Polyclonal Rabbit NOTCH1 Antibody
- Known as:
- Polyclonal Rabbit NOTCH1 Antibody
- Catalog number:
- abx000726
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Polyclonal Rabbit NOTCH1 Antibody
Related genes to: Polyclonal Rabbit 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: Polyclonal Rabbit NOTCH1 Antibody
Related articles to: Polyclonal Rabbit NOTCH1 Antibody
- Microglia are key regulators of neuroinflammation and neuronal survival after ischemic stroke. Emerging single-cell, transcriptomic, and metabolic studies show that ischemia induces rapid microglial reprogramming toward pro-inflammatory states that exacerbate neuronal death, oxidative stress, blood-brain barrier (BBB) disruption, and white-matter injury. Multiple pathways, including TLR4/NF-κB, NLRP3 inflammasome activation, Notch1-JAK/STAT signaling, epigenetic modulators such as HDAC3 and METTL14, and metabolic shifts involving AMPK/mTOR/HIF1α, collectively shape post-stroke microglial polarization. High-altitude hypoxia elicits similar inflammatory responses, activating microglia through RAGE-MAPK/NFκB signaling, CX3CL1/CX3CR1-dependent synaptic pruning, mitochondrial dysfunction, and lactate-mediated chromatin changes, highlighting hypoxia as a convergent driver of neuroinflammation. Modulating microglial activity, therefore, represents a promising therapeutic strategy. A wide range of natural compounds (e.g., curcumin, acteoside, astagaloside IV, artemisinin), synthetic agents (e.g., DBZ, resolvin D1), and cellular/molecular cellular interventions (e.g., rhFGF21, S100A9 inhibition, RBM3 induction) have shown efficacy in reducing inflammation, preserving BBB integrity, improving mitochondrial function, and promoting M2-like reparative phenotypes in preclinical models. Advances in understanding microglial subtypes, including CH25H, OASL, CD11c, and antioxidant Prdx1-enriched populations, further highlight their dynamic roles across injury and repair. This review presents current insights into microglial signalling, epigenetic and metabolic regulation, and therapeutic targeting in ischemic stroke, integrating parallel insights from high-altitude hypoxia. Together, these prospectives illuminate microglia as crucial mediators of neurovascular injury and recovery, and highlight opportunities for translating microglia-directed therapies into clinical interventions. - Source: PubMed
Publication date: 2026/05/06
Khan ShafaSultan ArmiyaSadik MohdAshraf Mohammad Zahid - Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by marked molecular heterogeneity and limited targeted therapeutic options. Its incidence is rising in many low- and middle-income countries, where genetic profiling of affected patients remains largely unexplored despite evident clinical disparities. This study aimed to characterize, for the first time in a Tunisian cohort, the spectrum of germline and somatic mutations in TNBC patients and to assess their potential impact on therapeutic response. Targeted next-generation sequencing (NGS) of hotspot regions across 50 cancer-related genes was performed in twelve patients using the AmpliSeq for Illumina Cancer Hotspot Panel v2, applied to both tumor tissues and matched adjacent non-tumoral tissues. Bioinformatics analysis revealed recurrent germline variants present in all samples, notably in TP53 (rs1042522), CSF1R (rs2066933), FGFR3 (rs7688609), RET (rs1800861), KDR (rs7692791), and PDGFRA (rs1873778). In tumor tissues, 32 deleterious somatic variants were detected across 20 oncogenes, with TP53 emerging as the most frequently mutated gene (58%). Distinct mutational patterns were observed in relation to treatment response. Notably, the co-occurrence of AKT1 (rs121434592) and TP53 (rs876660754) was observed in a patient with treatment resistance, whereas an in-frame deletion in NOTCH1 (p.Val1578del) was uniquely detected in patients who subsequently experienced disease recurrence. These findings provide the first comprehensive characterization of germline and somatic alterations in Tunisian TNBC patients, representing a North African cohort. They reveal the heterogeneity of mutation patterns linked to treatment response, and emphasize the importance of genomic profiling into clinical practice and guide personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/04/22
Mehri AsmaLaaribi Ahmed BalighJbir IchrafChelbi EmnaChelly BeyaChaabane AbirNechi SalwaOuzari Hadda-Imen - In pediatric patients, T-cell lymphoblastic lymphoma (T-LBL) survival exceeds 80%. Relapse remains associated with limited curative options. Frontline treatment is largely extrapolated from T-cell acute lymphoblastic leukemia (T-ALL) treatment, reflecting the ongoing debate, whether both entities represent distinct diseases or variants within one spectrum. This review focuses on T-LBL, summarizing shared and distinct clinical, pathological, and biological features in comparison to T-ALL. We address diagnostic and staging challenges, and current limitations of clinical risk stratification. Biomarkers, such as genetic variants in NOTCH1/FBXW7, are discussed in the context of dynamic risk assessment. Particularly emphasizing the molecular landscape of T-LBL and recurrent pathway alterations. NOTCH1 emerges as central determinant of disease biology. Activating NOTCH1 mutations (NOTCH1) are frequently associated with favorable outcomes and used for risk stratification in the ongoing trial LBL 2018 (EUCT number: 2023-508101-24-00). NOTCH1 fusions resulting in excessive NOTCH1 signaling are associated with increased relapse incidences, suggesting that the intracellular amount of NOTCH1 differentiates between tumor suppressive versus tumor supportive activity. These findings are placed in the context of recently described NOTCH1 variants in T-ALL, reported to similarly cause aberrant NOTCH1 activation. Future studies may consider incorporating detailed NOTCH1 status to understand disease dynamics and enhance therapeutic strategies. - Source: PubMed
Publication date: 2026/05/07
Heider Marie CAlfert AmelieHotfilder MarcBurkardt BirgitTe Vrugt Marcel - To analyze the clinical and genetic characteristics of patients with mucosa-associated lymphoid tissue (MALT) lymphoma transformed into diffuse large B-cell lymphoma (DLBCL). A retrospective analysis was performed on patients diagnosed with MALT lymphoma at Henan Provincial People's Hospital from January 2016 to December 2025. According to whether DLBCL transformation occurred, the patients were divided into the transformed group (MALT lymphoma patients who developed DLBCL transformation) and the non-transformed group. The patients were followed up until December 30, 2025, and the clinical and genetic characteristics were compared between the two groups. A total of 175 patients were included, including 13 patients in the transformation group, 4 males and 9 females, aged (58±18) years; and 162 pattients in the non-transformed group, 73 males and 89 females, aged (57±12) years.The incidence of B symptoms in the transformed group [46.2% (6/13) vs 16.7% (27/162), =0.018], the proportion with a MALT-international prognostic index (IPI) score≥2 point [69.2% (9/13) vs 17.3% (28/162), <0.001], and lactate dehydrogenase (LDH) levels [227 (194, 262) vs 173 (146, 196) U/L, <0.001] were all higher than those in the non-transformed group. The mutation rate of gene in the transformed group [84.6% (11/13) vs 45.7% (74/162), =0.007] and the mutation rate of ≥2 genes [69.2% (9/13) vs 17.3% (28/162), <0.001] were both higher than those in the non-transformed group. The mutation rates of the NOTCH1 gene [23.1% (3/13) vs 3.7% (6/162), =0.021], the SOCS1 gene [15.4% (2/13) vs 0, =0.005], and the KRAS gene [15.4% (2/13) vs 0, =0.005] were all higher in the transformed group than those in the non-transformed group. Patients with MALT lymphoma who transformed to DLBCL are often accompanied by B symptoms, a higher MALT-IPI score, elevated LDH and multiple gene mutations, and the mutation frequencies of NOTCH1, SOCS1, and KRAS are higher. - Source: PubMed
Publication date: 2026/05/07
Ma R JZhou PLiu Y BZhuo J HWang L FLi SLu W YPei X HZuo S QXu HJiang LChen X LYuan X LZhu Z M - Hypoxia is pervasive within the solid tumor microenvironment (TME), reshaping it through exosome release. As the main component of the tumor stroma, fibroblasts influence TME remodeling and tumor progression. Recent advances in targeting tumor-derived exosomes offer promising opportunities for innovative colorectal cancer (CRC) therapies. Here, we found that exosomes induced by hypoxia in CRC cells (H-Exo) can promote the activation of normal tissue-associated fibroblasts (NAFs) into cancer-associated fibroblasts (CAFs) phenotype, with a stronger effect compared to normoxic exosomes (N-Exo). Machine learning analysis identified HIF1A-AS2, induced by hypoxic tumor-derived exosomes, as a promising prognostic lncRNA in CRC. Pan-cancer and scRNA-seq analyses showed that high HIF1A-AS2 expression was characterized by hypoxia, angiogenesis, immunosuppression (e.g., CAFs), TGF-β, and fibroblast-CD44 interactions in CRC. HIF1A-AS2 expression progressively increased along pseudotime, shifting from early immune activation to late-stage extracellular matrix (ECM) organization, vascular niche formation, and fibroblast activation. HIF1A-AS2 in H-Exo was a key factor in the transformation of NAFs into CAFs. Exosomal HIF1A-AS2 sequesters miR-33, thereby derepressing HIF-1α, activating Notch1/ERK signaling, and upregulating angiogenic and matrix-remodeling factors (e.g., VEGF, MMP-7, and MMP-9). Further research revealed that exosomes with silenced HIF1A-AS2 or overexpressed miR-33 could inhibit CAF infiltration, tumor cell proliferation, angiogenesis, and ECM reorganization in xenografts, ultimately suppressing tumor growth. These findings highlight that simultaneously blocking tumor exosome-driven fibroblast activation and the HIF1A-AS2/miR-33/HIF-1α axis may serve as a promising therapeutic avenue for CRC intervention. - Source: PubMed
Publication date: 2026/05/06
Han SusuHuang TaoYin XiaolingWang TingShi QiTang YufeiZhu TingtingGao SongSui HuaHou Fenggang