Rat MIP-3a ELISA kit
- Known as:
- Rat MIP-3a Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- LF-EK50673
- Product Quantity:
- 1
- Category:
- Elisa Kits
- Supplier:
- Abfron
- Gene target:
- Rat MIP-3a ELISA kit
Related products to: Rat MIP-3a ELISA kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Sizeα - Calcitonin Gene Related Peptide, α - CGRP, rat'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit Related articles to: Rat MIP-3a ELISA kit
- Triple-negative breast cancer (TNBC) derives limited benefit from immune checkpoint blockade, largely owing to primary resistance shaped by the tumor immune microenvironment. Here, baseline transcriptomic profiling of a neoadjuvant chemoimmunotherapy cohort identified carbohydrate sulfotransferase 1 (CHST1) as a candidate resistance-associated gene. High CHST1 expression was associated with poor immunotherapy response and inferior clinical outcome across clinical datasets. Functionally, CHST1/Chst1 had minimal effects on tumor-cell-intrinsic proliferation, migration, or invasion in vitro, but promoted tumor growth in an immune context-dependent manner in vivo. Mechanistic analyses support a model in which CHST1 associates with NF-κB-repressing factor (NKRF) and limits its nuclear accumulation, a localization change associated with increased NF-κB-related CCL20 expression. Tumor-cell CCL20 perturbation and rescue experiments further supported a functional contribution of CCL20 to macrophage recruitment and M2-like remodeling. Pharmacologic CCR6 blockade enhanced the antitumor activity of anti-PD-1 therapy in syngeneic TNBC models. Finally, a CHST1-NKRF-CCL20 expression signature showed potential value for stratifying immunotherapy response. Collectively, this study supports a CHST1-NKRF-CCL20 regulatory model and identifies CCR6 blockade as a potential therapeutic strategy. - Source: PubMed
Publication date: 2026/08/24
Jiang Shu-HaoYing Xiao-HanWang Ruo-QingZhang QunChen LiShao Zhi-MingLi Jun-Jie - Multiple sclerosis (MS) is treated with branded or generic disease modifying therapies (DMTs), with increasing concern for the composition and quality of off-patent products. Our objective was to evaluate differences in disease-specific biomarkers, a potential indicator of suboptimal therapeutic exposure, between individuals treated with branded and generic DMTs. We compared biomarker variability in MS individuals (n = 1124) treated with generic or brand-name fumarates (diroximel fumarate, dimethyl fumarate (DMF)), fingolimod, and teriflunomide. In the generic DMF group, higher coefficients of variation (COV) for CXCL9, CCL20, and TNFSF13B were observed, with a paradoxically lower variability for CXCL13. Higher COVs for CXCL9 were observed with generic fingolimod and for CXCL9 and CXCL13 with generic teriflunomide when compared to brand. Additionally, all generic DMTs demonstrated higher multi-variable variability index values across 18 proteins associated with MS disease activity. Greater biomarker variability with generic formulations may reflect differences in therapeutic exposure and less consistent disease control. - Source: PubMed
Publication date: 2026/08/23
Okuda Darin TAnderson Benjamin JTaylor Sophia MJones-McCreary Morgan CBurgess Katy WWright Crystal MSantoyo Jose RSguigna Peter VStüve OlafTran Diem HLight David YMoog Tatum MPunnen Tom G - PIWILs are RNA-binding proteins whose role in ischemic stroke remains poorly defined. Here, we investigated the contribution of PIWILs to post-ischemic neuroinflammation by using a mouse model of 1 h transient middle cerebral artery occlusion (tMCAo), followed by 6 or 24 h of reperfusion. Brain tissues, blood, and peripheral organs were collected to assess PIWIL expression, inflammatory responses, and brain damage. PIWIL1 and PIWIL2 were significantly upregulated in the cortex and striatum at 24 h post-ischemia, with PIWIL2 also increased in blood and peripheral tissues. Immunofluorescence analyses revealed cell-type-specific localization of PIWILs in neurons, astrocytes, and endothelial cells. Notably, siRNA-mediated silencing of PIWIL2 significantly reduced infarct volume. PIWIL2 silencing also attenuated NF-κB-p65 and phospho-IκBα levels in the peri-infarct cortex but not in the striatum, indicating region-specific modulation of NF-κB signaling and differentially reprogrammed systemic chemokine profiles, with selective upregulation of CCL3, CCL5, and CXCL13 and downregulation of CCL2, CCL17, CCL20, and CXCL1. Mechanistically, PIWIL2 interacted with IKKα and promoted activation of the NF-κB pathway, leading to RelA- and RelB-dependent transcriptional regulation of pro-inflammatory chemokines. Together, these findings identify PIWIL2 as an upstream regulator of NF-κB-dependent neuroinflammation that exacerbates ischemic brain injury and suggest PIWIL2 as a promising therapeutic target targeting post-stroke inflammatory damage. - Source: PubMed
Publication date: 2026/07/24
Patil Rohan MaheshLaudati GiusyGuida NatasciaRuggiero SilviaDi Muraglia NoemiAnzilotti SerenellaLanthaler JulianCoppola LuigiFormisano LuigiAnnunziato LucioEsposito ElgaPignataro Giuseppe - Galectin-13 (GAL-13), also known as placental protein 13, is a lectin primarily studied in the context of pregnancy and immune regulation at the maternal-fetal interface. However, its potential roles in other tissues, including cancer, remain largely unknown. In this work, we provide new insights into the role of this protein while developing a comprehensive set of research tools to facilitate future studies. Our transcriptomic analyses reveal that GAL-13 reprograms gene expression in HepG2 liver cells, suggesting functions beyond placental physiology, potentially linked to inflammatory and tumor-related signaling. We generated a panel of 10 high-affinity nanobodies that enable detection, neutralization, and affinity-based purification of GAL-13, overcoming long-standing challenges in obtaining a soluble, functional form of the protein. Importantly, this large nanobody panel also provides an opportunity to map the functional epitopes of GAL-13, including those outside its classical carbohydrate-recognition domain (CRD). The purified GAL-13 retains its biological activities, notably inducing apoptosis in Jurkat T cells and stimulating CCL20 expression in HepG2 cells. This de novo induction of CCL20 was inhibited by our nanobodies, demonstrating their utility in dissecting GAL-13-mediated effects. Moreover, we observed extensive cross-reactivity of several nanobodies with GAL-16, reflecting the strong structural similarity between these two placental galectins and underscoring the need for careful validation of reagent specificity. Altogether, by integrating methodological innovation with functional analyses, our study provides essential molecular tools to advance GAL-13 research and reveals an emerging role for this understudied lectin in cancer biology. - Source: PubMed
Publication date: 2026/08/19
Fuselier CamilleJoly de Boissel Philippine GrangerNehmé RitaParé AlexFronton FannyAjarrag SammyBui Duong TFortier MarlèneDumoulin AlyssaKlassen John SDoucet NicolasChatenet DavidSt-Pierre Yves - BRAF-mutant colorectal cancer (CRC) is a clinically aggressive subtype arising from the serrated pathway and is associated with poor prognosis and therapy resistance. The mechanisms driving malignant transformation in microsatellite-stable (MSS) BRAF-mutant CRC remain incompletely understood. We aimed to define the role of WNT pathway activation in serrated CRC progression and tumor-immune interactions. - Source: PubMed
Publication date: 2026/08/18
Mastel ManuelGuiseris Martinez AitanaPozza UmbertoMeier JasminChiotakakos IoannisJaun SandraArtmann CarolinDiamante GabrieleGeorgakopoulos NikolaosAlbrecht PhilippPetersen YvonneReuter SaskiaSchmitt BarbaraGünther MichaelThiran AlexandraNurfauziah IstiffaGhezzi IanOuyang Kyanna SMilsom Michael DPuschhof JensReitsam Nic GBoonekamp Kim EBetge JohannesOrmanns SteffenBoutros MichaelJackstadt Rene