IRF1 antigen
- Known as:
- IRF1 antigenic
- Catalog number:
- 'H00003659-Q01-25
- Product Quantity:
- 25
- 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
'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Anti_Tg)Thyroglobulin Antigen(Des-Asp187)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187)-ME20M_ME20S (185-193) (human, bovine, mouse), (Des-Asp187)-Melanocyte Lineage-Specific Antigen GP100 (185-193) (hu(Des-Asp187,Met186)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187,Met186)-Melanoma-Associated ME20 Antigen (185-193) (human, bovine, mouse), (Des-Asp187,Met186)-95 kDa Melano(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Draxin) C1ORf187, Antigen blocking peptide(Val438)-Tyrosinase (432-444) (human)
(Val438)-LB24-AB (432-444) (human), (Val438)-Monophenol Monooxygenase (432-444) (human), (Val438)-SK29-AB (432-444) (human), (Val438)-Tumor Rejection Antigen AB (0x19 Antigen0x2 Antigen1,25-dihydroxyvitamin D3 Competitive ELISA, Coated with Antigen105 kDa islet cell antigen,BEM-3,Brain-enriched membrane-associated protein tyrosine phosphatase,ICA105,PTP IA-2,PTPLP,Ptprn,Rat,Rattus norvegicus,Receptor-type tyrosine-protein phosphatase-like N,R-P Related articles to: IRF1 antigen
- The immunosuppressive tumor microenvironment (TME) remains a major barrier to the efficacy of immune checkpoint blockade (ICB) therapy, underscoring the need for strategies that can safely reprogram the TME to enhance cancer immunity. - Source: PubMed
Publication date: 2026/05/29
Nguyen Dinh-HuyYou Sung-HwanVan Nguyen KhuynhNguyen Phuong Thi-MinhNgo Hien Thi-ThuTran Khang VuongTran Thanh QuangSong MiryoungHong YeongjinMin Jung-Joon - Hypoxia within the tumor microenvironment (TME) triggers the exosomal transfer of microRNAs (hypoxamirs) that reprogram tumor-associated macrophages (TAMs) toward a pro-tumorigenic M2 phenotype. This systematic review defines the molecular pathways and clinical consequences of the hypoxamir-TAM axis across solid malignancies to guide therapeutic translation. A systematic search of PubMed, Embase, and Cochrane library was conducted through February 1, 2026. Following PRISMA 2020 guidelines, 17 studies were included for analysis. Methodological quality was evaluated using the standard Office of Health Assessment and Translation (OHAT) tool. Analysis identified two primary regulatory tracks: a signaling axis mediated by targets such as PTEN, IRF1, and PHLPP2, and a metabolic axis driven by miR-210, let-7a, and miR-30c targeting the iron-sulfur cluster assembly protein (ISCU). These coordinated pathways drive an "angiogenic switch," facilitate "metabolic migration," and induce significant resistance to chemotherapies, including gemcitabine and temozolomide. Fourteen studies achieved a high-confidence Tier 1 OHAT rating. The hypoxamir-TAM axis is a fundamental driver of immune evasion and therapeutic failure. Targeting this dual-axis framework offers a viable strategy for restoring anti-tumor immunity, while circulating hypoxamirs represent high-value liquid biopsy biomarkers for real-time TME monitoring. - Source: PubMed
Publication date: 2026/05/28
Altobi AlmunthirHeo DanhuiBarman LinaRuiz Santiago - Peripheral nerve injury induces neuroinflammation in the dorsal root ganglion (DRG), which is a major cause of neuropathic pain. Interferon regulatory factors (IRFs) are a family of transcription factors that regulate the expression of inflammatory genes. Although several IRFs affect nociceptive transmission in the spinal cord, their roles in the DRG remain largely unknown. - Source: PubMed
Watanabe YujiMaruyama MotoyoYokoyama MikiArakawa RyosukeSakai Atsushi - : Resistance to sunitinib represents a major clinical obstacle in the management of clear cell renal cell carcinoma (ccRCC). This investigation aims to identify genes associated with sunitinib resistance and elucidate potential molecular pathways in ccRCC. : To identify differentially expressed genes (DEGs) in sunitinib-resistant ccRCC cells and their parental cells, bioinformatic analysis was performed on the GSE216494 dataset. Protein-protein interaction (PPI) network and topological analyses pinpointed a hub gene. Sunitinib-resistant A498 and 786-O cell lines were employed for validation. Sunitinib sensitivity and cell proliferation were evaluated using functional assays, such as colony formation and Cell Counting Kit-8 (CCK-8). Protein interactions and signaling pathway activity are investigated using co-immunoprecipitation (Co-IP), dual-luciferase reporter assays, and immunofluorescence. In resistant cells and patient-derived organoids (PDOs), the therapeutic potential of olaparib, either by itself or in conjunction with sunitinib, was assessed. : Sunitinib-resistant cells and patient tissues were shown to exhibit consistent upregulation of poly (ADP-ribose) polymerase 9 (). knockdown sensitized resistant cells to sunitinib, suppressing proliferation. Conversely, its overexpression induced resistance in parental cells. Additionally, STAT1 and PARP9 interact to promote nuclear translocation and STAT1 phosphorylation. Activation of the / axis further enhanced the expression of and . Olaparib treatment can increase sunitinib-resistant ccRCC cells. Olaparib can weaken the / signaling pathway and prevent sunitinib-resistant ccRCC cells from proliferating. Importantly, combination treatment with olaparib and sunitinib showed superior antitumor efficacy in ccRCC PDOs. : This study demonstrates that promotes sunitinib resistance in ccRCC by activating the / pathway and upregulating /. - Source: PubMed
Publication date: 2026/06/16
Luo LeiGuan FengjuWang ZhankunLi BinDing XuemeiSong LeileiSun Lijiang - Interferons (IFNs) play fundamental roles in cancer immunity. We have previously shown that conditional ablation of Notch pathway genes in a mouse model of glioma results in impaired IFNγ signaling and immunosuppressive tumors. However, it remained unclear whether the interaction between the Notch and IFN signaling pathways could be leveraged to counteract immune evasion in glioma. Here, we investigated whether expression of the intrinsically active Notch intracellular domain (NICD) could enhance IFN responses in glioma cells. Using a doxycycline (Dox)-inducible system, we overexpressed (OE) NICD in U-251MG human glioma cells. NICD-OE dramatically potentiated STAT1 phosphorylation in response to stimulation with either IFNγ or IFNα. Moreover, NICD-OE induced the expression of the transcription factor IRF1, a regulator of IFN signaling responses. Notably, NICD-OE in U-251MG human glioma cells boosted the IFNγ-dependent transcription of the and genes, which encode cytokines that regulate T cell function. Accordingly, NICD-OE in vivo promoted cytotoxic T lymphocyte recruitment to the tumor and reduced tumor cell proliferation in a murine glioma model. Hence, we have identified a signaling network that could be exploited to enhance anti-tumor immunity in glioma subtypes. - Source: PubMed
Publication date: 2026/05/23
Giannaki MarinaParmigiani ElenaBurger KarinTaylor VerdonGiachino Claudio