Notch1 Monoclonal Antibody (3E12)
- Known as:
- Notch1 Monoclonal Antibody (3E12)
- Catalog number:
- ASA905-897
- Product Quantity:
- 100 µL
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Notch1 Monoclonal Antibody (3E12)
Related genes to: Notch1 Monoclonal Antibody (3E12)
- 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 Monoclonal Antibody (3E12)
Related articles to: Notch1 Monoclonal Antibody (3E12)
- The mutational landscape of head & neck and cutaneous squamous cell carcinomas (HNSCC, cSCC) has major gene alterations involving PIK3CA, NOTCH1, and TP53 among others that contribute to tumorigenesis. In this study, we focused on somatostatin receptor 4 (SSTR4), which was identified in a recent in vivo HNSCC CRISPR screen. Mutations in the SSTR protein family are more commonly implicated in neuroendocrine tumors, and to date, no studies have shown a link between SSTR4 and cSCC/HNSCC. To understand the role of Sstr4 in skin keratinocytes, we employed transcriptomic profiling and proteomic methods and identified enriched pathways and protein-protein interactions (PPIs) networks. Sstr4 activation by J-2156 agonist regulated MAPK-ERK signaling pathway, which simultaneously limited G1 to S phase cell cycle progression. To validate Sstr4 as a driver of cSCC/HNSCC tumorigenesis, we performed a localized and clonal Sstr4 knockout in basal keratinocytes of the Pik3ca oncogenic mouse model using ultrasound-guided in-utero lentivirus injection technology. Tumor formation in mice following Sstr4 knockout occurred rapidly around 12 weeks. Our study is the first to uncover Sstr4 role in cSCC/HNSCC through in-vivo models. - Source: PubMed
Publication date: 2026/08/07
Taqvi AliHuynh Tuan KhangKadam AdwayKardan ZahraYan YueLaham Amina JamalLoganathan Sampath Kumar - DLL4-NOTCH1 signaling mediates juxtacrine communication between tip- and stalk-like endothelial cells during vascular sprouting, contributing to complementary aspects of endothelial function. Thus, simultaneous modulation of DLL4 and NOTCH1 may provide a strategy to broadly interfere with the endothelial functions involved in tumor angiogenesis. Accordingly, this study aimed to identify a novel natural compound capable of modulating DLL4-NOTCH1-mediated endothelial communication and to investigate how such modulation influences tumor angiogenesis and growth. - Source: PubMed
Publication date: 2026/06/19
Ha SeunghwanYou JihyeBae So HeeKim Hyoung-GeunBaek Nam-InJeong Ji-HakKim Jeong AhLee You Mie - Tumor-induced manipulations of myelomonocytic differentiation have been widely reported. Here, we describe the elicitation of a tumor-supportive cell type in a T lymphoma model in mice. We observed that the development of T lymphoma coincided with the appearance of a lymphoma-associated monocytic cell type (LAM) of host origin accompanied by a diminished dendritic cell (DC) population. RNA-sequencing and cytometric analyses revealed that LAMs shared markers with both DCs and with resident macrophages, most closely resembling monocyte-derived DCs (moDCs). The numbers of T lymphoma cells were negatively affected by reducing LAMs suggesting a helper function of LAMs for tumor growth. LAMs expressed Notch ligands, and treatments of lymphoma-carrying mice with Notch signaling-inhibitors LY3039478 and DAPT selectively decreased expansions of T lymphomas with or without Notch1 mutations, respectively. Mature LAMs did not proliferate in the periphery. Instead, their expansion resulted from altered myelomonocytic differentiation in the bone marrows of lymphoma-carrying mice with increases in common monocyte/DC precursors but with reduced granulocyte, monocyte and DC precursor populations. These data suggest that developing T lymphomas are capable of reprogramming monocyte/DC differentiation to increase the numbers of a tumor-promoting DC type, attract it to tumor locations and may engage in Notch ligand-dependent signaling to support lymphoma survival. - Source: PubMed
Publication date: 2026/08/05
Dubois SigridClaudio-Medina YetzaliMarte Jennifer LGulley James LMueller Juergen R - The NOTCH1 gene and its signaling pathway play a critical role in the oncogenesis and progression of various carcinomas through complex cellular and molecular mechanisms. This integrative literature review examines 21 selected studies across multiple carcinoma types, including head and neck, prostate, penis, breast, and hepatocellular carcinomas, to elucidate the functional impact of notch1 alterations on tumor behavior and clinical outcomes. NOTCH1 functions as a context-dependent regulator, acting either as an oncogene or tumor suppressor according to cellular environment and molecular context. Aberrations in notch1 signaling influence cell proliferation, differentiation, apoptosis, and angiogenesis, thereby contributing to cancer initiation and progression. Despite some variability in findings, the majority of studies indicate that notch1-related molecular changes have significant implications for prognosis and potential therapeutic targeting. This review highlights the importance of understanding notch1 signaling pathways in the cellular and molecular biology of carcinomas, aiming to pave the way for novel diagnostic and treatment strategies. - Source: PubMed
Publication date: 2026/04/30
Silva Leticia Milene Silva daMatos Ana Gabrielly de MeloKwang Ii Marciaga Teófilo Carvalho João VictorDuarte Denner Rodrigo DinizSousa Bruna Larissa NolêtoCarmo Juliana Martins da Guia Ribeiro doBeltrammi Daniel Gomes MonteiroLages Joyce SantosFrazão Rita da Graça CarvalhalTeixeira Júnior Antonio Augusto LimaPinho Jaqueline DinizSilva Gyl Eanes Barros - This study aimed to investigate the mechanism by which Xinfeng Capsules(XFC), a traditional Chinese medicine preparation, ameliorates interstitial lung disease(ILD) in adjuvant arthritis(AA) model rats. It exerts the effect by regulating the adsorption of microRNA155(miR155) by metastasis-associated lung adenocarcinoma transcript 1(MALAT1), thereby ameliorating the abnormal expression of miR155 and subsequently modulating the neurogenic locus Notch homolog protein(Notch)-recombination signal binding protein for immunoglobulin kappa J region(RBP-Jκ) signaling pathway. An AA rat model was established, and after intragastric administration of XFC, pharmacodynamic evaluation was conducted on rats in each group, including arthritis index scoring, paw swelling measurement, pulmonary function test, and histopathological examinations of lung tissue and ankle joint synovium. ELISA was used to detect the levels of related inflammatory cytokines. RT-qPCR was performed to determine the expression levels of long non-coding RNA(lncRNA) MALAT1, miR155 and genes related to the Notch-RBP-Jκ signaling pathway, while Western blot was applied to examine the protein expression of ETS transcription factor-1(ETS-1) and RBP-Jκ. The results showed that, compared with the model group, XFC significantly improved pulmonary function, alleviated paw swelling, and inhibited fibrous hyperplasia and inflammatory cell infiltration in synovial and lung tissue of AA rats. It also reduced the serum levels of pro-inflammatory cytokines such as tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β) and interleukin-6(IL-6), thereby alleviating the systemic inflammatory responses. In addition, XFC ameliorated the aberrant expression of lncRNA MALAT1 and miR155, inhibited the transcription of Notch homolog 1(Notch1), Jagged canonical Notch ligand 1(Jagged1), nuclear factor of activated T cells cytoplasmic 1(NFATC1) and interferon regulatory factor 8(IRF8), and further promoted the protein expression of ETS-1 while suppressing RBP-Jκ protein expression. In summary, XFC may exert its effects by enhancing the roles of lncRNA MALAT1 as a molecular sponge to adsorb miR155, thereby inhibiting the aberrant expression of miR155, which in turn modulates the overactivation and transcription of the Notch-RBP-Jκ signaling pathway, suppresses the articular inflammatory response and ameliorates ILD lesions in AA rats. - Source: PubMed
Li Meng-QiWang Dian-LeiFang WeiZhu Wen-TaoWei Wen-BinYan Gui-MingZhang Xiao-Jun