EPCAM_RAT Epcam ELISA tesk kit
- Known as:
- EPCAM_RAT Epcam Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16502
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- EPCAM_RAT Epcam ELISA tesk kit
Related genes to: EPCAM_RAT Epcam ELISA tesk kit
- Gene:
- EPCAM NIH gene
- Name:
- epithelial cell adhesion molecule
- Previous symbol:
- M4S1, MIC18, TACSTD1
- Synonyms:
- Ly74, TROP1, GA733-2, EGP34, EGP40, EGP-2, KSA, CD326, Ep-CAM, HEA125, KS1/4, MK-1, MH99, MOC31, 323/A3, 17-1A, TACST-1, CO-17A, ESA
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-10-02
- Date modifiied:
- 2019-04-23
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- This study examined the ability of established brain biomarkers, glial fibrillary acid protein (GFAP), neuro-filament light chain (NFL), ubiquitin carboxy hydrolase-L1(UCH-L1), tau, and phosphorylated tau (p-tau), and novel biomarkers from blood collected sub-acutely after concussion to determine prediction of persisting post-concussion symptoms (PPCS) beyond 3 months. We hypothesized that a combination of established and novel proteins would predict high PPCS burden. - Source: PubMed
Publication date: 2026/08/14
Gill JessicaLim ArumDennis EmilyBickart KevinYun SijungYun JosephAlice JohnMiles ChristopherChrisman Sara PdVaughan ChristopherCullum C MunroCook Lawrence JGioia GerardRivara Frederick PGiza Christopher CBazarian Jeffrey J - Tumor cells exhibit a hyper-glycolytic phenotype, resulting in massive lactic acid (LA) production that acidifies the tumor microenvironment (TME) and fosters immunosuppression. Current lactate-targeted therapies often lack synergistic dual-directional regulation. Herein, we engineer an exosomal nanoplatform, PpIX/siRNA@EXO-LOD, to simultaneously disrupt intra- and extracellular LA homeostasis, thereby enabling synergistic metabolic and photodynamic therapy (PDT). The system integrates three key components: protoporphyrin IX (PpIX) for PDT, siRNA targeting monocarboxylate transporter 4 (MCT4) for intracellular metabolic interference, and surface-displayed lactate oxidase (LOD) for extracellular catalytic starvation. Upon epithelial cell adhesion molecule (EpCAM)-mediated targeting, the nanovesicle triggers a cascade of synergistic effects. Crucially, siRNA-mediated silencing of MCT4 induces lethal intracellular acidosis, leading to significant intracellular HO accumulation. This elevated HO level acts as a booster for PpIX-generated reactive oxygen species (ROS) upon laser irradiation, creating an amplified oxidative stress burst that overwhelms tumor cell defenses. Concurrently, surface-anchored LOD consumes extracellular LA, alleviates lactate-induced immunosuppression. In vivo studies demonstrate that this dual-regulation strategy effectively inhibits tumor growth, downregulates metastasis-related factors (amphiregulin (AREG), ATP-binding cassette sub-family B member 1 (ABCB1)), and reprograms the TME from an immunosuppressive state to an immunologically active state. This work presents a precision nanomedicine strategy that leverages the interplay between metabolic modulation and photodynamic amplification for enhanced cancer treatment. - Source: PubMed
Publication date: 2026/08/28
Zhou SisiCao YuWang XianbiaoLiu Songqin - Breast cancer (BC) is the most commonly diagnosed malignancy in women, with triple-negative breast cancer (TNBC) representing the most aggressive subtype that is associated with poor clinical outcomes. Identifying novel biomarkers or therapeutic targets is therefore of great importance. Nectin cell adhesion molecule-2 (NECTIN2) is an immunoglobulin-like glycoprotein involved in cell adhesion and immune regulation that is highly expressed in several cancers but its role in the progression of BC is unclear. Using publicly available data sets, we found that NECTIN2 expression is elevated in BC compared to normal tissues and is associated with poorer recurrence-free survival in TNBC patients. Among TNBC cell lines, MDA-MB-231 cells exhibited the highest expression of NECTIN2 at gene and protein levels, consistent with a more aggressive phenotype. To investigate its functional role, we silenced NECTIN2 in MDA-MB-231 and MDA-MB-468 cells. Relative cell viability was modestly reduced in NECTIN2-depleted MDA-MB-231 cells at later time points, but no significant changes were observed in MDA-MB-468 cells. Interestingly, NECTIN2 depletion significantly reduced migration and invasion in MDA-MB-231 cells, but not in MDA-MB-468 cells. Given this cell line-specific effect, subsequent mechanistic investigations focused on the MDA-MB-231 model. Gene expression profiling suggested a reduction in LIMK1, a regulator of cytoskeletal dynamics and cell motility, following NECTIN2 depletion. Furthermore, ectopic expression of LIMK1 in NECTIN2-deficient MDA-MB-231 cells partially restored migratory capacity and was associated with partial epithelial-mesenchymal transition (EMT)-like changes, including a decrease in E-cadherin and ZO-1, and a higher level of fibronectin and Slug. Collectively, these findings suggest that NECTIN2 contributes to migratory and invasive phenotypes in MDA-MB-231 cells, potentially through LIMK1-associated cytoskeletal remodeling and EMT-related marker changes. However, this mechanism requires further investigation because it appears to be context-dependent and may not be universally applicable across TNBC subtypes. - Source: PubMed
Publication date: 2026/08/28
Klaihmon PhatchanatMuangtate PattaratornThongphayong SudaratSaetan PuretatChanthateyanonth SupasornThuwajit ChanitraIssargrisil SurapolPhannasil Phatchariya - Accurate cell segmentation in high-plex imaging remains challenging because no single biomarker channel captures the full structural diversity of cells, and many practical segmentation backbones are trained on a small, fixed-channel input convention. In this work, we study channel complementarity under the standard three-channel input convention of Cellpose-SAM using a systematic fused-evaluation framework with combination-specific operating-point calibration. On a primary healthy salivary gland region, we show that multi-channel gains are selective but meaningful: the strongest pair improves over the single-channel baseline, and the strongest triplet further improves over the best pair. On a second held-out diseased tissue region, we identify strong auxiliary combinations centered on EPCAM, and the triplet combination (DAPI, EPCAM, CD31) remains beneficial across both regions. To test whether these gains are artifacts of conservative post-processing, we additionally perform controlled-merge sensitivity analysis across the merge hyperparameter grid. These analyses do not reproduce the fused triplet gains, suggesting that the observed improvements arise from joint multi-channel inference rather than from the merge heuristic itself. Together, our results show that higher-order channel complementarity is real but selective under the standard three-channel input convention of Cellpose-SAM, and that reproducible triplet benefits can be identified through systematic search. - Source: PubMed
Publication date: 2026/07/28
Ma HaotianLin YiGodschall ElizabethMatuck BrunoByrd Kevin MatthewPeng YifanLiu Jinze - Despite advances in lupus nephritis (LN) management, its heterogenous nature poses challenges in predicting treatment response. Multiplexed spatial proteomics offers a potential solution to dissect the heterogeneity of treatment response in LN. - Source: PubMed
Publication date: 2026/08/12
Tay Sen HeeLouis Sam Titus Anto Sam CrossleeMaruvada VinaikaLee Bernett Teck KwongChan Gek CherWong Alvin Seng CheongCho JiacaiThamboo Thomas PaulrajMohan Chandra