IFI204 protects host defense against Staphylococcus aureus-induced pneumonia by promoting extracellular traps formation. | IFI204 protects host defense against Staphylococcus aureus-induced pneumonia by promoting extracellular traps formation. Zhang JG, Chen W, Zhou CK, Ma K, Liu ZZ, Gao Y, Lin XQ, Yang YJ. | 01/14/2023 |
Interferon activated gene 204 protects against bone loss in experimental periodontitis. | Interferon activated gene 204 protects against bone loss in experimental periodontitis. Swanson KV, Girnary M, Alves T, Ting JP, Divaris K, Beck J, Pucinelli CM, da Silva RAB, Uyan D, Wilson JE, Seaman WT, Webster-Cyriaque J, Vias N, Jiao Y, Cantley L, Marlier A, Arnold RR, Marchesan JT., Free PMC Article | 10/15/2022 |
Interferon-gamma inducible protein 16 and type I interferon receptors expression in experimental apical periodontitis induced in wild-type mice. | Interferon-gamma inducible protein 16 and type I interferon receptors expression in experimental apical periodontitis induced in wild-type mice. Pucinelli CM, Lima RB, Almeida LKY, Lucisano MP, Córdoba AZ, Marchesan JT, da Silva LAB, da Silva RAB. | 09/24/2022 |
Structural mechanism of DNA recognition by the p204 HIN domain. | Structural mechanism of DNA recognition by the p204 HIN domain. Fan X, Jiang J, Zhao D, Chen F, Ma H, Smith P, Unterholzner L, Xiao TS, Jin T., Free PMC Article | 03/27/2021 |
SENP3 senses oxidative stress to facilitate STING-dependent dendritic cell antitumor function. | SENP3 senses oxidative stress to facilitate STING-dependent dendritic cell antitumor function. Hu Z, Teng XL, Zhang T, Yu X, Ding R, Yi J, Deng L, Wang Z, Zou Q. | 03/20/2021 |
DNA Sensor IFI204 Contributes to Host Defense Against Staphylococcus aureus Infection in Mice. | DNA Sensor IFI204 Contributes to Host Defense Against Staphylococcus aureus Infection in Mice. Chen W, Yu SX, Zhou FH, Zhang XJ, Gao WY, Li KY, Liu ZZ, Han WY, Yang YJ., Free PMC Article | 09/12/2020 |
Silencing of Ifi204/p204 induces resistance to IFNgamma-mediated cell growth arrest in SCCVII cells. | Silencing of the interferon-inducible gene Ifi204/p204 induces resistance to interferon-γ-mediated cell growth arrest of tumor cells. Yamaguchi H, Hiroi M, Ohmori Y. | 07/11/2020 |
The results reveal that the interferon-inducible IFI204 could negatively regulate the IRF7-mediated type I interferon response after RNA virus infection to avoid unnecessary host damage from hyper-inflammatory responses. | P200 family protein IFI204 negatively regulates type I interferon responses by targeting IRF7 in nucleus. Cao L, Ji Y, Zeng L, Liu Q, Zhang Z, Guo S, Guo X, Tong Y, Zhao X, Li CM, Chen Y, Guo D., Free PMC Article | 02/8/2020 |
p204 is a critical component of canonical LPS-TLR4 signaling pathway, and these studies also suggest that p204 could be a potential target to prevent and treat inflammatory and infectious diseases. | p204 Is Required for Canonical Lipopolysaccharide-induced TLR4 Signaling in Mice. Yi YS, Jian J, Gonzalez-Gugel E, Shi YX, Tian Q, Fu W, Hettinghouse A, Song W, Liu R, He M, Qi H, Yang J, Du X, Xiao G, Chen L, Liu CJ., Free PMC Article | 09/8/2018 |
Importantly, knocking down p204, which is reported as the mouse orthologous of human IFI16, inhibited epidermal hyperplasia in mice with imiquimod-induced psoriasiform dermatitis. These findings indicate that IFI16 plays a critical role in the pathogenesis of psoriasis and may be a potential therapeutic target | Up-regulation of Interferon-inducible protein 16 contributes to psoriasis by modulating chemokine production in keratinocytes. Cao T, Shao S, Li B, Jin L, Lei J, Qiao H, Wang G., Free PMC Article | 02/3/2018 |
Ifi204 is required for EPC differentiation. | Regulatory roles of interferon-inducible protein 204 on differentiation and vasculogenic activity of endothelial progenitor cells. Yang J, Zhang X, Zhao Z, Li X, Wang X, Chen M, Song B, Ii M, Shen Z., Free PMC Article | 11/18/2017 |
study identifies the AIM2 inflammasome and cGAS/IFI16-STING-type I IFN pathway as a novel mechanism for host innate immunity to the ALVAC vaccine vector. | Priming and Activation of Inflammasome by Canarypox Virus Vector ALVAC via the cGAS/IFI16-STING-Type I IFN Pathway and AIM2 Sensor. Liu F, Niu Q, Fan X, Liu C, Zhang J, Wei Z, Hou W, Kanneganti TD, Robb ML, Kim JH, Michael NL, Sun J, Soong L, Hu H., Free PMC Article | 10/28/2017 |
p204 initiated innate antiviral responses in adipose cells, thereby modulating adipocyte function. | p204-Mediated innate antiviral responses in mouse adipose cells and their effects on cell functions. Yu L, Liu P, Liu Z, Zhu W, Yan K, Chen Q, Han D. | 12/19/2015 |
cGAS and Ifi204 cooperate to produce type I IFNs in response to Francisella infection. | cGAS and Ifi204 cooperate to produce type I IFNs in response to Francisella infection. Storek KM, Gertsvolf NA, Ohlson MB, Monack DM., Free PMC Article | 06/20/2015 |
The present study demonstrated that mouse Leydig cells had innate antiviral activities in response to viral DNA challenge through p204 activation. | p204-initiated innate antiviral response in mouse Leydig cells. Zhu W, Liu P, Yu L, Chen Q, Liu Z, Yan K, Lee WM, Cheng CY, Han D. | 02/21/2015 |
confers resistance to HSV-1 infection in the corneal epithelium | Resistance to HSV-1 infection in the epithelium resides with the novel innate sensor, IFI-16. Conrady CD, Zheng M, Fitzgerald KA, Liu C, Carr DJ., Free PMC Article | 06/9/2012 |
Data indicate that the transient expression of p204 in the early stage is indispensable for adipocyte differentiation. Disruption of p204 expression patterns at this stage leads to irreversible damage in fat formation. | Transient expression of interferon-inducible p204 in the early stage is required for adipogenesis in 3T3-L1 cells. Xiao J, Sun B, Cai GP. | 07/12/2010 |
IFI16 exerts in vivo anti-tumoral activity by promoting apoptosis of tumor cells. | In vivo growth inhibition of head and neck squamous cell carcinoma by the Interferon-inducible gene IFI16. Mazibrada J, De Andrea M, Rittà M, Borgogna C, Dell'eva R, Pfeffer U, Chiusa L, Gariglio M, Landolfo S. | 02/22/2010 |
p204, a murine member of the p200 family regulates cell proliferation, cell and tissue differentiation (e.g. of skeletal muscle myotubes, beating cardiac myocytes, osteoblasts, chondrocytes and macrophages) and signaling by Ras proteins[review] | p204, a p200 family protein, as a multifunctional regulator of cell proliferation and differentiation. Luan Y, Lengyel P, Liu CJ., Free PMC Article | 01/21/2010 |
Cbfa1, p204, and Id proteins form a regulatory circuit and act in concert to regulate osteoblast differentiation. | p204 protein overcomes the inhibition of core binding factor alpha-1-mediated osteogenic differentiation by Id helix-loop-helix proteins. Luan Y, Yu XP, Yang N, Frenkel S, Chen L, Liu CJ., Free PMC Article | 01/21/2010 |
p204 is a novel regulator of chondrocyte differentiation by (1) acting as a coactivator of Cbfa1 and (2) affecting IHH/PTPrP signaling. | Cbfa1-dependent expression of an interferon-inducible p204 protein is required for chondrocyte differentiation. Zhang Y, Kong L, Carlson CS, Liu CJ. | 01/21/2010 |
p204 may serve as a negative feedback inhibitor of Ras activity. | p204 protein is a novel modulator of ras activity. Ding B, Lengyel P. | 01/21/2010 |
Ifi204 is a regulator of monocyte/macrophage differentiation and make possible a connection with other myeloid regulators [review] | The biological role of interferon-inducible P204 protein in the development of the mononuclear phagocyte system. Bourette RP, Mouchiroud G. | 01/21/2010 |
This gene product interacts with the Tpr protein, a component of the nuclear pore complex. | The mouse interferon-inducible gene Ifi204 product interacts with the Tpr protein, a component of the nuclear pore complex. De Andrea M, Zannetti C, Noris E, Gariglio M, Azzimonti B, Landolfo S. | 01/21/2010 |
acquires malignant transformation capability upon mutation at the Rb-binding sites | The interferon-inducible gene, Ifi204, acquires malignant transformation capability upon mutation at the Rb-binding sites. De Andrea M, Ravotto M, Noris E, Ying GG, Gioia D, Azzimonti B, Gariglio M, Landolfo S. | 01/21/2010 |