Ask about this productRelated genes to: SETD7 Blocking Peptide
- 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 Blocking Peptide
Related articles to: SETD7 Blocking Peptide
- Pre-eclampsia (PE) is a severe pregnancy-specific hypertensive disorder that poses significant risks to both maternal and fetal health. This study seeks to elucidate the mechanism by which SETD7 regulates trophoblast cell pyroptosis in PE through epigenetic mechanisms. - Source: PubMed
Publication date: 2026/05/23
Zhao XiaolanLi LinglingWang YujueZheng Zhenrong - The innate immune signaling pathway cGAS-STING plays an important role in the recognition of cytosolic nucleic acids and the induction of the interferon-dependent antiviral response. Despite the significant research interest in this cascade in the context of immune system function, the mechanisms regulating cGAS-STING signaling and the switch between its pro-inflammatory and pro-apoptotic effects remain largely underexplored. According to publicly available RNA-seq data and microarray analyses, SETD7 lysine methyltransferase participates in interferon signaling in cancer cells. This study aims to elucidate the role of SETD7 in the regulation of the STING-dependent immune response in human lung adenocarcinoma (LUAD) cells. For this purpose, we developed a reproducible and cost-effective method for inducing the STING cascade by transfecting cells with salmon sperm DNA (sspDNA). We demonstrated that sspDNA efficiently induces phosphorylation of the key components of the STING-TBK1-IRF3 signaling pathway and activates the expression of interferons and pro-inflammatory cytokines. Using this approach, we further demonstrated that SETD7 is involved in the regulation of the IRF3-dependent transcriptional program. Suppression of SETD7 was associated with changes in the expression of genes related to innate immune response and apoptosis, including increased levels of , , , (PUMA), and . Furthermore, attenuation of SETD7 expression reduced the lentiviral transduction efficacy in H1299 cells. These results suggest that SETD7 may play a role in regulating the switch in STING signaling between pro-inflammatory and pro-apoptotic responses in LUAD cells. - Source: PubMed
Publication date: 2026/04/30
Nevzorov Ivan AKorableva PolinaShuvalov OlegParfenyev SergeyBarlev Nickolai ADaks Alexandra - ATG16L1 (autophagy related 16 like 1) is a core macroautophagy/autophagy protein essential for autophagosome formation. It also functions in non-canonical autophagy pathways such as LC3-associated phagocytosis (LAP) and in other processes including immunity, inflammation, and membrane trafficking. This review synthesizes recent advances and proposes that ATG16L1 functions as a central molecular integrator governed by a multi-layered regulatory code. This framework includes genetic polymorphisms, transcriptional control, and diverse post-transcriptional and post-translational mechanisms. We detail how these regulatory layers collectively fine-tune ATG16L1 function in response to cellular stress. Dysregulation of this network contributes broadly to human diseases including inflammatory bowel disease, cancer, and neurodegenerative disorders. Notably, the functional impact of specific regulatory events is highly context dependent, a principle exemplified by the Crohn disease-associated T300A polymorphism. Deciphering this regulatory landscape and its crosstalk with both autophagy-dependent and autophagy-independent functions positions ATG16L1 as a pivotal node in cellular homeostasis and as an emerging therapeutic target. ATG: autophagy related; CASM: conjugation of Atg8-family proteins to single membranes; CCD: coiled-coil domain; CEBPA/CEBPα: CCAAT enhancer binding protein alpha; CHUK/IKKA: component of inhibitor of nuclear factor kappa B kinase complex; circRNA: circular RNA; CPT1A: carnitine palmitoyltransferase 1A; CREB: cAMP responsive element binding protein; CSNK2: casein kinase 2; FTO: FTO alpha-ketoglutarate dependent dioxygenase; GJA8/connexin 50: gap junction protein alpha 8; H/R: hypoxia-reoxygenation; HDAC: histone deacetylase; KAT2B/PCAF: lysine acetyltransferase 2B; KDM1A: lysine demethylase 1A; LAP: LC3-associated phagocytosis; lncRNA: long non-coding RNA; LRRK2: leucine rich repeat kinase 2; mA: N6-methyladenosine; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; miRNA/MIR: microRNA; Mtb: ; ncRNA: non-coding RNA; PE: phosphatidylethanolamine; PI3K: phosphoinositide 3-kinase; PRKA/PKA: protein kinase cAMP-activated; PPP1: protein phosphatase 1; RAB33B: RAB33B, member RAS oncogene family; RB1CC1/FIP200: RB1 inducible coiled-coil 1; SETD7: SET domain containing 7, histone lysine methyltransferase; SQSTM1/p62: sequestosome 1; TNF/TNF-α: tumor necrosis factor; ULK: unc-51 like autophagy activating kinase; V-ATPase: vacuolar-type H-translocating ATPase; VDR: vitamin D receptor; WIPI2B: WD repeat domain, phosphoinositide interacting 2B; YTHDF2: YTH N6-methyladenosine RNA binding protein F2; ZDHHC7: zDHHC palmitoyltransferase 7. - Source: PubMed
Publication date: 2026/05/14
Wei FujingLiu ZhenzhenYu XiaoyingSun YinqiZhao YuanyuanWang YuFeng ZilingZhao XiaozhuKe XiaoxueYang AiminCui Hongjuan - Endothelial plasticity, the capacity of endothelial cells (ECs) to reversibly alter their phenotype in response to environmental cues, typically enables adaptive vascular remodeling and tissue homeostasis. In diabetes, this plasticity becomes maladaptive, driving pathological transitions across interconnected axes: dysregulated angiogenesis with barrier destabilization, inflammatory reprogramming through immune-endothelial crosstalk, metabolic dysfunction spanning mitochondrial stress to senescence, and endothelial-to-mesenchymal transition with fibrosis. In this review, we synthesize mechanistic insights across endothelial state transitions and highlight how single-cell approaches have reframed diabetic vascular disease as a disorder of maladaptive endothelial plasticity. By integrating single-cell insights from diabetic mouse models and human patient samples, we demonstrate that restoring adaptive endothelial plasticity requires coordinated multi-dimensional intervention targeting the intersecting pathways that perpetuate pathological transitions, timed to disease stage and calibrated to vascular bed-specific context. For example, combining metabolic therapies such as GLP-1 receptor agonists or SGLT2 inhibitors with anti-inflammatory agents targeting IL-17A or IL-1β, pairing anti-VEGF treatments with inhibitors of MFAP4 or ANGPTL4 to overcome angiogenic bypass pathways, or coupling senolytics, such as UBX1325, with anti-fibrotic strategies like TGF-β or SETD7 inhibition to prevent irreversible EndoMT. We identify candidate therapeutic targets across angiogenic, inflammatory, metabolic, and fibrotic domains, and highlight critical knowledge gaps, most notably the limited characterization of human diabetic ECs, that must be addressed to translate these insights into effective clinical strategies for preventing diabetic vascular complications. - Source: PubMed
Publication date: 2026/05/06
Alnuaimi Noura SLößlein LenaMousa MiraKhader Thanumol AbdulAlkhaaldi AyeshaAzzam Sarah KVan Craenenbroeck Amaryllis HAshraf Syed SalmanCarmeliet PeterAlsafar Habiba - Hydroquinone (HQ), a major metabolite of benzene, is a recognized risk factor for acute myeloid leukemia (AML). However, the mechanisms underlying HQ-associated leukaemogenesis remain incompletely understood. Increasing evidence suggests that defective osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), contributes to HQ-induced hematopoietic dysfunction and leukemic progression. SET domain-containing 7 (SETD7) has been found to regulate the proliferation and differentiation of BMSCs, while autophagy is known to play a crucial role in promoting osteogenic differentiation. Therefore, this study aimed to investigate the regulatory roles of SETD7 and autophagy in the osteogenic differentiation of HQ-exposed BMSCs. The results demonstrated that HQ exposure was associated with decreased histone 3 lysine 4 monomethylation (H3K4me1) and SETD7 protein levels, autophagy, and osteogenic differentiation capacity in BMSCs. Activation of autophagy by rapamycin (Rapa) effectively rescued the BMSCs osteogenic differentiation reduced by HQ. Moreover, overexpression of SETD7 restored both autophagic activity and osteogenic differentiation capacity suppressed by HQ. Notably, co-treatment with the autophagy inhibitor 3-methyladenine (3-MA) abrogated the pro-osteogenic effects induced by SETD7 overexpression in HQ-exposed BMSCs. Collectively, these findings indicated that SETD7 promoted osteogenic differentiation in HQ-exposed BMSCs via autophagy-dependent mechanism. This study provides mechanistic insight into how HQ may disrupt the bone marrow microenvironment, highlights the role of SETD7 in maintaining osteogenic differentiation and autophagy in HQ-exposed BMSCs, and contributes to a better understanding of the epigenetic and cellular pathways involved in HQ-induced hematotoxicity. - Source: PubMed
Publication date: 2026/02/23
Shen YilinNiu YiboXu TaoLuo ZhilongSong DonghaoLuo ChihengLiu YanCui QilinChen DongxiaoZhao XinyuLuo HaoGao Yuting