Goat DEFB2 ELISA
- Known as:
- Goat DEFB2 Enzyme-linked immunosorbent assay test
- Catalog number:
- kt-52868
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Goat DEFB2 ELISA
Ask about this productRelated genes to: Goat DEFB2 ELISA
- Gene:
- DEFB4A NIH gene
- Name:
- defensin beta 4A
- Previous symbol:
- DEFB102, DEFB2, DEFB4
- Synonyms:
- SAP1, HBD-2, DEFB-2
- Chromosome:
- 8p23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-28
- Date modifiied:
- 2017-04-21
Related products to: Goat DEFB2 ELISA
Related articles to: Goat DEFB2 ELISA
- To evaluate whether systemic supplementation with L. rhamnosus LR-04 and L. acidophilus LA-14 modulates the expression of TLR4, hBD-2, and hBD-3 in a rat model of experimental apical periodontitis (AP), and to assess potential histopathological alterations in the liver. - Source: PubMed
Publication date: 2026/05/22
Cosme-Silva LeopoldoDal-Fabbro RenanTenorio Gabrielle Cabral Melville de SouzaSilva José Alex daErvolino EdilsonCapalbo Letícia CabreraGomes-Filho João Eduardo - Recent studies have shown that zinc finger protein 750 (ZNF750), a key tumor suppressor in esophageal squamous cell carcinoma (ESCC), is associated with defective epithelial differentiation. At the same time, mucosal immune dysfunction is increasingly recognized as a key factor in the development of ESCC. Exploring the role of ZNF750 in regulating the mucosal immune microenvironment provides a new perspective on its tumor suppression mechanism. - Source: PubMed
Publication date: 2026/04/14
Zhou TongFan JingyueWang MengyaoCheng CaixiaYuan FajiaLi JunliWan HuiliCui DongdongMiao YaruBi Yanghui - Chronic inflammatory skin diseases such as psoriasis and hidradenitis suppurativa are driven by cytokines, including IL-17A and TNF. Although biologics targeting these cytokines have transformed therapy, the transcriptional contributions of individual skin-resident cell types remain unclear, and dermal fibroblasts have been largely overlooked compared with keratinocytes. To address this, we compared the transcriptional responses of primary human dermal fibroblasts and keratinocytes following in vitro stimulation with IL-17A, TNF, or both, using bulk RNA sequencing and Western blotting. Dermal fibroblasts mounted a stronger and broader proinflammatory response than keratinocytes. This was particularly evident in response to TNF and combined TNF/IL-17A stimulation, with enrichment for immune signalling and chemotaxis pathways and robust induction of chemokine genes, including CCL20, CXCL8, and IL6. Keratinocytes primarily upregulated genes associated with epithelial differentiation, barrier function, and protein regulation, including IL36G, S100A7A, and DEFB4A. The heightened fibroblast responsiveness correlated with increased TNF sensitivity and substantially higher TNFR2 (TNFRSF1B) expression and signalling compared with keratinocytes, suggesting a fibroblast-specific mechanism amplifying inflammatory responses. These findings challenge the keratinocyte-centric view of skin inflammation and identify dermal fibroblasts as active contributors and potential therapeutic targets in TNF- and Th17-driven skin diseases. - Source: PubMed
Svraka LejlaAbdallah Hakim BenBertelsen TrineVestergaard ChristianJohansen Claus - The aim of this study was to compare the presence of human ß defensin-2 (hBD-2) in GCF and microbial flora in the subgingival plaque, among the patients treated with fixed orthodontic braces and aligners. - Source: PubMed
Publication date: 2026/01/23
Sharma AditiKumar MukeshYadav EktaKumar SumitGoyal ManishRastogi Sonal - Cytokine storm is a critical driver of acute respiratory distress syndrome and multiple organ failure. Human β-defensin 2 (HBD-2) is the first inducible defensin discovered in human body. Defensin can resist pathogenic microorganisms invading the body through direct bactericidal effect and also modulates acquired immune response. Albumin exhibits immunomodulatory properties and can reduce the level of inflammatory cytokines to improve the systemic inflammatory response. We previously engineered a recombinant fusion protein, DF-HSA, comprising two HBD-2 molecules linked to human serum albumin. Here, we evaluated its effect on cytokine storm using a lipopolysaccharide (LPS)-induced cytokine storm murine model (BALB/c athymic mice, female). DF-HSA reduced the mortality in cytokine storm murine model and prolonged the retention time of HBD-2 in the body. A Luminex assay showed that DF-HSA reduced the production of multiple inflammatory cytokines in cytokine storm murine model. Evans blue staining showed that DF-HSA reduced vascular leakage. Transmission electron microscopy showed that DF-HSA reduced the lung injury of cytokine storm mice. The pathological results showed that DF-HSA alleviated the lung and small intestine damage of cytokine storm mice. In summary, DF-HSA effectively inhibits cytokine storms and ameliorates associated tissue damage. - Source: PubMed
Publication date: 2026/01/21
Du YiboYu ZhuojunSheng WeijinLi YiHou LeiZheng YanboLiu XiujunZhen Yongsu