Relevant bibliographies by topics / IFI16

Academic literature on the topic 'IFI16'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "IFI16"

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Fujiuchi, Nobuko, Jason A. Aglipay, Takao Ohtsuka, Naoki Maehara, Fikret Sahin, Gloria H. Su, Sam W. Lee, and Toru Ouchi. "Requirement of IFI16 for the Maximal Activation of p53 Induced by Ionizing Radiation." Journal of Biological Chemistry 279, no. 19 (February 27, 2004): 20339–44. http://dx.doi.org/10.1074/jbc.m400344200.

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IFI16 is a member of the PYRIN superfamily that has been implicated in BRCA1-mediated apoptosis and inflammation signaling pathways. Here we report that most breast cancer cell lines examined expressed decreased mRNA and protein levels of IFI16, although IFI16 is expressed in human primary normal mammary epithelial cells. Significantly, immunohistochemical analysis of tissues from 25 breast cancer patients demonstrated that carcinoma cells showed negative or weaker staining of IFI16 compared with positive nuclear staining in normal mammary duct epithelium. si-RNA-mediated reduction of IFI16 resulted in perturbation of p53 activation when treated with ionizing radiation (IR). Expression of IFI16 enhanced p53 transcriptional activity in cells exposed to IR. Adenovirus expression of IFI16 in IFI16-deficient MCF7 induced apoptosis, which was enhanced by radiomimetic neocarcinostatin treatment. Tetracycline-regulated IFI16 also induced apoptosis when coexpressed with p53 in p53-deficient EJ cells subjected to IR, suggesting that IFI16 is involved in p53-mediated transmission of apoptosis signaling. Consistent with these results, expression of IFI16 enhanced activation of the known p53 target genes, includingp21, Hdm2, andbaxin MCF7 cells. These results suggest that loss of IFI16 results in deregulation of p53-mediated apoptosis, leading to cancer development.
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Alunno, A., V. Caneparo, F. Carubbi, O. Bistoni, S. Caterbi, M. Gariglio, E. Bartoloni, S. Landolfo, and R. Gerli. "Interferon gamma-inducible protein 16 (IFI16) and anti-IFI16 antibodies in primary Sjögren’s syndrome: findings in serum and minor salivary glands." Reumatismo 67, no. 3 (February 9, 2016): 85. http://dx.doi.org/10.4081/reumatismo.2015.839.

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The interferon (IFN) signature, namely the overexpression of IFN-inducible genes is a crucial aspect in the pathogenesis of primary Sjögren’s syndrome (pSS). The IFN-inducible IFI16 protein, normally expressed in cell nuclei, may be overexpressed, mislocalized in the cytoplasm and secreted in the extracellular milieu in several autoimmune disorders including pSS. This leads to tolerance breaking to this self-protein and development of anti-IFI16 antibodies. The aim of this study was to identify pathogenic and clinical significance of IFI16 and anti-IFI16 autoantibodies in pSS. IFI16 and anti-IFI16 were assessed in the serum of 30 pSS patients and one-hundred healthy donors (HD) by ELISA. IFI16 was also evaluated in 5 minor salivary glands (MSGs) of pSS patients and 5 MSGs of non-pSS patients with sicca symptoms by immunohistochemistry. Normal MSGs do not constitutively express IFI16. Conversely, in pSS-MSGs a marked expression and cytoplasmic mislocalization of IFI16 by epithelial cells was observed with infiltrations in lymphocytes and peri/ intra-lesional endothelium. pSS patients display higher serum levels of both IFI16 and anti-IFI16 autoantibodies compared to HD. Our data suggest that IFI16 protein may be involved in the initiation and perpetuation of glandular inflammation occurring in pSS.
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Chang, Xiaobo, Xibao Shi, Xiaozhuan Zhang, Li Wang, Xuewu Li, Aiping Wang, Ruiguang Deng, Enmin Zhou, and Gaiping Zhang. "IFI16 Inhibits Porcine Reproductive and Respiratory Syndrome Virus 2 Replication in a MAVS-Dependent Manner in MARC-145 Cells." Viruses 11, no. 12 (December 16, 2019): 1160. http://dx.doi.org/10.3390/v11121160.

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Porcine reproductive and respiratory syndrome virus (PRRSV) is a single-stranded positive-sense RNA virus, and the current strategies for controlling PRRSV are limited. Interferon gamma-inducible protein 16 (IFI16) has been reported to have a broader role in the regulation of the type I interferons (IFNs) response to RNA and DNA viruses. However, the function of IFI16 in PRRSV infection is unclear. Here, we revealed that IFI16 acts as a novel antiviral protein against PRRSV-2. IFI16 could be induced by interferon-beta (IFN-β). Overexpression of IFI16 could significantly suppress PRRSV-2 replication, and silencing the expression of endogenous IFI16 by small interfering RNAs led to the promotion of PRRSV-2 replication in MARC-145 cells. Additionally, IFI16 could promote mitochondrial antiviral signaling protein (MAVS)-mediated production of type I interferon and interact with MAVS. More importantly, IFI16 exerted anti-PRRSV effects in a MAVS-dependent manner. In conclusion, our data demonstrated that IFI16 has an inhibitory effect on PRRSV-2, and these findings contribute to understanding the role of cellular proteins in regulating PRRSV replication and may have implications for the future antiviral strategies.
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Biolatti, Matteo, Valentina Dell'Oste, Sara Pautasso, Jens von Einem, Manfred Marschall, Bodo Plachter, Marisa Gariglio, Marco De Andrea, and Santo Landolfo. "Regulatory Interaction between the Cellular Restriction Factor IFI16 and Viral pp65 (pUL83) Modulates Viral Gene Expression and IFI16 Protein Stability." Journal of Virology 90, no. 18 (July 6, 2016): 8238–50. http://dx.doi.org/10.1128/jvi.00923-16.

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ABSTRACTA key player in the intrinsic resistance against human cytomegalovirus (HCMV) is the interferon-γ-inducible protein 16 (IFI16), which behaves as a viral DNA sensor in the first hours postinfection and as a repressor of viral gene transcription in the later stages. Previous studies on HCMV replication demonstrated that IFI16 binds to the viral protein kinase pUL97, undergoes phosphorylation, and relocalizes to the cytoplasm of infected cells. In this study, we demonstrate that the tegument protein pp65 (pUL83) recruits IFI16 to the promoter of the UL54 gene and downregulates viral replication, as shown by use of the HCMV mutant v65Stop, which lacks pp65 expression. Interestingly, at late time points of HCMV infection, IFI16 is stabilized by its interaction with pp65, which stood in contrast to IFI16 degradation, observed in herpes simplex virus 1 (HSV-1)-infected cells. Moreover, we found that its translocation to the cytoplasm, in addition to pUL97, strictly depends on pp65, as demonstrated with the HCMV mutant RV-VM1, which expresses a form of pp65 unable to translocate into the cytoplasm. Thus, these data reveal a dual role for pp65: during early infection, it modulates IFI16 activity at the promoter of immediate-early and early genes; subsequently, it delocalizes IFI16 from the nucleus into the cytoplasm, thereby stabilizing and protecting it from degradation. Overall, these data identify a novel activity of the pp65/IFI16 interactome involved in the regulation of UL54 gene expression and IFI16 stability during early and late phases of HCMV replication.IMPORTANCEThe DNA sensor IFI16, a member of the PYHIN proteins, restricts HCMV replication by impairing viral DNA synthesis. Using a mutant virus lacking the tegument protein pp65 (v65Stop), we demonstrate that pp65 recruits IFI16 to the early UL54 gene promoter. As a putative counteraction to its restriction activity, pp65 supports the nucleocytoplasmic export of IFI16, which was demonstrated with the viral mutant RV-VM1 expressing a nuclearly retained pp65. These data reveal a dual role of pp65 in IFI16 regulation: in the early phase of HCMV infection, it contributes to viral evasion from IFI16 restriction activity, while at later time points, it promotes the nuclear delocalization of IFI16, thereby stabilizing and protecting it from degradation. In the present work, we further clarify the mechanisms HCMV relies on to overcome intracellular innate immune restriction and provide new insights into the relevance of DNA-sensing restriction factor IFI16 during HCMV infection.
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Caposio, Patrizia, Francesca Gugliesi, Claudia Zannetti, Simone Sponza, Michele Mondini, Enzo Medico, John Hiscott, et al. "A Novel Role of the Interferon-inducible Protein IFI16 as Inducer of Proinflammatory Molecules in Endothelial Cells." Journal of Biological Chemistry 282, no. 46 (August 14, 2007): 33515–29. http://dx.doi.org/10.1074/jbc.m701846200.

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The human IFI16 gene is an interferon-inducible gene implicated in the regulation of endothelial cell proliferation and tube morphogenesis. Immunohistochemical analysis has demonstrated that this gene is highly expressed in endothelial cells in addition to hematopoietic tissues. In this study, gene array analysis of human umbilical vein endothelial cells overexpressing IFI16 revealed an increased expression of genes involved in immunomodulation, cell growth, and apoptosis. Consistent with these observations, IFI16 triggered expression of adhesion molecules such as ICAM-1 and E-selectin or chemokines such as interleukin-8 or MCP-1. Treatment of cells with short hairpin RNA targeting IFI16 significantly inhibited ICAM-1 induction by interferon (IFN)-γ demonstrating that IFI16 is required for proinflammatory gene stimulation. Moreover, functional analysis of the ICAM-1 promoter by deletion- or site-specific mutation demonstrated that NF-κB is the main mediator of IFI16-driven gene induction. NF-κB activation appears to be triggered by IFI16 through a novel mechanism involving suppression of IκBα mRNA and protein expression. Support for this finding comes from the observation that IFI16 targeting with specific short hairpin RNA down-regulates NF-κB binding activity to its cognate DNA and inhibits ICAM-1 expression induced by IFN-γ. Using transient transfection and luciferase assay, electrophoretic mobility shift assay, and chromatin immunoprecipitation, we demonstrate indeed that activation of the NF-κB response is mediated by IFI16-induced block of Sp1-like factor recruitment to the promoter of the IκBα gene, encoding the main NF-κB inhibitor. Activation of NF-κB accompanied by induction of proinflammatory molecules was also observed when IκBα expression was down-regulated by specific small interfering RNA, resulting in an outcome similar to that observed with IFI16 overexpression. Taken together, these data implicate IFI16 as a novel regulator of endothelial proinflammatory activity and provide new insights into the physiological functions of the IFN-inducible gene IFI16.
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Xiao, Tsan, and Tengchuan Jin. "Ligand binding and signaling by IFI16 (INM8P.400)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 195.8. http://dx.doi.org/10.4049/jimmunol.194.supp.195.8.

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Abstract IFI16 plays important roles in inflammatory immune responses to viral infections as well as in autoimmune disorders such as lupus. It has been implicated in interferon induction through a STING-mediated pathway, as well as in inflammasome activation during recognition of viral DNA in the nucleus. Despite recent progress that highlighted the mechanisms of dsDNA binding by the IFI16 HINb domain, there are major gaps in our understanding of the ligand-induced structural changes, the polymerization of IFI16 mediated by dsDNA and its PYD domain, its interaction with downstream signaling partners, the regulation of IFI16 by host and microbe-derived molecules, and the cell-type specific immune responses mediated by IFI16. We have characterized the key structural determinants in both the recognition of dsDNA by IFI16 and the potential downstream signaling events. We will outline the implications of our findings and discuss future directions in clarifying the structure and function of IFI16 in infectious diseases and autoimmune disorders.
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Orzalli, Megan H., Nicole M. Broekema, and David M. Knipe. "Relative Contributions of Herpes Simplex Virus 1 ICP0 and vhs to Loss of Cellular IFI16 Vary in Different Human Cell Types." Journal of Virology 90, no. 18 (July 13, 2016): 8351–59. http://dx.doi.org/10.1128/jvi.00939-16.

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ABSTRACTThe herpes simplex virus 1 (HSV-1) ICP0 protein is an E3 ubiquitin ligase that promotes the degradation of several host cell proteins. Most studies have found that ICP0 promotes the loss of IFI16 in infected cells, but one study reported that ICP0 was not necessary or sufficient for loss of IFI16 in a tumor-derived cell line. Therefore, in this study, we examined the requirement for ICP0 in promoting the loss of IFI16 in several normal and tumor-derived cell lines. HSV-1 infection resulted in an observable decrease of IFI16 protein levels in normal human foreskin fibroblasts (HFFs), normal oral keratinocytes (NOKs), and HeLa cells but not in U2OS cells. During infection with an ICP0-null virus, we observed a reduced loss of IFI16 in HFFs and NOKs but not in HeLa cells. Ectopic expression of ICP0 from a transfected plasmid was sufficient to promote the loss of IFI16 in HFFs and NOKs. In the absence of ICP0, we observed a delayed reduction of IFI16 protein that correlated with a reduction in the steady-state levels ofIFI16mRNA. In addition, we show that the ICP0-independent loss of IFI16 in HeLa cells is dependent in part on the activity of the viral virion host shutoff (vhs) tegument protein. Together, these results demonstrate that HSV-1 promotes the loss of IFI16 through at least two mechanisms: (i) by ICP0-dependent degradation of IFI16 and (ii) by vhs-dependent turnover ofIFI16mRNA. In addition, this study highlights a potential intrinsic difference between normal and tumor-derived cells for the activities of IFI16 and HSV-1 ICP0.IMPORTANCEHSV-1 is a ubiquitous virus that establishes a lifetime persistent infection in humans. The relative success of HSV-1 as a pathogen is, in part, dependent on the expression of viral proteins that counteract host intrinsic defense mechanisms and that modulate immune responses during viral infection. In this study, we examined the relative roles of two viral gene products for the ability to promote loss of the antiviral IFI16 DNA sensor. We demonstrate that the viral immediate early ICP0 protein plays a dominant role in the loss of IFI16 in normal, but not tumor-derived, human cell lines. In contrast, viral vhs-mediated loss of IFI16 by mRNA destabilization is revealed to be dominant in tumor-derived cells in which ICP0 is nonfunctional. Together, these results contribute to our understanding of how HSV-1 modulates IFI16 protein levels and highlight cell-type-dependent differences between normal and tumor-derived cells.
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De Andrea, M., M. De Santis, V. Caneparo, E. Generali, S. Sirotti, N. Isailovic, G. M. Guidelli, et al. "Serum IFI16 and anti‐IFI16 antibodies in psoriatic arthritis." Clinical & Experimental Immunology 199, no. 1 (October 15, 2019): 88–96. http://dx.doi.org/10.1111/cei.13376.

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Yamauchi, Moriyasu, Takafumi Nakano, Torahiko Nakashima, Ryuji Yasumatsu, Kazuki Hashimoto, Satoshi Toh, Hideki Shiratsuchi, Yoshinao Oda, and Shizuo Komune. "Interferon Inducible IFI16 Expression in p16 Positive Squamous Cell Carcinoma of the Oropharynx." ISRN Otolaryngology 2013 (July 11, 2013): 1–7. http://dx.doi.org/10.1155/2013/263271.

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Human-papillomavirus- (HPV-) positive oropharyngeal squamous cell carcinomas (OPSCC) are reported to be more responsive to treatment and to be related to a favorable prognosis compared with non-HPV carcinomas. However, the molecular basis of the responsiveness is unclear. Interferon inducible IFI16, which is implicated in the control of cell growth, apoptosis, angiogenesis, and immunomodulation in various types of cancers, is reported to be frequently expressed in the HPV-positive head and neck SCC and to correlate with a better prognosis. In this study, we hypothesized that HPV related OPSCC expresses IFI16 resulting in favorable prognosis. To clarify the relationship between the prognosis of HPV related OPSCC patients and IFI16 status, we examined immunohistologically the pretreatment specimens of OPSCC for the expression of p16 as a surrogate marker of HPV infection and IFI16. We could not show that the expression of IFI16 is associated with that of p16. There was no significant difference in the survival rate between IFI16 positive and negative groups. Patients with p16 negative tumor exhibited worse survival rate regardless of IFI16 status. In this limited case series, we could not conclude that IFI16 expression is altered in p16 positive OPSCC and that it would be a new predictive marker or a useful therapeutic tool.
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Roy, Arunava, Dipanjan Dutta, Jawed Iqbal, Gina Pisano, Olsi Gjyshi, Mairaj Ahmed Ansari, Binod Kumar, and Bala Chandran. "Nuclear Innate Immune DNA Sensor IFI16 Is Degraded during Lytic Reactivation of Kaposi's Sarcoma-Associated Herpesvirus (KSHV): Role of IFI16 in Maintenance of KSHV Latency." Journal of Virology 90, no. 19 (July 27, 2016): 8822–41. http://dx.doi.org/10.1128/jvi.01003-16.

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ABSTRACTIFI16 (interferon gamma-inducible protein 16) recognizes nuclear episomal herpesvirus (Kaposi's sarcoma-associated herpesvirus [KSHV], Epstein-Barr virus [EBV], and herpes simplex virus 1 [HSV-1]) genomes and induces the inflammasome and interferon beta responses. It also acts as a lytic replication restriction factor and inhibits viral DNA replication (human cytomegalovirus [HCMV] and human papillomavirus [HPV]) and transcription (HSV-1, HCMV, and HPV) through epigenetic modifications of the viral genomes. To date, the role of IFI16 in the biology of latent viruses is not known. Here, we demonstrate that knockdown of IFI16 in the latently KSHV-infected B-lymphoma BCBL-1 and BC-3 cell lines results in lytic reactivation and increases in levels of KSHV lytic transcripts, proteins, and viral genome replication. Similar results were also observed during KSHV lytic cycle induction in TREX-BCBL-1 cells with the doxycycline-inducible lytic cycle switch replication and transcription activator (RTA) gene. Overexpression of IFI16 reduced lytic gene induction by the chemical agent 12-O-tetradecoylphorbol-13-acetate (TPA). IFI16 protein levels were significantly reduced or absent in TPA- or doxycycline-induced cells expressing lytic KSHV proteins. IFI16 is polyubiquitinated and degraded via the proteasomal pathway. The degradation of IFI16 was absent in phosphonoacetic acid-treated cells, which blocks KSHV DNA replication and, consequently, late lytic gene expression. Chromatin immunoprecipitation assays of BCBL-1 and BC-3 cells demonstrated that IFI16 binds to KSHV gene promoters. Uninfected epithelial SLK and osteosarcoma U2OS cells transfected with KSHV luciferase promoter constructs confirmed that IFI16 functions as a transcriptional repressor. These results reveal that KSHV utilizes the innate immune nuclear DNA sensor IFI16 to maintain its latency and repression of lytic transcripts, and a late lytic KSHV gene product(s) targets IFI16 for degradation during lytic reactivation.IMPORTANCELike all herpesviruses, latency is an integral part of the life cycle of Kaposi's sarcoma-associated herpesvirus (KSHV), an etiological agent for many human cancers. Herpesviruses utilize viral and host factors to successfully evade the host immune system to maintain latency. Reactivation is a complex event where the latent episomal viral genome springs back to active transcription of lytic cycle genes. Our studies reveal that KSHV has evolved to utilize the innate immune sensor IFI16 to keep lytic cycle transcription in dormancy. We demonstrate that IFI16 binds to the lytic gene promoter, acts as a transcriptional repressor, and thereby helps to maintain latency. We also discovered that during the late stage of lytic replication, KSHV selectively degrades IFI16, thus relieving transcriptional repression. This is the first report to demonstrate the role of IFI16 in latency maintenance of a herpesvirus, and further understanding will lead to the development of strategies to eliminate latent infection.
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Dissertations / Theses on the topic "IFI16"

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Johnson, Lacey Nicole St George Clinical School UNSW. "Molecular regulation of Megakaryopoiesis: the role of Fli-1 and IFI16." Awarded by:University of New South Wales. St George Clinical School, 2006. http://handle.unsw.edu.au/1959.4/26819.

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Megakaryocytes (Mks) are unique bone marrow cells, which produce platelets. Dysregulated Mk development can lead to abnormal platelet number and the production of functionally defective platelets, causing bleeding, thrombotic events, and leukaemia. Understanding the molecular mechanisms driving megakaryopoiesis may yield insights into the molecular genetics and cellular pathophysiology of a diversity of disorders. The primary aim of this thesis was to gain insight into the molecular events required for normal Mk development. As transcription factors and cytokines play a central role in driving Mk development, both of these processes were investigated. Fli-1 and GATA-1 are key transcription factors regulating Mk-gene expression, alone and co-operatively. To understand the mechanism of transcriptional synergy exerted by Fli-1 and GATA-1, in vitro assays were carried out investigating the interactions between Fli-1, GATA-1 and DNA that mediate synergy. A novel mechanism of synergy was identified, where Fli-1 DNA binding is not required, although an interaction between Fli-1 and GATA-1, and GATA-1 DNA binding is required. Importantly, the results demonstrate that Fli-1 DNA binding is not essential for promoting Mk-gene expression in primary murine bone marrow cells. Thrombopoietin (TPO) is the primary cytokine responsible for Mk and platelet development. Identifying novel TPO gene-targets may provide invaluable information to aid the understanding of the complex and unique processes required for Mk development. Using microarray technology, IFI16 was identified as a TPO-responsive gene that has not previously been studied in the Mk lineage. This work demonstrated that IFI16 is expressed in CD34+ HSC-derived Mks, and that the Jak/STAT pathway is essential for the activation of IFI16 by both TPO and IFN-??. Of biological significance, IFI16 was found to regulate both the proliferation and differentiation of primary Mks, suggesting that IFI16 may control the balance between these two essential processes. In conclusion, the data in this thesis presents a novel mechanism through which Fli-1 and GATA-1 regulate the synergistic activation of Mk genes. The identification and functional characterisation of a novel TPO-inducible gene, IFI16, involved in regulating the proliferation and differentiation of Mks is also described. These findings have implications for several congenital and malignant conditions affecting Mk and platelet development, and possibly a mechanism for IFN-induced thrombocytopaenia.
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Iannucci, Andrea. "Toll-like receptor 4-mediated inflammation triggered by extracellular IFI16 is enhanced by lipopolysaccharide binding." Doctoral thesis, Università del Piemonte Orientale, 2021. http://hdl.handle.net/11579/127593.

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A cornucopia of biological activities has been attributed to the IFI16 protein, including cell cycle regulation, tumor suppression, DNA damage signaling, virus sensing, and virus restriction. In addition, aberrant IFI16 expression and release in the extracellular space has been reported in a series of inflammatory conditions. The current hypothesis is that overexpression of the IFI16 protein occurs in tissue compartments where it is not physiologically expressed during inflammation. The ensuing release of the IFI16 protein into the extracellular space may allow it to behave like a damage-associated molecular pattern (DAMP) that signals through the Toll-like receptor 4 (TLR4) triggering inflammation by itself or through interaction with exogenous molecules, e.g., lipopolysaccharide (LPS). Pull down assays and ELISA were used to characterize IFI16 binding activity to LPS. Human and murine cells were used as target cells to define IFI16-induced proinflammatory activity. Co-IP, SPR, and silencing experiments were used to define IFI16 signaling. We show that the IFI16 HINB domain binds to the lipid A moiety of different LPS variants. Treatment of target cells with IFI16 led to increased production of proinflammatory cytokines, which was further enhanced when IFI16 was pre-complexed with sub-toxic doses of high TLR4 agonist LPS but not low agonists. Silencing of TLR4/MD-2 or MyD88 abolished cytokine production. These findings alongside with other in vitro binding experiments indicate that PYRIN domain of IFI16 interacts and signals through TLR4. Collectively, our data provide compelling evidence that: i) IFI16 is a DAMP that triggers inflammation through the TLR4/MD2-MyD88 pathway; and ii) its activity is strongly enhanced upon binding to LPS variants regarded as full TLR4 activators. These data strengthen the notion that extracellular IFI16 functions as DAMP and point to new pathogenic mechanisms involving the crosstalk between IFI16 and subtoxic doses of LPS.
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BAWADEKAR, MANDAR. "DAMP-ening inflammation caused by Interferon Inducible Protein 16 (IFI16) in systemic autoimmunity." Doctoral thesis, Università del Piemonte Orientale, 2014. http://hdl.handle.net/11579/46148.

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O'Hare, Craig. "An examination of the role of IFI16 in detecting viral DNA in human immortalised keratinocytes." Thesis, Lancaster University, 2017. http://eprints.lancs.ac.uk/88908/.

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The presence of exogenous DNA in the cytosol results in the activation of the DNA sensor cyclic GMP-AMP synthase (cGAS). cGAS produces the second messenger cyclic GMP-AMP (cGAMP) which binds to and activates the endoplasmic reticulum adapter STimulator of INterferon Genes (STING). Activated STING initiates transcription of the anti-viral cytokine interferon-b, and by extension, induces activation of the anti-viral immune response. Other DNA sensors have been proposed to recognise exogenous DNA via STING but their relevance to the cGAS-STING pathway is unclear. Interferon-g inducible protein 16 (IFI16) is a putative DNA sensor that has also been proposed to induce interferon-b transcription via STING. This thesis demonstrates that both IFI16 and cGAS are required for full activation of immune responses to DNA and DNA virus infection in human immortalised keratinocytes (HaCaT). The cGAS-STING pathway was examined in IFI16(-/-) HaCaT cell lines to conclusively determine the contribution of IFI16 to DNA sensing. IFI16(-/-) HaCaT cell lines produced drastically reduced levels of interferon-b, interferon-stimulated genes and pro-inflammatory cytokine mRNAs following stimulation with exogenous DNA due to reduced activation of the STING pathway. IFI16 was observed not influence cGAS activity as DNA-induced cGAMP levels were comparable between Wild type and IFI16(-/-) cell lines. IFI16 was required for STING signalling following cGAMP stimulation. IFI16 was found to interact with STING promoting STING phosphorylation and translocation to peri-nuclear foci. Additionally, in preliminary experiments we observe that IFI16 may be required for STING palmitoylation. Thus, we propose that IFI16 and cGAS co-operate for the full activation of DNA sensing in HaCaT cells.
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Orzalli, Megan Jenkins. "Inhibition of Nuclear DNA Sensing by Herpes Simplex Virus 1." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10779.

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The detection of immunostimulatory DNA is well documented to occur at several cellular sites, but there is limited evidence of nuclear innate DNA sensing. Prior to this study, the detection of herpesviral DNA was thought to be restricted to the cytosol so as to limit the sensing of host DNA in the nucleus. However, given the nuclear lifecycle of these viruses, we hypothesized that viral DNA could be sensed in the nucleus of infected cells. To test this hypothesis we examined the activation of interferon regulatory factor 3 (IRF-3) in response to herpes simplex virus 1 (HSV-1) infection of primary human foreskin fibroblasts (HFF). Using a mutant defective for expression of all viral genes, we observed that the release of viral DNA into the nucleus is necessary to activate IRF-3 signaling. Furthermore, we determined this response to be dependent on nuclear-localized interferon inducible protein 16 (IFI16) and the cytoplasmic stimulator of interferon genes (STING) adaptor protein.
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LO, CIGNO IRENE. "The Nuclear DNA Sensor IFI16 Acts as a Restriction Factor for Human Papillomavirus Replication through Epigenetic Modifications of the Viral Promoters." Doctoral thesis, Università del Piemonte Orientale, 2015. http://hdl.handle.net/11579/115207.

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Albertini, Silvia. "The Everlasting Fight between Host and Pathogens: Unveiling Common Strategies Adopted by Small DNA Tumour Viruses to Dampen Innate Immunity." Doctoral thesis, Università del Piemonte Orientale, 2018. http://hdl.handle.net/11579/104067.

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Samimuthu, Karthika, and Karthika Samimuthu. "To examine the role of IFI16 in cisplatin resistance." Thesis, 2019. http://ndltd.ncl.edu.tw/cgi-bin/gs32/gsweb.cgi/login?o=dnclcdr&s=id=%22107CGU05538001%22.&searchmode=basic.

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Book chapters on the topic "IFI16"

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Appleton, Kathryn M., Ian Cushman, Yuri K. Peterson, Balachandran Manavalan, Shaherin Basith, Sangdun Choi, Akihiro Kimura, et al. "IFI10." In Encyclopedia of Signaling Molecules, 891. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100636.

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Dell’Oste, Valentina, Valeria Caneparo, Marco de Andrea, Marisa Gariglio, and Santo Landolfo. "IFI16 Autoantibodies." In Autoantibodies, 333–40. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-444-56378-1.00040-x.

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RIBOLDI, PIERSANDRO, MARIA GEROSA, MICHELE MONDINI, and SANTO LANDOLFO. "INTERFERON-INDUCIBLE PROTEIN IFI16 AUTOANTIBODIES." In Autoantibodies, 331–37. Elsevier, 2007. http://dx.doi.org/10.1016/b978-044452763-9/50048-2.

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"IFI10." In Encyclopedia of Signaling Molecules, 2511. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101801.

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Conference papers on the topic "IFI16"

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Lim, Gayoung, Na-Lee Ka, and Mi-Ock Lee. "Abstract 4914: IFI16 is increased in response to chemotherapeutic agents in breast cancer cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4914.

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Kobayashi, Yuta, Matias Bustos, Qiang Yu, and Dave Hoon. "962 IFI16 promotes immune responses through IFN-γ pathway activation in metastatic cutaneous melanomas." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0962.

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