Human Cellexp Human Recombinant IL-29 proteins
- Known as:
- Human Cellexp Human Recombinant Interleukin-29 proteins
- Catalog number:
- 6473-10
- Product Quantity:
- 10
- Category:
- Proteins
- Supplier:
- Biovis
- Gene target:
- Human Cellexp Recombinant IL-29 proteins
Related genes to: Human Cellexp Human Recombinant IL-29 proteins
- Gene:
- IFNL1 NIH gene
- Name:
- interferon lambda 1
- Previous symbol:
- IL29
- Synonyms:
- IL-29
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-02
- Date modifiied:
- 2016-10-11
Related products to: Human Cellexp Human Recombinant IL-29 proteins
Related articles to: Human Cellexp Human Recombinant IL-29 proteins
- Neuroinflammation of the central nervous system (CNS) triggers long-lasting neurodegenerative changes associated with the development of neurogenic dysfunction in the pelvic organs. We previously described the symptoms of voiding dysfunction in a mouse model of multiple sclerosis (MS) induced by a coronaviral infection with mouse hepatitis virus (MHV). The aim of the current study was to identify immune, inflammatory and neuronal changes in the lumbosacral (L6-S2) dorsal root ganglia (DRG) innervating the lower urinary tract (LUT) after severe neurodegeneration in the CNS. - Source: PubMed
Publication date: 2025/06/15
Foley Taylor CYesupatham Sathish KMiller-Dawson JakeMalykhina Anna P - Cytokine therapy, a non-antigen-specific strategy, has led to several FDA-approved drugs. Given the role of dysregulated cytokine expression in diseases such as COVID-19, accurate quantification is critical in both clinical and research settings. While antibody-based assays offer high sensitivity, their reliance on specific antibodies limits multiplexing and increases analytical complexity. Conversely, mass spectrometry methods like multiplexed reaction monitoring provide higher throughput but lack the sensitivity to detect physiological cytokine levels and the resolution to distinguish structural isomers. Thus, a new MS-based approach is needed that integrates high sensitivity with the ability to resolve structurally similar cytokines. We developed an ion mobility-mass spectrometry (IM-MS)-based parallel reaction monitoring (PRM) method to establish the first Cytokine Ion Mobility Peptide (CIMP) databank and enable high-throughput cytokine profiling in serum samples from COVID-19 patients. By introducing ion mobility as an additional gas-phase separation dimension alongside liquid chromatography, the method enhances analyte resolution based on structural differences, facilitating the separation of isomers within the ion mobility trap. The incorporation of ion mobility as a complementary separation parameter enables the distinction of homologous cytokines and structural isomers (e.g., IFNA1/IFNA2, IFNL1/IFNL3, and peptide isomers), which remains challenging for conventional antibody-based assays. The method achieved a limit of detection of 62.9 fmol/L and a limit of quantification of 210 fmol/L across 31 cytokines, demonstrating greater sensitivity than traditional multiple reaction monitoring (MRM) approaches and enabling quantification at physiological concentration levels, assuming comparable background signal across platforms. The IM-MS-PRM method offers a multiplexed, high-throughput, and adaptable platform that eliminates the need for multiple assays while delivering excellent reproducibility. It enables accurate and sensitive cytokine quantification from minimal volumes of COVID-19 patient serum. Combined with the CIMP databank, this approach allows precise differentiation between early and late severe COVID-19 cases, supporting improved diagnostic and therapeutic decision-making. - Source: PubMed
Publication date: 2025/05/20
Yan LingYuan ChenruiZhou RunhouZhong LiKai-Wang To KelvinLiu NaDiao XinXie GuangshanZhao HongzhiWu HaijiangZhu LinChen ZhiweiCai Zongwei - Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies and most often diagnosed at an advanced stage. Identification of markers for the early diagnosis of PDAC is crucial. In this study, we aimed to identify novel mRNA biomarkers for diagnosing PDAC, focusing on early-stage tumorigenesis and associated immunological changes. - Source: PubMed
Publication date: 2025/04/23
Lee Jong-ChanKang Sung WonSim Eun-JinBae Jin-SikKoo Seong-MoByoun Mun-SubKwon SerinHong SeoiKim YunjiYoun YunaJung KwangrokKim JaihwanJeong Hyoung HwaKim JihieHwang Jin-Hyeok - In this study, we used a three-dimensional airway "organ tissue equivalent" (OTE) model at an air-liquid interface (ALI) to mimic human airways. We investigated the effects of three viruses (Influenza A virus (IAV), Human metapneumovirus (MPV), and Parainfluenza virus type 3 (PIV3) on this model, incorporating various control conditions for data integrity. Our primary objective was to assess gene expression using the NanoString platform in OTE models infected with these viruses at 24- and 72-hour intervals, focusing on 773 specific genes. To enhance the comprehensiveness of our analysis, we introduced a novel algorithm, namely MAS (Magnitude-Altitude Score). This innovative approach uniquely combines biological significance, as indicated by fold changes in gene expression, with statistical rigor, as represented by adjusted p-values. By incorporating both dimensions, MAS ensures that the genes identified as differentially expressed are not mere statistical artifacts but hold genuine biological relevance, providing a more holistic understanding of the airway tissue response to viral infections. Our results unveiled distinct patterns of gene expression in response to viral infections. At 24 hours post-IAV infection, a robust interferon-stimulated gene (ISG) response was evident, marked by the upregulation of key genes including IFIT2, RSAD2, IFIT3, IFNL1, IFIT1, IFNB1, ISG15, OAS2, OASL, and MX1, collectively highlighting a formidable antiviral defense. MPV infection at the same time point displayed a dual innate and adaptive immune response, with highly expressed ISGs, immune cell recruitment signaled by CXCL10, and early adaptive immune engagement indicated by TXK and CD79A. In contrast, PIV3 infection at 24 hours triggered a transcriptional response dominated by ISGs, active immune cell recruitment through CXCL10, and inflammation modulation through OSM. The picture evolved at 72 hours post-infection. For IAV, ISGs and immune responses persisted, suggesting a sustained impact. MPV infection at this time point showed a shift towards IL17A and genes related to cellular signaling and immune responses, indicating adaptation to the viral challenge over time. In the case of PIV3, the transcriptional response remained interferon-centric, indicating a mature antiviral state. Our analysis underscored the pivotal role of ISGs across all infections and time points, emphasizing their universal significance in antiviral defense. Temporal shifts in gene expression indicative of adaptation and fine-tuning of the immune response. Additionally, the identification of shared and unique genes unveiled host-specific responses to specific pathogens. IAV exerted a sustained impact on genes from the initial 24 hours, while PIV3 displayed a delayed yet substantial genomic response, suggestive of a gradual and nuanced strategy. - Source: PubMed
Publication date: 2024/11/26
Rezapour MostafaWalker Stephen JOrnelles David ANiazi Muhammad Khalid KhanMcNutt Patrick MAtala AnthonyGurcan Metin Nafi - Janus kinases (JAKs) bind to class I and II cytokine receptors, activating signaling and regulating gene transcription through signal transducer and activator of transcription (STAT) proteins. Type I interferons (IFNs) require the JAK members TYK2 and JAK1, which bind to the receptor subunits IFNAR1 and IFNAR2, respectively. We investigated the role of JAKs in regulating IFNAR signaling activity. Synthetic IFNARs in which the extracellular domains of IFNAR1 and IFNAR2 are replaced with nanobodies had near-native type I IFN signaling, whereas the homomeric variant of IFNAR2 initiated much weaker signaling, despite harboring docking sites for JAKs and STATs. Cells with JAK1 and TYK2 knockout (KO) showed residual signaling, suggesting partial complementation by the remaining JAKs, particularly when they were overexpressed. Live-cell micropatterning experiments confirmed the promiscuous binding of JAK1, JAK2, and TYK2 to IFNAR1 and IFNAR2, and their recruitment correlated with their relative cellular abundances. However, each JAK had a different efficacy in inducing cross-phosphorylation and downstream signaling. JAK binding was also promiscuous for other cytokine receptors, including IFN-L1, IL-10Rβ, TPOR, and GHR, but not for EPOR, which activated different downstream signaling pathways. These findings suggest that competitive binding of JAKs to cytokine receptors together with the varying absolute and relative abundances of the JAKs in different cell types can account for the cell type-dependent signaling pleiotropy of cytokine receptors. - Source: PubMed
Publication date: 2024/11/19
Zoler EyalMeyer ThomasBellón Junel SotolongoMönnig MiaSun BoyuePiehler JacobSchreiber Gideon