RTCD1 Blocking Peptide
- Known as:
- RTCD1 Blocking Peptide
- Catalog number:
- 33r-9747
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- RTCD1 Blocking Peptide
Related genes to: RTCD1 Blocking Peptide
- Gene:
- RTCA NIH gene
- Name:
- RNA 3'-terminal phosphate cyclase
- Previous symbol:
- RTCD1
- Synonyms:
- RPC, RTC1
- Chromosome:
- 1p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-10
- Date modifiied:
- 2016-10-05
Related products to: RTCD1 Blocking Peptide
Related articles to: RTCD1 Blocking Peptide
- The molecular mechanisms and interactions for the complex cancer pathogenesis are still poorly understood. Traditional and conventional endpoint migration assays such as MTT/XTT/CCK-8, transwell migration, clonogenic, and false positives/negatives assays, do not capture the kinetics of the 3D tumor microenvironment. Therefore, there is the need for high-resolution kinetic data on cancer cell invasion, proliferation, migration, cytotoxicity, adhesion, and differentiation, to understand transient and adaptive responses that are often missed by static measurements for highly effective cancer immunotherapeutics. Here, we review the xCELLigence™ Real-Time Cell Analysis (RTCA) system that represents a major advancement in cancer research by enabling non-invasive, label-free, and continuous monitoring of cellular behaviour through impedance-based technology. Over the years, and particularly since 2020, RTCA has been increasingly applied and relied upon across diverse areas of cancer research, including kinase inhibition, gene silencing, metabolic targeting, immunotherapy, nanomedicine, and three-dimensional tumour models. We first analyse the recent advances in the applications of xCELLigence™ RTCA, with a specific emphasis on how impedance-derived kinetic signatures enhance mechanistic understanding of tumor cell behaviour. We then critically discuss quantitative metrics derived from real-time impedance measurements, compare RTCA with conventional endpoint assays, and highlight its translational relevance for drug development and precision oncology. Finally, we outline current limitations and emerging directions that may further consolidate RTCA as a predictive and integrative platform in preclinical cancer research. - Source: PubMed
Publication date: 2026/05/26
Andraos CharleneJoseph Jitcy SajiUtembe WellsMagogotya MillicentOriyomi OlumayowaFagbohun Oladapo - Endometriosis is a common gynecological disease with high recurrence rates after surgery and the lesions keep unlimited proliferative capacity. The effect of garcinol on cell proliferation has not been investigated in endometriosis. Herein, we studied the effect of garcinol on endometriosis by using the immortalized human endometriotic epithelial cell line 12Z and stromal cell line iheESCs. RTCA and EdU assays were used to assess cell proliferation. RNA-Seq was used to discover the differential expression gene (DEG) profile and GSEA, KEGG, protein-protein interaction network and the transcription factor interaction network were analyzed. We found that garcinol inhibited the cell proliferation and S phase DNA synthesis of 12Z and iheESCs cells. There were 548 DEGs in the transcription profiles of the two cell lines. The GSEA results showed that garcinol could inhibit the DNA replication and cell cycle pathways. Among the cell cycle related genes, p21 was increased, while cyclin B1, cyclin E1, CDK2, CDK4, Myc, p27 and E2F1 were significantly decreased after garcinol treatment. The level of cell cycle M phase marker, pH3 Ser10, was also reduced by garcinol. Garcinol could regulate the Akt/c-Jun/ERK1/2 signaling pathways. Garcinol could regulate the protein-protein interaction network and the transcription factor interaction network, in which garcinol increased the transcription factor ATF3 and FOSB expression. In conclusion, garcinol could inhibit the proliferation of endometriosis cells in vitro. - Source: PubMed
Liu JingZhao BinYe YixinOu DeqiongGan XiaowenChen MiaojuanNing FenZhao MingguangZhang ZidiLiu HongyangHuang YanqingDu MiaomiaoLi LiQin ShuangSha XiaoyanLi PingZhang LindongLash Gendie ELu Qinsheng - Neuroinflammation involves all central nervous system cells, activated by factors such as genetics, trauma, and age. The activation of microglia signals the onset of neuroinflammation, with these resident macrophages playing a crucial role in defense and repair. Tumor microenvironments, comprising non-cancer cells and structures within tumor tissue, actively influence angiogenesis, drug resistance, and tumor progression. Gliomas, especially glioblastoma, display aggressive traits, with neuroinflammation playing a key role in shaping the complex environment that fuels rapid proliferation, invasiveness, and other aggressive features inherent to these brain tumors. Fungi from extreme environments, such as the halotolerant Penicillium flavigenum isolated from Tuz Lake, possess biotechnological potential. Despite increasing interest in fungal-derived compounds, studies investigating sorbicillin water fraction in glioblastoma models, particularly under co-culture conditions with microglia, remain limited. - Source: PubMed
Publication date: 2026/05/25
Engür-Öztürk SelinKaya-Tilki ElifÖzarda Mustafa GüçlüCantürk ZerrinDikmen Miriş - The reductive citric acid (rTCA) and reverse oxidative TCA (roTCA) cycles are used by autotrophic to fix dissolved inorganic carbon (DIC) at deep-sea and terrestrial hot springs, water treatment facilities, acid rock drainage, sediments and aquatic habitats including lake redoxclines, and more. rTCA and roTCA cycles operating in these contexts likely reflect selective pressures present in them. This genome survey examines the versions of the rTCA and roTCA cycles present in the completed genome sequences of several phyla of . The versions of these cycles correlate in part with the phyla to which the organisms belong, as well as with their habitats. There are many potential mechanisms for navigating the carboxylation of C compounds, which may diminish its metabolic cost. There are variations in electron donors for reductive steps in these cycles that could push them in a reductive direction. The predicted O sensitivity of several enzymes correlates with organisms' lifestyles. The presence of genes encoding DIC transporters and carbonic anhydrases correlates with habitat pH. Understanding how these cycles have responded to billions of years of selective pressure in a variety of habitats may provide insights into engineering autotrophic biochemistries to function well in a variety of industrial contexts. - Source: PubMed
Publication date: 2026/04/09
Scott Kathleen MWalsh Daniel PNapier LydiaBohdanovska MarynaConde QuinnMachado-Olavarria Ana CMadala SanjayMeade Samantha MNguyen Kim TNguyen TammyO'Malley DarynPalmer HaleyParbhoo Kavita JPfent AlexandraPhillips RileyBusato Victoria PontesRakhmonova MadinaRuiz DesireeSmall ErinSpence Shaniah SThakur Anjali - Epithelial-mesenchymal transition (EMT) is a fundamental biological process involved in normal functions such as embryonic development and tissue repair, as well as in pathological conditions including cancer progression, metastasis, and fibrosis. TGF-β1 is a key inducer of EMT, activating pathways that alter cell morphology and gene expression (e.g., downregulation of E-cadherin, upregulation of α-smooth muscle actin (α-SMA)). EMT contributes to fibrotic tissue remodeling in idiopathic pulmonary fibrosis (IPF), a chronic and progressive lung disease characterized by excessive scarring of lung tissue. To achieve a comprehensive evaluation of EMT in respiratory epithelial cells (A549), we employed the standard Operetta CLS platform to assess morphological changes and protein expression of key biomarkers (E-cadherin, α-SMA), alongside an advanced approach that monitored cellular dynamics using the xCELLigence Real-Time Cell Analysis (RTCA) system and quantified biomarker gene expression via RT-qPCR. In Operetta experiments, TGF-β1 reduced cell roundness and E-cadherin protein levels, while it increased cell length and α-SMA protein levels. In xCELLigence RTCA experiments, TGF-β1 reduced the cellular index and E-cadherin gene expression while increasing α-SMA expression. SB-525334 blocked all effects of TGF-β1, whereas nintedanib was more effective in counteracting the stimulatory effects of TGF-β1 on cell length and α-SMA. Interestingly, nintedanib, per se, evoked small but consistent effects opposite to those of TGF-β1. In conclusion, integrating these experimental approaches provides a powerful platform for detailed investigation of EMT mechanisms and for the identification of novel drug candidates that counteract EMT. - Source: PubMed
Publication date: 2026/05/05
Djeujo Francine MedjiofackNegrini Marco SolimanoFerri PietroMion AndreaRuscitti FrancescaPitozzi VanessaMalfacini DavideTrevisani MarcelloMarchini GessicaCalò Girolamo