MALT EXTRACT AGAR
- Known as:
- MALT EXTRACT AGAR
- Catalog number:
- m13-113
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- AlphaBio Alpha Bioscience
- Gene target:
- MALT EXTRACT AGAR
Related genes to: MALT EXTRACT AGAR
- Gene:
- BIRC3 NIH gene
- Name:
- baculoviral IAP repeat containing 3
- Previous symbol:
- API2
- Synonyms:
- cIAP2, hiap-1, MIHC, RNF49, MALT2, c-IAP2
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-10
- Date modifiied:
- 2016-10-05
Related products to: MALT EXTRACT AGAR
Related articles to: MALT EXTRACT AGAR
- Acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors remains the principal barrier to durable responses in non-small cell lung cancer (NSCLC), yet how the molecular interaction networks underlying this resistance reorganize over time is poorly understood. We reasoned that a systems-level signature of resistance should be visible in the way protein interaction networks remodel under sustained drug exposure, and therefore applied time-resolved network analysis to isogenic gefitinib-sensitive PC9 and gefitinib-resistant PC9R cells across 24 h of gefitinib treatment, computing network entropy and centrality measures for temporal protein interaction networks and interrogating co-expression-augmented networks for candidate resistance-associated bottleneck proteins. Network entropy rose in both phenotypes, indicating that entropic remodeling is a general response to EGFR pathway perturbation rather than a signature of resistance. In contrast, eigenvector entropy was higher in resistant cells at the earliest post-treatment time point, and resistant cells preserved giant-component connectivity and small-world topology early before fragmenting later. Temporal centrality analysis nominated BIRC3 as a resistant-cell-associated high-centrality node at 24 h, and co-expression analysis identified delta-catenin (CTNND1) as a high-betweenness bottleneck in the PC9R network, topologically bridging EGFR, VAV3, HIF3A, and NOTCH2. These findings nominate early post-treatment eigenvector entropy and a CTNND1-centered, EGFR-enriched subnetwork as candidate resistance-associated features that require validation in independent datasets and functional models. - Source: PubMed
Publication date: 2026/09/21
Tsakona Dimitra CPapanikolaou Nikolaos A - L.f., a traditional medicinal plant widely distributed in South and Southeast Asia, has long been used in ethnomedicine to treat respiratory disorders, inflammation and tumor-related conditions. Although previous studies have suggested that possesses cytotoxic and anti-inflammatory activities, the antitumor efficacy and underlying mechanisms of its fruit-derived dichloromethane extract remain unclear. This study aimed to investigate the anti-lung cancer activity of the dichloromethane extract of fruits (FHF-DE) using integrated phytochemical, cellular, transcriptomic and approaches. FHF-DE inhibited the proliferation of multiple human lung cancer cell lines (including H1299, A549, H1975, H460, and PC9 cells) as well as murine Lewis lung carcinoma (LLC) line. Flow cytometry indicated G0/G1 arrest in LLC cells and S-phase arrest in H1975 cells. FHF-DE also promoted apoptotic cell death, as indicated by increased Bax expression, decreased Bcl-2 expression, and caspase-3 activation. Transcriptome sequencing and reverse transcription-quantitative (RT-q) PCR analyses indicated enrichment of the TNF signaling pathway, with increased TNF- and related gene expression (e.g., IRF1, BIRC3). In an LLC allograft mouse model, daily oral administration of FHF-DE (200-400 mg/kg) significantly suppressed tumor growth, without evident hepatotoxicity or nephrotoxicity in H&E staining. This finding demonstrates the antitumor efficacy of FHF-DE, although, molecular validation of the proposed mechanism in tumor tissues was not performed. Collectively, our in vitro data demonstrate that FHF-DE induces apoptosis and cell cycle arrest in lung cancer cells, with transcriptomic and pharmacological data suggesting a functional association with TNF-related signaling pathways. However, definitive mechanistic proof of direct TNFR1 engagement or extrinsic apoptotic pathway activation, particularly in vivo, requires further investigation. The present study provides preclinical evidence supporting further pharmacological and toxicological evaluation of fruit-derived extracts as natural-product-based candidates for lung cancer intervention. - Source: PubMed
Publication date: 2026/07/15
Yang JuanWu WenmingPeng JiahuiLiu XiaoyuYing DongmeiZhou XinyiWang JunanDuan YoufaXiong WenchaoJin An - Nasopharyngeal carcinoma (NPC) is a head and neck cancer characterized by highly locoregionally invasive behavior attributable to the latent infection with Epstein-Barr virus (EBV) and genomic instability. It is well established that EBV-encoded oncogenic molecules actively contribute to the malignant behavior of NPC cells. However, the mechanism by which aberrant genomic alterations enable NPC cells to become aggressive remains largely unknown. In the present study, whole-exome sequencing (WES) revealed that the gene encoding the baculoviral IAP repeat-containing 3 (BIRC3) protein was frequently mutated in circulating tumor cells (CTCs) but not in paired primary tumor cells from patients with metastatic NPC. A minigene assay indicated that the c.637 A > G mutation disrupted normal mRNA splicing, resulting in the partial deletion of Exons 2 and 3 and altered stability of BIRC3 mRNA. In vitro experiments demonstrated that ectopic expression of the BIRC3 mutant enhanced NPC cell invasive properties, including proliferation, resistance to apoptosis, migration, and invasion. Furthermore, overexpression of wild-type BIRC3 promoted invasive characteristics in NPC cells through the TRAF2-NF-κB signaling axis. In summary, BIRC3 acts as a regulator of the malignant features of NPC cells. Frequent BIRC3 mutations in CTCs, such as the c.637 A > G mutation, further enhance the metastatic potential of disseminated NPC cells by inducing aberrant alternative splicing. These findings suggest the therapeutic feasibility of targeting the BIRC3/TRAF2/NF-κB axis in the treatment of NPC. - Source: PubMed
Publication date: 2026/08/11
Liu XueLiu YupingZhu BiyunHuang YujuanChen YongLi QiuyunDeng YayanHuang LihongCai BinliFan QianqingLuo WenhuiYe JiaxiangLi YongqiangWei JiazhangZhang Jinyan - Primary cutaneous T-cell lymphomas (CTCL), particularly in their early stages, frequently present with clinical and histopathologic features that overlap with atopic dermatitis (AD) and psoriasis, contributing to diagnostic delay and ineffective, or even deleterious, treatment approaches. Minimally invasive molecular tests capable of distinguishing CTCL from benign inflammatory dermatoses are thus urgently needed. - Source: PubMed
Publication date: 2026/08/07
Fleischli AbigailBar JonathanManson MeredithNg Brandon DMeledathu ShannonBurnett AmeliaChefitz GabriellaEstrada Yeriel DGour DigpalCices AhuvaCorrea da Rosa JoelBrunner Patrick MGuttman-Yassky Emma - Pulmonary extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (pulmonary MALT lymphoma) is an indolent B-cell lymphoma that can mimic infection, inflammatory disease, or epithelial malignancy. Indeterminate fluorodeoxyglucose-avid abnormalities may complicate staging and lead to overinterpretation of disease extent. - Source: PubMed
Publication date: 2026/07/17
Zhang HongliangCai Helun