CLIA Homo sapiens,Human,Signal transducer and activator of transcription 1-alpha_beta,STAT1,Transcription factor ISGF-3 components p91_p84
- Known as:
- CLIA Homo sapiens,Human,Signal transducer activator transcription 1-alpha_beta,STAT1,Transcription factor ISGF-3 components p91_p84
- Catalog number:
- U1740h
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- EIAab
- Gene target:
- CLIA Homo sapiens Human Signal transducer and activator transcription 1-alpha_beta STAT1 Transcription factor ISGF-3 components p91_p84
Related genes to: CLIA Homo sapiens,Human,Signal transducer and activator of transcription 1-alpha_beta,STAT1,Transcription factor ISGF-3 components p91_p84
- Gene:
- IRF9 NIH gene
- Name:
- interferon regulatory factor 9
- Previous symbol:
- ISGF3G
- Synonyms:
- -
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-21
- Date modifiied:
- 2016-10-05
- Gene:
- STAT1 NIH gene
- Name:
- signal transducer and activator of transcription 1
- Previous symbol:
- -
- Synonyms:
- STAT91, ISGF-3
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
- Gene:
- STAT2 NIH gene
- Name:
- signal transducer and activator of transcription 2
- Previous symbol:
- -
- Synonyms:
- STAT113
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: CLIA Homo sapiens,Human,Signal transducer and activator of transcription 1-alpha_beta,STAT1,Transcription factor ISGF-3 components p91_p84
Related articles to: CLIA Homo sapiens,Human,Signal transducer and activator of transcription 1-alpha_beta,STAT1,Transcription factor ISGF-3 components p91_p84
- Immune cells need to sustain a state of constant alertness over a lifetime. Yet, little is known about the regulatory processes that control the fluent and fragile balance that is called homeostasis. Here we demonstrate that JAK-STAT signaling, beyond its role in immune responses, is a major regulator of immune cell homeostasis. We investigated JAK-STAT-mediated transcription and chromatin accessibility across 12 mouse models, including knockouts of all STAT transcription factors and of the TYK2 kinase. Baseline JAK-STAT signaling was detected in CD8 T cells and macrophages of unperturbed mice-but abrogated in the knockouts and in unstimulated immune cells deprived of their normal tissue context. We observed diverse gene-regulatory programs, including effects of STAT2 and IRF9 that were independent of STAT1. In summary, our large-scale dataset and integrative analysis of JAK-STAT mutant and wild-type mice uncovered a crucial role of JAK-STAT signaling in unstimulated immune cells, where it contributes to a poised epigenetic and transcriptional state and helps prepare these cells for rapid response to immune stimuli. - Source: PubMed
Publication date: 2024/04/24
Fortelny NikolausFarlik MatthiasFife VictoriaGorki Anna-DorotheaLassnig CarolineMaurer BarbaraMeissl KatrinDolezal MarliesBoccuni LauraRavi Sundar Jose Geetha AarathyAkagha Mojoyinola JoannaKarjalainen AnzhelikaShoebridge StephenFarhat AsmaMann UlrikeJain RohitTikoo ShwetaZila NinaEsser-Skala WolfgangKrausgruber ThomasSitnik KatarzynaPenz ThomasHladik AnastasiyaSuske TobiasZahalka SophieSenekowitsch MartinBarreca DanieleHalbritter FlorianMacho-Maschler SabineWeninger WolfgangNeubauer Heidi AMoriggl RichardKnapp SylviaSexl VeronikaStrobl BirgitDecker ThomasMüller MathiasBock Christoph - Identifying the molecular mechanisms behind SARS-CoV-2 disparities and similarities will help find new treatments. The present study determines networks' shared and non-shared (specific) crucial elements in response to HCoV-229E and SARS-CoV-2 viruses to recommend candidate medications. - Source: PubMed
Publication date: 2024/04/23
Dehghan ZeinabMirmotalebisohi Seyed AmirMozafar MaryamSameni MarziehSaberi FatemehDerakhshanfar AminMoaedi JavadZohrevand HassanZali Hakimeh - IRF9 is a crucial component in the JAK-STAT pathway. IRF9 interacts with STAT1 and STAT2 to form IFN-I-stimulated gene factor 3 (ISGF3) in response to type I IFN stimulation, which promotes ISG transcription. However, the mechanism by which IFN signaling regulates Malabar grouper (Epinephelus malabaricus) IRF9 is still elusive. Here, we explored the nd tissue-specific mRNA distribution of the MgIRF9 gene, as well as its antiviral function in E. malabaricus. MgIRF9 encodes a protein of 438 amino acids with an open reading frame of 1317 base pairs. MgIRF9 mRNA was detected in all tissues of a healthy M. grouper, with the highest concentrations in the muscle, gills, and brain. It was significantly up-regulated by nervous necrosis virus infection and poly (I:C) stimulation. The gel mobility shift test demonstrated a high-affinity association between MgIRF9 and the promoter of zfIFN in vitro. In GK cells, grouper recombinant IFN-treated samples showed a significant response in ISGs and exhibited antiviral function. Subsequently, overexpression of MgIRF9 resulted in a considerable increase in IFN and ISGs mRNA expression (ADAR1, ADAR1-Like, and ADAR2). Co-immunoprecipitation studies demonstrated that MgIRF9 and STAT2 can interact in vivo. According to the findings, M. grouper IRF9 may play a role in how IFN signaling induces ISG gene expression in grouper species. - Source: PubMed
Publication date: 2024/03/31
Periyasamy ThirunavukkarasuMing-Wei LuVelusamy SharmilaAhamed AnisKhan Javed MasoodPappuswamy ManikantanViswakethu Velavan - We hypothesized that the hCG modulates the expression of IFNT-pathway and ISGs in bovine endometrium during early pregnancy. The aim of the current study is to evaluate the effect of hCG on IFNT-pathway signals and ISGs expression in endometrial cells. For this, 29 non-lactating cross-bread cows were used in the study and submitted to a 9-day fixed-time artificial insemination (FTAI) protocol. The day of the AI was considered Day 0 (D0), and five days (D5) after the FTAI, the cows were allocated into two groups: Control and hCG group, when a hCG group received a single dose of 2.500UI of hCG. On day 18 after FTAI (D18) cows were slaughtered and endometrial tissue samples were collected. There was no difference between the embryo recovery rate of the cows in C compared to the hCG. The hCG group increased the accessory corpus luteum formation rate. The hCG resulted in greater serum progesterone concentration in the hCG group compared to the C on Day 14. Only the expression of IFNAR2 and STAT1 were upregulated on pregnant cows of the hCG group compared to the C group. The pathway genes (JAK1, STAT2, and IRF9) were not regulated. The mRNA abundance of ISG15, MX1, MX2, and OAS1 was upregulated in pregnant cows for hCG group, compared to C group. The results show that the administration of hCG, 5 days after AI, in addition to increasing the serum progesterone, modulates the expression of IFNT-pathway and ISGs on bovine endometrium on Day 18 of pregnancy. - Source: PubMed
Publication date: 2024/03/29
Manta Manuela Wolkerda Silva Eduardo PradebonFeltrin Suzana RossatoPrante Amanda LuizaAires Karine de Vargasde Andrade Leonardo Guedesda Silva Ana PaulaAmaral Carolina Dos SantosWink Letícia MinussiPortela Valério MarquesAntoniazzi Alfredo Quites - The tick-borne encephalitis virus (TBEV) serocomplex includes several medically important flavivirus members endemic to Europe, Asia, and North America, which can induce severe neuroinvasive or viscerotropic diseases with unclear mechanisms of pathogenesis. Langat virus (LGTV) shares a high sequence identity with TBEV but exhibits lower pathogenic potential in humans and serves as a model for virus-host interactions. In this study, we demonstrated that LGTV infection inhibits the activation of gp130/JAK/STAT (Janus kinases (JAK) and signal transducer and activator of transcription (STAT)) signaling, which plays a pivotal role in numerous biological processes. Our data show that the LGTV-infected cells had significantly lower phosphorylated STAT3 (pSTAT3) protein upon oncostatin M (OSM) stimulation than the mock-infected control. LGTV infection blocked the nuclear translocation of STAT3 without a significant effect on total STAT3 protein level. LGTV inhibited JAK1 activation and reduced gp130 protein expression in infected cells, with the viral NS5 protein mediating this effect. TBEV infection also reduces gp130 level. On the other hand, pretreatment of Vero cells with OSM significantly reduces LGTV replication, and STAT1/STAT2 knockdown had little effect on OSM-mediated antiviral effect, which suggests it is independent of STAT1/STAT2 and, instead, it is potentially mediated by STAT3 signlaing. These findings shed light on the LGTV and TBEV-cell interactions, offering insights for the future development of antiviral therapeutics and improved vaccines. - Source: PubMed
Lin ShaoliWang XiaochunSallapalli Bhargava TejaHage AdamChang PeixiHe JiaBest Sonja MZhang Yanjin