BD-3, Human Protein
- Known as:
- BD-3, Human Protein
- Catalog number:
- z02756-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- BD-3 Human Protein
Related genes to: BD-3, Human 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, Human Protein
Related articles to: BD-3, Human Protein
- 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 - 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 - Metastatic castration resistance prostate cancer (mCRPC) is the advanced state of prostate cancer where majority of patients succumb to ineffective treatment perspectives like androgen deprivation alongside salvage therapies. mCRPC is predominantly orchestrated by androgen receptor (AR)-dependent gene expression. On the account of AR being a "potentially attractive immunological target", an immunoinformatics pipeline was built to identify and screen mutation-independent, broad MHC covering, potential antigenic, non-allergenic, non-toxic and soluble epitopes. The filtered epitopes required assembly into a unified construct with interconnecting linkers and adjuvant and further TLR3-docking. We chose TLR3 because of its pro-apoptotic activity in prostate cancer, to check active immune response by the vaccine. Our study was not confined to the use of a conventional adjuvant like human beta defensin-3 but it extended to the scope of utilization of a protein-based TLR3-specific agonist as an adjuvant for assembling the second composite construct. Our path was guided by the discovery of TLR3-specific agonist minibinder 8.6 (a small, hyperstable protein) by Adams et al. An extensively comparative molecular dynamics study of the free state and bound states of the two constructs unveiled a more stable interaction, complex stability and immune response attributing to the specificity of the minibinder-based construct towards TLR3. Our work circumscribes a multi-headed approach beginning with peptide subunit multi-epitope vaccine construct design for mitigating mCRPC; secondarily, endorsing the advocacy of TLR3-agonizing minibinders as vaccine adjuvants for enhanced immunity and finally posing a comparative framework of minibinder 8.6 over HBD3, as a more potential adjuvant, apprehending wet-lab proof. - Source: PubMed
Publication date: 2026/02/20
Paul IshaniRay SoumyadeepTewari MuskanSaha MowmitaRay Sujay - Human β-defensin 3 (hBD-3) is a multifunctional host defense peptide with exceptional antimicrobial, immunomodulatory, and tissue-repair properties. Beyond its potent activity against gram-positive and gram-negative bacteria, fungi, and selected viruses, hBD-3 plays a central role in epithelial barrier integrity, chemotactic signaling, and wound healing. Its expression is tightly regulated by an intricate network of pattern-recognition receptors, inflammatory cytokines, growth factors, vitamins, and endocrine mediators. Emerging evidence indicates that hBD-3 functions as a transcriptional convergence point, integrating signals from NF-κB, AP-1, STATs, and nuclear receptors to coordinate antimicrobial and immune responses. Notably, glucocorticoids selectively modulate hBD-3 in ways that differ from other defensins, suggesting unique regulatory mechanisms within immune-endocrine environments. hBD-3 also contributes to angiogenesis, fibroblast activation, and keratinocyte migration, supporting its role in tissue repair and chronic wound management, including in diabetic microenvironments. Recent promoter analyses further reveal potential non-classical regulatory elements that expand current understanding of hBD-3 transcriptional control. Despite these advances, therapeutic manipulation of hBD-3 remains controversial due to its context dependent immunologic effects, potential oncogenic implications, and delivery challenges. This review synthesizes current knowledge on hBD-3 biology, regulation, and function, and discusses the opportunities and limitations for its therapeutic application in infectious and inflammatory diseases. - Source: PubMed
Publication date: 2026/02/16
Jacobo-Delgado Yolanda MHuerta-Elías Jaime EduardoCabral-Venegas ValeriaGarcía-Hernández MarianaRivas-Santiago Bruno