BD-3, Mouse Protein
- Known as:
- BD-3, Mouse Protein
- Catalog number:
- z02895-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- BD-3 Mouse Protein
Related genes to: BD-3, Mouse Protein
- Gene:
- CTU1 NIH gene
- Name:
- cytosolic thiouridylase subunit 1
- Previous symbol:
- ATPBD3
- Synonyms:
- MGC17332, NCS6
- Chromosome:
- 19q13.41
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-24
- Date modifiied:
- 2014-11-19
- Gene:
- DEFB103A NIH gene
- Name:
- defensin beta 103A
- Previous symbol:
- DEFB3, DEFB103
- Synonyms:
- HBD-3, HBP-3, HBD3, HBP3, DEFB-3
- Chromosome:
- 8p23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-25
- Date modifiied:
- 2017-04-21
- Gene:
- MBD3L1 NIH gene
- Name:
- methyl-CpG binding domain protein 3 like 1
- Previous symbol:
- MBD3L
- Synonyms:
- -
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-21
- Date modifiied:
- 2016-03-15
- Gene:
- NACC1 NIH gene
- Name:
- nucleus accumbens associated 1
- Previous symbol:
- BTBD14B
- Synonyms:
- NAC1, NAC-1, BEND8, BTBD30
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-15
- Date modifiied:
- 2018-06-04
- Gene:
- NACC2 NIH gene
- Name:
- NACC family member 2
- Previous symbol:
- BTBD14A
- Synonyms:
- MGC23427, BEND9, BTBD31
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-15
- Date modifiied:
- 2016-02-12
Related products to: BD-3, Mouse Protein
Related articles to: BD-3, Mouse Protein
- Psoriasis is a chronic inflammatory autoimmune skin disease for which no standardised and reliable molecular biomarkers of disease course or activity are currently available. Here, we aimed to identify serum biomarkers of psoriasis. Serum samples from 40 patients with psoriasis and 40 healthy volunteers were analysed using ELISA and Proximity Extension Assay proteomics. ELISA revealed significantly increased serum levels of AGO2 and APOA1 in psoriatic patients versus controls, with a strong association between APOA1 and psoriasis (OR = 20.72, 95% CI of 4.57-93.87, = 0.000137). Targeted serum proteomics additionally identified 35 differentially expressed proteins, including well-known psoriasis drivers (e.g., top upregulated IL17A and SERPINB4). The most downregulated was adrenomedullin (ADM, FC = -10.12). For 14 altered proteins, no previous direct associations with psoriasis were reported. Among them, DEFB103A_DEFB103B and DSG3 showed the best discrimination between psoriasis and control samples, while SERPINB4 correlated with psoriasis severity. APOA1, DEFB103A_DEFB103B, and DSG3 emerge as novel candidate circulating psoriasis biomarkers, and SERPINB4 as a biomarker of psoriasis severity. The functional role of DSG3 and other newly identified proteins (ACRV1, HAO1, ADH4, GPD1, GFER, PTGES2, DSG3, AFAP1L1, GALNT3, RASGRP2, MAP2K6, LXN, NBEAL2, and VPS54) in psoriasis requires further studies. - Source: PubMed
Publication date: 2026/06/26
Dźwigała MonikaSys DorotaŻycka-Krzesińska JoannaRybicka BeataPopławski PiotrWalecka-Herniczek IrenaPiekiełko-Witkowska AgnieszkaBogusławska Joanna - Candida auris (C. auris) is an emerging fungal pathogen with a remarkable ability to persist on human skin, but how structural skin cells respond to colonization is unclear. We used ex vivo human skin models, together with primary keratinocytes and fibroblasts, to characterize epithelial and stromal responses to C. auris compared with Candida albicans. C. auris formed biofilms and induced a wound-model-dependent pattern of cytokine secretion dominated by IL-1β and IL-6, yet caused minimal epithelial damage and modest reductions in leukocyte viability. RNA sequencing revealed complementary but cell-type-specific responses. Keratinocytes and fibroblasts both amplified a pro-inflammatory IL-6/CXCL8 response, while keratinocytes additionally upregulated antimicrobial genes such as RNASE7, TSLP, DEFB103A (encoding hBD-3), and the neutrophil-recruiting chemokines CXCL2 and CXCL3. Fibroblasts further induced CCL28, supporting T cell recruitment, alongside transcriptional programs associated with tissue remodeling. Recombinant RNase 7 and short form TSLP directly inhibited C. auris growth in vitro in a dose-dependent manner. Together, these findings identify keratinocytes as epithelial sentinels that integrate inflammatory and antimicrobial defenses against skin-tropic C. auris and suggest that fibroblast-driven cytokine amplification and especially antimicrobial peptides from within the skin barrier may provide therapeutic targets to limit C. auris skin colonization. - Source: PubMed
Publication date: 2026/06/26
Seiser SaskiaBrezovec HelenaPenninger PhilippPhan-Canh TrinhMoser DorisAssen Frank PAyub TanyaRademacher FranziskaGläser RegineCerbu DianaKienzl PhilipFreystätter ChristianHarder JürgenKuchler KarlElbe-Bürger Adelheid - Periodontitis arises from dysregulated host-microbe interactions, driving progressive tissue degradation. Matrix metalloproteinases (MMPs) and antimicrobial peptides like human β-defensin-3 (HBD-3) serve as pivotal biomarkers in periodontal pathogenesis. This study quantified gingival mRNA expression of MMP-1, MMP-9, and HBD-3 across health, gingivitis, and chronic periodontitis to assess their diagnostic and therapeutic relevance. Gingival biopsies were collected from 23 healthy controls (probing depth [PD] < 3 mm), 18 gingivitis patients, and 19 moderate-to-severe chronic periodontitis patients (PD > 5 mm). RNA extraction utilized FavorPrep™ kits, followed by cDNA synthesis and quantitative real-time PCR (qRT-PCR) with GAPDH normalization. Gene expression was calculated via the 2 method. Statistical analyses included Kruskal-Wallis, Games-Howell post-hoc, and Spearman's correlation (SPSS v20.0; α = 0.05). Chronic periodontitis exhibited significantly elevated MMP-1 expression (31.00 ± 7.1) versus healthy controls (21.26 ± 4.3; p = 0.001), with overall intergroup differences (p = 0.001). HBD-3 expression demonstrated significant variation across groups (p = 0.045), peaking in periodontitis (38.22 ± 9.6), though pairwise comparisons were non-significant. MMP-9 expression showed no intergroup differences (p = 0.688). Critically, HBD-3 expression correlated positively with clinical attachment loss (CAL) in periodontitis (ρ = 0.497; p = 0.030). MMP-1 overexpression in chronic periodontitis underscores its role as a primary mediator of tissue destruction and potential diagnostic biomarker. The HBD-3/CAL correlation suggests compensatory antimicrobial responses during disease progression. These findings nominate MMP-1 as a promising therapeutic target for mitigating periodontal breakdown. Longitudinal validation is warranted for clinical translation. - Source: PubMed
Publication date: 2026/06/10
Ramezani MahyaBazargan MahsaSattari Mandana - The expression of hBD-3 and quantification of immune and inflammatory response cells (non-degranulated and degranulated mast cells, mature and immature plasmacytoid dendritic cells, mature and immature Tregs, T lymphocytes, cytotoxic T lymphocytes, and B lymphocytes) were evaluated in the radicular cysts (epithelium/capsule) of primary and permanent teeth. The relationship between the size of the radiographic lesion and expression of hBD-3 was also evaluated. Radicular cysts were subjected to immunohistochemical analysis to quantify the immune and inflammatory response cells and to evaluate hBD-3 staining and its relationship with radiographic lesion size. The results were analyzed using the D'Agostino & Pearson, Mann-Whitney, t-test, Kruskal-Wallis, and Dunn's post-tests (5%). hBD-3 was expressed in cysts of primary and permanent teeth. In primary teeth, hBD-3 expression was higher in small lesions than in large lesions (p < 0.05). All the evaluated cell types were detected in all radicular cysts. Cysts of primary teeth showed a higher expression of plasmacytoid dendritic cells, B lymphocytes, and T lymphocytes (p < 0.05), whereas those of permanent teeth showed a higher expression of T lymphocytes, immature plasmacytoid dendritic cells, cytotoxic T lymphocytes, and B lymphocytes (p < 0.05). hBD-3 was expressed in the epithelium/capsule of primary and permanent teeth radicular cysts. Immature plasmacytoid dendritic cells were the predominant cells in radicular cysts of primary teeth, whereas T lymphocytes were more abundant in permanent teeth. - Source: PubMed
Publication date: 2026/05/18
Bertasso Amanda SilvaLéon Jorge EsquicheJorge Olívia SantanaSilva Raquel Assed Bezerra daLucisano Marília PacíficoQueiroz Alexandra Mussolino deSilva Evânio Vilela daSilva Léa Assed Bezerra daNelson-Filho Paulo - Human β defensin type 3 (hBD-3) is recognized as one of the most intriguing antimicrobial peptides (AMPs) that holds the promise of solving drug resistance issues. hBD-3 can function (disruption of membrane integrity) in high salt environments, where most other AMPs fail. However, its functional mechanism at the molecular level remains elusive. To characterize its structure and dynamics during membrane crossing, long-time (a total of 57.0 μs) all-atom molecular dynamics simulations were conducted on hBD-3 monomers and dimers in both wild-type and analog (in which all three disulfide bonds are broken) forms that are embedded in four types of lipid membranes. Trajectory analysis was carried out using a statistical method─conformational dynamics analysis to calculate contact matrices and then principal component analysis (PCA) and linear discriminant analysis (LDA), in order to discern structural changes upon various physical and chemical perturbations. The result shows that the major collective coordinate primarily distinguishes between the wild-type and analog forms of hBD-3. For the hBD-3 monomer, the analog undergoes significant structural loss due to the lack of stabilizing disulfide bonds; salt exerts a nearly consistent effect on the contact degrees of freedom of the protein, whereas changes in lipid membrane composition have an insignificant effect. For the hBD-3 dimer, no consistent relationship between structure and salt concentration is indicated, and variations in the chemical composition of model bacterial membranes have a limited effect on its dynamics. These results suggest that the wild-type and analog forms of hBD-3 may employ different mechanisms when crossing bacterial membranes. The effect of salt on hBD-3 dynamics can be mitigated by the high net charge density of the protein. Additionally, the hBD-3 dimer can distinguish between model Gram-positive and Gram-negative membranes, whereas the monomer cannot. Overall, these findings provide unique insights into the structure, dynamics, and membrane-disrupting mechanism of hBD-3. - Source: PubMed
Publication date: 2026/04/30
Penfield JacksonShen TongyeRucker George RZhang Liqun