Ask about this productRelated genes to: ISG15 antibody
- Gene:
- ISG15 NIH gene
- Name:
- ISG15 ubiquitin like modifier
- Previous symbol:
- G1P2
- Synonyms:
- IFI15, UCRP
- Chromosome:
- 1p36.33
- Locus Type:
- gene with protein product
- Date approved:
- 1990-10-16
- Date modifiied:
- 2019-04-23
Related products to: ISG15 antibody
Related articles to: ISG15 antibody
- Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease characterized by chronic inflammation and dysregulated interferon (IFN) signaling. Many patients remain refractory to existing treatments, underscoring the need for novel therapeutic approaches achievable through drug repurposing. Fluvoxamine, an antidepressant with anti-inflammatory and immunomodulatory properties, has not been systematically studied in SLE. - Source: PubMed
Publication date: 2026/05/19
Dulcic DorianDumancic LucijaMarcec RobertPadjen IvanMayer MiroslavLikic Robert - Macrophage fate decisions during infection are commonly framed as receptor-proximal transcriptional choices. We propose that the functional outcome results from a "kinetic race," a dynamic proteostatic competition among protein synthesis, post-translational modifications (PTMs), and degradation. Building on experimental evidence of infection-induced proteostasis, we outline a conceptual "turnover-first" framework. In this model, we hypothesize that the ubiquitin proteasome system (UPS), autophagy, and translational control create a master molecular timer that licenses or restrains pyroptosis, apoptosis, necroptosis, and PANoptosis. We detail how PTMs act as decision codes and present examples of how bacterial pathogens and viruses hijack this network, deploying specialized effectors to move death thresholds by host shutoff, ubiquitin/ISG15 editing, and autophagy evasion. We summarize the emerging chemical biology platforms allowing quantification of these "death competence codes" in real-time, and map drug-addressable nodes offering a systems level strategy to tune macrophage longevity and inflammatory output in sepsis and infectious disease. - Source: PubMed
Publication date: 2026/05/18
Saha SandhiniVerma RohitNita-Lazar Aleksandra - Porcine deltacoronavirus (PDCoV) is an emerging enteropathogenic coronavirus that causes severe diarrhea in swine industries worldwide. However, the interactions between PDCoV and host cells remain poorly understood. In this study, we employed transcriptomic and proteomic analyses to investigate host responses to PDCoV infection. Our results identified 1448 differentially expressed genes (DEGs) at 1.5 h post-PDCoV infection and 11,753 DEGs, along with 898 differentially expressed proteins (DEPs) at 18 h post-PDCoV infection. Furthermore, several signaling pathways, including innate immunity, autophagy, and ferroptosis, were primarily enriched following an integrated analysis of the transcriptome and proteome. Protein-protein interaction (PPI) analysis indicated that proteins closely associated with these pathways, such as interferon-induced protein with tetratricopeptide repeats 1 (IFIT1), myxovirus resistance 2 (MX2), interferon-stimulated gene 15 (ISG15), radical S-adenosyl methionine domain containing 2 (RSAD2), 2'-5'-oligoadenylate synthetase like (OASL), autophagy related 14 (ATG14), and glutathione peroxidase 4 (GPX4), were central to the interaction network. Importantly, we demonstrated that autophagy and ferroptosis were induced upon PDCoV infection, and that inhibition of autophagy significantly suppressed the induction of PDCoV-induced ferroptosis, which decreases the viral proliferation. Overall, our findings provide a comprehensive overview of transcriptomic and proteomic changes following PDCoV infection and enhance the understanding of PDCoV pathogenesis, which will be beneficial for improving strategies for the prevention and control of PDCoV infection. - Source: PubMed
Publication date: 2026/05/18
Yang XiaozhuMi XingyuLiu WeiZainab FarwaWu MinruiYin HanweiLiu MengyuanZhang TingSun ZilongZhang DingTang PanSong TaoDuan LiqiangXi YiboWang ChenyangLi WeiWang HaidongYang Bo - Interferon (IFN) alpha (IFNα) and lambda3 (IFNλ3) constitute first line responses of immunity against SARS-CoV-2 infection by increasing interferon-stimulated genes (ISGs). Prolonged IFN production may exacerbate inflammation, contributing to endotheliitis and vascular dysfunction in COVID-19. We investigated whether spike protein S1 (SP1) of SARS-CoV-2 via IFN influences inflammation in human vascular and lymphatic endothelial cells (EC) and whether these processes contribute to vascular dysfunction in the context of hypertension. We focused on ISG15, a crucial immune protein that is also implicated in hypertension-associated vascular injury. - Source: PubMed
Publication date: 2026/05/18
Rios Francisco JMontezano Augusto CCamargo Livia LLopes Rheure AGarcía-Redondo Ana BAranday-Cortes ElihuBriones Ana MMcLauchlan JohnTouyz Rhian M - Interferon-stimulated gene 15 (ISG15) is a ubiquitin-like modifier that plays a central role in innate immune signaling and antiviral defense. Increasing evidence indicates that ISG15 and its conjugation system (ISGylation) extend far beyond canonical antiviral activity to critically regulate neuroinflammatory responses in the central nervous system (CNS), contributing to the pathogenesis of viral encephalitis, neurodegenerative disorders, autoimmune demyelination, and certain neuropsychiatric conditions. Mechanistically, ISG15 functions in both conjugated and free forms, exerting context-dependent effects on key inflammatory pathways, including JAK-STAT , NF-κB, inflammasome activation, and cGAS-STING signaling. Through these coordinated actions, ISG15 acts as a molecular rheostat that fine-tunes neuroimmune responses, with outcomes determined by cell type, disease stage, and the balance between intracellular ISGylation and extracellular ISG15 signaling. This functional versatility underscores its translational relevance, as multiple components of the ISGylation machinery, such as the E1 enzyme UBE1L, the E2 enzyme UBE2L6, the E3 ligase HERC5, and the deISGylating Ubiquitin-specific protease 18 (USP18), representing emerging druggable nodes within interferon-driven networks. In this review, we summarize current insights into the molecular and cellular roles of ISG15 in neuroinflammation, highlight its dual protective and pathogenic functions, and discuss therapeutic strategies and future directions for targeting ISG15-related pathways in CNS diseases. - Source: PubMed
Publication date: 2026/05/14
Chen XinXiao XiaoLuo WeiLiu HaoranLiu MaoSima XiutianGao Linbo