Ask about this productRelated genes to: NOTCH1 antibody
- Gene:
- NOTCH1 NIH gene
- Name:
- notch receptor 1
- Previous symbol:
- TAN1
- Synonyms:
- -
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-13
- Date modifiied:
- 2019-04-23
Related products to: NOTCH1 antibody
Related articles to: NOTCH1 antibody
- Chronic, non-healing wounds are a severe diabetic complication. The underlying mechanisms are not fully understood, and the role of ATF7 in this context has not been well characterized. In our study, we utilized db/db diabetic mice and AAV-mediated keratinocyte-specific Atf7 overexpression in vivo. HaCaT keratinocyte/THP-1 macrophage cocultures under high glucose were used in vitro. Our results showed that ATF7 was upregulated in diabetic wounds. Keratinocyte-specific Atf7 overexpression accelerated diabetic wound closure, enhanced re-epithelialization, granulation tissue formation, and keratinocyte proliferation, while suppressing macrophage M1 polarization and inflammation. Multiomics screening identified NOTCH1 as a key ATF7 target. ATF7 transcriptionally repressed NOTCH1 by recruiting Suv39h1, increasing H3K9me3 at the NOTCH1 promoter. This reduced NOTCH1 protein and its active intracellular domain (N1ICD) within keratinocyte-derived exosomes. ATF7-overexpressing keratinocyte exosomes carried less N1ICD, leading to decreased N1ICD transfer to macrophages and subsequent inhibition of M1 polarization. Notably, local injection of exosomes from ATF7-overexpressing keratinocytes accelerated wound healing in db/db mice. In summary, ATF7 promotes diabetic wound healing by repressing NOTCH1 transcription via H3K9me3, thereby reducing exosomal N1ICD secretion from keratinocytes and inhibiting macrophage M1 polarization. This identifies the ATF7/NOTCH1/exosome axis as a therapeutic target. - Source: PubMed
Publication date: 2026/08/24
Xu PengchengXue YuanFeng LinlinKuang JingwenHu XiaochenTang HuiyiCheng BiaoWei Limin - Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) driven by autoimmune mechanisms. However, growing evidence indicates that B lymphocytes may contribute to the disease through antigen presentation and the production of proinflammatory mediators. This study aimed to examine the effect of JNJ 10191584 (JNJ), a potent and selective H4R antagonist, on the progression of EAE and to uncover the underlying mechanisms. The research explored the potential impact of H4R antagonists on inflammatory responses in B cells within an EAE mouse model of MS. EAE mice received an oral dose of JNJ at 6 mg/kg daily, starting on day 10 and continuing until day 42. Flow cytometry assessed JNJ's effect on the expression of NF-κB p65, IκBα, Notch1, Notch3, IL-2, IL-6, GM-CSF, iNOS, TNF-α, and MCP-1 in CD19 B cells. RT-PCR was used to evaluate the impact of JNJ on mRNA levels of these inflammatory markers in brain tissue. In EAE mice, JNJ treatment reduced the number of CD19 cells expressing NF-κB p65, IκBα, Notch1, Notch3, IL-2, IL-6, GM-CSF, iNOS, and MCP-1. Additionally, JNJ decreased mRNA expression of inflammatory markers in brain tissue compared with vehicle-treated mice. These results suggest that targeting H4R with antagonists could offer a new therapeutic approach for MS by specifically modulating B-cell-mediated inflammation. - Source: PubMed
Publication date: 2026/08/24
Al-Mazroua Haneen AAlhamami Hussain NNadeem AhmedAnsari Mushtaq ABakheet Saleh AAttia Sabry MSarawi Wedad SAlomar Hatun AAlsaad Abdulaziz M SAlshamrani Ali AAhmad Sheikh F - Poor early treatment response in T-cell lymphoblastic lymphoma (T-LBL) is associated with an unfavorable prognosis. This multicenter prospective study evaluated the efficacy of the response-adjusted Chinese Children's Cancer Group (CCCG-LBL-2016) protocol for pediatric T-LBL and examined clinical and molecular prognostic factors. - Source: PubMed
Publication date: 2026/08/22
Guo XiaWang Chao-BanTang Yue-JiaFang Yong-JunYan JieJu Xiu-LiLiu Ai-GuoYang Liang-ChunGao JuGao Yi-Jin - Reliable prognostic biomarkers are urgently needed for operable esophageal squamous cell carcinoma (ESCC), as conventional histopathology often fails to detect minimal residual disease and accurately predict patient outcomes. - Source: PubMed
Publication date: 2026/08/22
Lu DiTong YuHe ChunhongChen ZhimingWang ZhizhiLiu JingwenYin Jiani CLi ShaobinMai ShijieRao XuguangCai Kaican - Parkinson's disease (PD) remains a neurodegenerative disorder without effective disease-modifying therapies, largely due to its multifactorial pathogenesis. We report that the natural flavonoid Astragalin (AST) concurrently addresses three core pathological processes in PD, namely dopaminergic neuron degeneration, α-synucleinopathy, and neuroinflammation, through coordinated modulation of interconnected molecular pathways. In both subacute MPTP- and chronic rotenone-induced murine PD models, AST preserved 85% of nigral tyrosine hydroxylase-positive neurons, fully prevented motor deficits, and suppressed phosphorylated α-synuclein (α-Syn) accumulation and Lewy body-like inclusion formation. Mechanistically, AST activated the BDNF-TrkB/AKT pro-survival pathway, enhanced NRF2-mediated antioxidant defense, and suppressed neuroinflammatory cascades by dual inhibition of Notch1/HES-1 and COP1-C/EBPβ signaling, leading to attenuated microglial and astrocytic activation. These findings position AST as a promising multi-target therapeutic neuroprotective candidate with disease-modifying potential, providing a structural scaffold for developing combination-inspired anti-PD strategies. - Source: PubMed
Publication date: 2026/08/20
Wang JunHe Jie-YuHuang QinMa Hui-YongCao Min-MinQin Xiao-YanHu YangLan Rongfeng