Ask about this productRelated genes to: SETD7 antibody
- Gene:
- SETD7 NIH gene
- Name:
- SET domain containing 7, histone lysine methyltransferase
- Previous symbol:
- -
- Synonyms:
- KIAA1717, SET7, SET7/9, Set9, KMT7
- Chromosome:
- 4q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-15
- Date modifiied:
- 2018-12-21
Related products to: SETD7 antibody
Related articles to: SETD7 antibody
- SET7 belongs to the SET domain (SETD) methyltransferase family, which catalyzes the monomethylation of lysine residues in histones and nonhistone proteins. This process can either enhance or suppress gene activation. Interferon regulatory factor 3 (IRF3) is a key transcription factor in the type I interferon (IFN) signaling pathway. This pathway is controlled by multiple posttranslational modifications that finely tune IRF3's function. Here, we identify SET7 as a negative regulator of IRF3. SET7 interacts with IRF3 and catalyzes the monomethylation of IRF3 at lysine 98. This modification decreases IRF3 phosphorylation, dimerization, and subsequent nuclear translocation, thereby inhibiting the production of downstream type I interferons. Furthermore, zebrafish lacking , as well as those treated with the inhibitor (R)-PFI-2, exhibits greater resistance to viral infection. -deficient mice also exhibit greater resistance to RNA and DNA viral infections. Our findings reveal a role for SET7 in regulating antiviral innate immunity and provide insight into the IRF3 monomethylation that affects its activation. - Source: PubMed
Publication date: 2026/08/25
Deng HongyanSun XueyiZha HuangyuanWang ZixuanTang JinhuaChen XiaoyunZhu ChunchunHua JialeLiu WenJia ShukeLuo YimanXiang YuhanLi WenhuaLiu XingXiao Wuhan - Diabetic retinopathy (DR) has traditionally been viewed as a consequence of cumulative oxidative damage. However, the clinical phenomenon of metabolic memory, whereby prior hyperglycemia continues to exert adverse effects despite subsequent glucose normalization, indicates a more complex redox biology. This review advances a paradigm shift from considering reactive species merely as markers of injury to interpreting oxidative signatures as a dynamic, compartment-specific code that records glycemic history, predicts disease trajectory, and enables therapeutic subtyping. We synthesize evidence across multiple redox layers, including protein oxidative post-translational modifications such as S-glutathionylation and tyrosine nitration, lipid peroxidation products, mitochondrial DNA damage, and epigenetic rewriting mediated by SET domain-containing lysine methyltransferase 7 (SETD7, also known as SET7/9)-dependent monomethylation of histone H3 lysine 4 (H3K4me1). Persistent failure of mitochondrial quality control and maladaptive chromatin remodeling may stabilize hyperglycemia-induced redox programs after glucose normalization, whereas exosomal signaling may contribute to their intercellular propagation. In this context, metabolic memory refers to the durable yet potentially modifiable maintenance of these molecular programs rather than absolute biological irreversibility. Moving beyond the failure of generic antioxidant approaches, we introduce a clinical taxonomy of redox subphenotypes, glutathione-deficient, lipid-peroxidation-dominant, mitochondrial reactive oxygen species (ROS)-driven, and epigenetic redox-lock, each linked to candidate, predominantly preclinical, mechanism-matched interventions, including thiol-repleting agents, ferroptosis inhibitors, mitophagy-enhancing or mitochondrial-protective agents, and epigenetic modulators. Finally, we outline an integrated roadmap combining single-cell redox profiling, liquid-biopsy multi-omics, and biomarker-enriched clinical trial designs to translate redox signatures into precision management. Decoding the redox code may extend the traditional oxidative stress paradigm by revealing biologically heterogeneous molecular states with distinct therapeutic implications. - Source: PubMed
Publication date: 2026/08/14
Mohammad Suleiman IbrahimVasudevan AsokanNuseir MuslemBaig Mirza RYakhshieva ZukhraTurakulov RustamSharma ChandanSinghal DivyaAlghazali TawfeeqAbdelgawwad El-Sehrawy Amr Ali Mohamed - Early-life stress increases gene expression, neurophysiological, and behavioral responses to subsequent stress. Here, we determined the role of chromatin in such long-lasting sensitivity. We used a combination of bottom-up mass spectrometry, viral-mediated epigenome editing, RNA sequencing, patch-clamp electrophysiology of dopamine neurons, and behavioral quantification in a mouse model of early-life stress, focusing on the ventral tegmental area (VTA), a key dopaminergic brain region. We found that early-life stress enriches histone-3 lysine-4 monomethylation-associated with open chromatin and primed or active enhancers-and the H3K4 monomethylase SETD7. Mimicking early-life stress through postnatal overexpression of Setd7 and enrichment of H3K4me1 in the VTA sensitizes transcriptional, physiological, and behavioral responses to adult stress, while Setd7 knockdown ameliorates the impact of early-life stress. These findings link early-life stress experience to long-term stress hypersensitivity within the brain's dopaminergic circuitry, providing a mechanism by which early-life stress increases risk for mood and anxiety disorders later in life. - Source: PubMed
Publication date: 2026/08/07
Kim Hye Ji JGeiger Luke TBalouek Julie-AnneFang Lisa ZBarrett Mason RThompson Jeremy MFarrelly Lorna AHage TravisLin RixingChen Andy STang MeganHuang HaoBuretta AnnaChan AgathaBennett Shannon NGarcia Benjamin AMaze IanCreed Meaghan CPeña Catherine Jensen - Early life stress (ELS) sensitizes individuals to subsequent stressors to increase lifetime risk for psychiatric disorders. Within the nucleus accumbens (NAc)-a key limbic and reward-associated brain region-ELS sensitizes both cellular and transcriptional response to later stress, which are programmed by enduring epigenetic changes. Among the histone modifications persistently enriched by ELS in NAc is H3K4me1, which is associated with open chromatin and epigenetic priming of genomic enhancers. Here, we sought to determine whether H3K4me1 enrichment in NAc was sufficient to prime cellular and behavioral responses to adult stress. Viral-mediated overexpression of the histone H3 monomethyltransferase in juvenile NAc of male and female mice induced persistent chromatin changes and predominately opened chromatin at long-range cis-regulatory elements predicted to enhance immediate early genes and transcriptional regulators of mesolimbic development and synaptic activity. These epigenetic changes altered physiological properties of D2-type medium spiny neurons in NAc to resemble neurons of stressed mice, without significantly altering D1-type neurons. Finally, juvenile-but not adult- overexpression and H3K4me1 enrichment in NAc enhanced behavioral sensitivity to future stress. Together, these data indicate that altered postnatal chromatin development in NAc by H3K4me1 enrichment is sufficient to prime long-lasting transcriptional, physiological, and behavioral stress sensitivity. - Source: PubMed
Publication date: 2026/08/26
Rashford Rebekah LFang Lisa ZDeBerardine MichaelKim Hye Ji JHirschfield Laura WCervi EllaBarrett Mason RThompson Jeremy MCreed Meaghan CPeña Catherine Jensen - Small extracellular vesicles (sEVs) are cell-released lipid vesicles that facilitate intercellular communication by transferring bioactive cargo to recipient cells. We previously showed that a single intrathecal administration of RAW 264.7 macrophage-derived sEVs, given two weeks prior to complete Freund's adjuvant (CFA)-induced inflammation, resulted in earlier recovery from mechanical and thermal hypersensitivity. How this long-term memory develops, and how sEVs regulate immune responses, are unknown. Recent studies have shown that priming microglia with inflammatory stimuli can enhance or suppress responses to a delayed secondary insult via epigenetic modifications. We hypothesized that prophylactic intrathecal administration of macrophage-derived sEVs confers accelerated resolution of inflammatory pain by reprogramming epigenetic memory in spinal microglia. - Source: PubMed
Publication date: 2026/07/09
Luo XuanWickman Jason RDaCunza Jason TTian YuzhenSacan AhmetAjit Seena K