance Asc expression through p65/RelA in MCF7 cell lines (35). Furthermore, p205 has been shown to co-localize and bind directly with the CCAAT/enhancer binding protein-β (c/EBPβ) in mouse adipose-derived stem cells (27). Furthermore, c/EBPβ has also been implicated in the induction of several proinflammatory genes in macrophages (36).…”

Section: Resultsmentioning

confidence: 99%

The PYHIN Protein p205 Regulates the Inflammasome by Controlling Asc Expression

Ghosh

Wallerath

Covarrubias

et al. 2017

The Journal of Immunology

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Members of the interferon-inducible PYHIN protein family such as Absent in Melanoma-2 and Interferon Gamma Inducible Protein (IFI) 16 bind double-stranded DNA (dsDNA) and form caspase-1 activating inflammasomes, important in immunity to cytosolic bacteria, DNA viruses or Human Immunodeficiency Virus. IFI16 has also been shown to regulate transcription of type I Interferons during Herpes Simplex Virus infection. The role of other members of the PYHIN protein family in the regulation of immune responses is much less clear. Here, we identified an immune regulatory function for a member of the murine PYHIN protein family, p205 (also called Ifi205). Examination of immune responses induced by dsDNA and other microbial ligands in bone marrow derived macrophages lacking p205 revealed that inflammasome activation by dsDNA as well as ligands that engage the NLRP3 inflammasome was severely compromised in these cells. Further analysis revealed that p205 knockdown cells showed reduced expression of Asc at the protein and RNA level. p205 knockdown resulted in reduced binding of actively transcribing RNA Polymerase II to the endogenous Asc gene resulting in decreased transcription and processing of Asc pre-mRNA. Deletion of p205 in B16 melanoma cells using CRISPR/Cas9 showed similar loss of Asc expression. Ectopic expression of p205 induced expression of an Asc promoter-luciferase reporter gene. Together these findings suggest that p205 controls expression of Asc mRNA to regulate inflammasome responses. These findings expand on our understanding of immune regulatory roles for the PYHIN protein family.

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“…Interferon inducible gene 205 ( Ifi205 ) belongs to the HIN-200 family, and is a regulator of type I interferon (IFN) production 7,8 . HIN-200 family members are characterized by at least one HIN-200 domain (hematopoietic interferon-inducible nuclear proteins with a 200-amino-acid repeat), which binds double-stranded DNA via an oligonucleotide/oligosaccharide binding (OB) fold 9,10 . HIN-200 family members also contain an N terminal pyrin domain, which mediates assembly into innate immune effector complexes 8,11 .…”

Section: Introductionmentioning

confidence: 99%

Chronic Interferon Stimulated Gene Transcription Promotes Oncogene Induced Breast Cancer

Wang,

Canasto-Chibuque,

Kim

et al. 2023

Preprint

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The Mre11 complex (comprising Mre11, Rad50, Nbs1) is integral to the maintenance of genome stability. We previously showed that a hypomorphicMre11mutant mouse strain (Mre11ATLD1/ATLD1) was highly susceptible to oncogene induced breast cancer. Here we used a mammary organoid system to examine which Mre11 dependent responses are tumor suppressive. We found thatMre11ATLD1/ATLD1organoids exhibited an elevated interferon stimulated gene (ISG) signature and sustained changes in chromatin accessibility. ThisMre11ATLD1/ATLD1phenotype depended on DNA binding of a nuclear innate immune sensor, IFI205. Ablation ofIfi205inMre11ATLD1/ATLD1organoids restored baseline and oncogene-induced chromatin accessibility patterns to those observed inWT. Implantation ofMre11ATLD1/ATLD1organoids and activation of oncogene led to aggressive metastatic breast cancer. This outcome was reversed in implantedIfi205-/-Mre11ATLD1/ATLD1organoids. These data reveal a connection between innate immune signaling and tumor suppression in mammary epithelium. Given the abundance of aberrant DNA structures that arise in the context of genome instability syndromes, the data further suggest that cancer predisposition in those contexts may be partially attributable to tonic innate immune transcriptional programs.

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Interferon-inducible protein 205 (p205) plays a role in adipogenic differentiation of mouse adipose-derived stem cells

Cited by 9 publications

References 20 publications

AIM2-Like Receptors Positively and Negatively Regulate the Interferon Response Induced by Cytosolic DNA

AIM2-Like Receptors Positively and Negatively Regulate the Interferon Response Induced by Cytosolic DNA

The PYHIN Protein p205 Regulates the Inflammasome by Controlling Asc Expression

Chronic Interferon Stimulated Gene Transcription Promotes Oncogene Induced Breast Cancer

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