IRF1 antigen

Price:

636.35 €

Known as:: IRF1 antigenic
Catalog number:: 'H00003659-Q01-10
Product Quantity:: 10
Category:: -
Supplier:: ACR
Gene target:: IRF1 antigen

Related genes to: IRF1 antigen

Gene:: IRF1 ^{NIH gene}
Name:: interferon regulatory factor 1
Previous symbol:: -
Synonyms:: MAR
Chromosome:: 5q31.1
Locus Type:: gene with protein product
Date approved:: 1991-05-09
Date modifiied:: 2016-10-05

Related products to: IRF1 antigen

Related articles to: IRF1 antigen

IRF-1 modulates hepatic ferroptosis and aggravates liver ischemia/reperfusion injury via DYRK1α.
The purpose is to define the contribution of the interferon regulatory factor-1-dual-specificity tyrosine phosphorylation-regulated kinase 1α (IRF-1-DYRK1α) axis to hepatocellular ferroptosis during liver ischemia/reperfusion injury (LIRI). - Source: PubMed
Publication date: 2026/06/16
Zhang JinpingZhang JinmingSong SiyuanLi MingyangSun LiyingZhu ZhijunLin Dongdong
IRF1 Inhibits the Proliferation and Metastasis of Colorectal Cancer by Suppressing the RAS-RAC1 Pathway [Retraction].
[This retracts the article DOI: 10.2147/CMAR.S186236.]. - Source: PubMed
Publication date: 2026/06/05
DHODH regulates trophoblast fusion via IFITM-reduced plasma membrane fluidity: Implications for hypertensive disorders of pregnancy.
Hypertensive disorders of pregnancy (HDPs) affect 5%-10% of pregnant women and, in the absence of established therapies, remain a leading cause of maternal and perinatal mortality. HDPs have been associated with disruption of cytotrophoblast fusion into syncytiotrophoblasts, a process essential for placental development. Here, we identified altered expression of mitochondrial dihydroorotate dehydrogenase (DHODH) and interferon-induced transmembrane proteins (IFITMs), using HDP placentas, and investigated their functional roles in trophoblast fusion and membrane dynamics. In trophoblast cells, the inhibition of DHODH led to upregulated expression of IFITM1-3 through transcription factor IRF1 and suppression of syncytialization. IFITMs also increased the proportion of saturated fatty acids, thereby decreasing plasma membrane fluidity. Furthermore, IFITM2 increased the soluble fms-like tyrosine kinase-1/placental growth factor (sFlt1/PlGF) ratio, a key biomarker of HDP severity. These results suggest that DHODH deficiency activates IRF1-mediated IFITM2 expression, leading to impaired trophoblast fusion via biophysical remodeling of the membrane and contributing to HDP pathogenesis. - Source: PubMed
Publication date: 2026/06/08
Yoshida KanokoKusama KazuyaKojima JunyaKawaguchi YuSuzuki KaitoShimooki TomokaTsuru AtsuyaYoshie MikihiroOno MasanoriNishi HirotakaKato KiyokoTamura Kazuhiro
Patient-matched transcriptomics of in vivo and in vitro colonic epithelium substantiate organoids as a translational model for ulcerative colitis.
Ulcerative colitis (UC) is characterized by cytokine-driven inflammation and barrier disruption in the colon, making epithelial dysfunction central to disease pathology. Intestinal epithelial organoids (IEOs) preserve donor-specific genetics and architecture, offering a promising model, but their ability to replicate patient-specific epithelial inflammation remains undetermined. To directly compare in vivo epithelial transcriptional states with defined cytokine-induced responses in vitro, we analyzed patient-matched transcriptomics from laser microdissected inflamed and uninflamed colonic epithelium and IEOs derived from uninflamed biopsies of the same UC patients. IEOs were stimulated with UC-relevant cytokines (TNF, IFNγ, IFNλ1, or TNF + IFNγ) or a cytokine cocktail (TNF, IL17, IL1β, IL22, Poly(I:C), IFNγ). Key inflammatory genes were validated by immunoblotting and immunostaining. Cytokine-stimulated IEOs recapitulated key in vivo epithelial inflammation, including interferon signaling, antigen presentation, and unfolded protein response pathways. Among the tested conditions, TNF + IFNγ combination and the cytokine cocktail most closely replicated UC epithelial inflammation, with concordance for over 350 UC-relevant genes and protein-level validation of IRF1, ERAP2, NOS2, DUOX2 confirmed patient-dependent expression between inflamed epithelium and cytokine-stimulated IEOs. Our study shows that cytokine-stimulated IEOs provide a robust, personalized platform for modeling epithelial inflammation, enabling discovery of epithelial-specific disease mechanisms and therapeutic targets. - Source: PubMed
Publication date: 2026/06/14
Walaas Gunnar Andreas EnerhaugSridhar ArunKuraas Lusie FrostvollSæterstad SiriSchioldborg Amanda YinVan Beelen Granlund AtleSandvik Arne KristianØstvik Ann ElisabetBakke IngunnBruland Torunn
Intra-articular metformin and chlorogenic acid synergistically protect against cartilage degeneration by suppressing NF-κB/NLRP3 inflammasome axis in osteoarthritis.
Osteoarthritis (OA) is a leading cause of disability, driven by cartilage degradation, subchondral bone remodeling, and synovial inflammation. Activation of the NF-κB/NLRP3 inflammasome axis contributes to disease progression. This study investigated the chondroprotective and anti-inflammatory effects of intra-articular (IA) metformin (MET) and chlorogenic acid (CGA), alone or in combination, in a rabbit model of OA. OA was induced by monosodium iodoacetate (MIA) injection into the knee joints of male rabbits The rabbits were randomized into six groups: Control, MET + CGA, OA, OA + MET, OA + CGA, and OA + MET + CGA. Disease severity was evaluated via radiography, gross morphology, histopathology, and hematological and synovial fluid analyses. MIA induced OA manifested by joint space narrowing, osteophyte formation, and cartilage erosion, accompanied by elevated serum CRP, increased synovial IL-1β, IL-6, and TNF-α, and upregulation of NF-κB, NLRP3, caspase-1, GSDMD, IRF-1, and cartilage-degrading enzymes. MET or CGA alone significantly attenuated these changes, improving joint architecture, lowering inflammatory cytokines, and suppressing pyroptotic signaling. Combination therapy produced the most pronounced benefits, restoring near-normal cartilage structure, normalizing leukocyte profiles, and reducing molecular markers toward baseline. In silico findings revealed the affinity of CGA to bind with NLRP3 PYD, ASC PYD, IRF-1 and NF-κB p65. In conclusion, IA MET + CGA synergistically ameliorated structural and molecular hallmarks of OA via coordinated inhibition of NF-κB/NLRP3 inflammasome activation and pyroptosis. These findings highlight the translational potential of this dual therapy as a disease-modifying approach for OA management, pending further investigations. - Source: PubMed
Publication date: 2026/06/09
Abdel-Kareem Mona AAbd-Elrafea NourhanAbdo WaliedAtiba Ayman SElsisy Rasha AAlnasser Sulaiman MAlruhaimi Reem SMahmoud Ayman MFarage Amira E

IRF1 antigen

Related genes to: IRF1 antigen

Related products to: IRF1 antigen

Related articles to: IRF1 antigen

IRF-1 modulates hepatic ferroptosis and aggravates liver ischemia/reperfusion injury via DYRK1α.

IRF1 Inhibits the Proliferation and Metastasis of Colorectal Cancer by Suppressing the RAS-RAC1 Pathway [Retraction].

DHODH regulates trophoblast fusion via IFITM-reduced plasma membrane fluidity: Implications for hypertensive disorders of pregnancy.

Patient-matched transcriptomics of in vivo and in vitro colonic epithelium substantiate organoids as a translational model for ulcerative colitis.

Intra-articular metformin and chlorogenic acid synergistically protect against cartilage degeneration by suppressing NF-κB/NLRP3 inflammasome axis in osteoarthritis.