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Human Polyclonal DEFB103A Primary Antibody for ELISA, WB - ABIN2473299
Ulick, Tedde, Mantero: Pathogenesis of the type 2 variant of the syndrome of apparent mineralocorticoid excess. in The Journal of clinical endocrinology and metabolism 1990
Show all 2 Pubmed References
this study shows that hBD3 amplifies the response to bacterial DNA in both mouse and human immune cells in a TLR9-dependent manner
the role of DEFB103 gene copy number variation (CNV) in ankylosing spondylitis (AS) susceptibility, was investigated.
It may be concluded hepatitis B virus up-regulates HBD-3 and A3G expression in vivo and in vitro in placental trophoblast and lack of this up-regulation is possibly associated with intrauterine transmission of hepatitis B.
The encoded peptide displays antimicrobial activity against S. aureus and E. faecium.
these observations suggest that there may be an interracial difference in DEFB4/103A copy numbers between admixed populations and a relationship between DEFB1 single nucleotide polymorphisms and DEFB4/103A copy number variation
Human beta-defensin 3 peptide is increased and redistributed in Crohn's ileitis
study demonstrates that HBD2 and 3 activate plasmacytoid dendritic cells by enhancing the intracellular uptake of CpG and self DNA and promote DNA-induced IFN-alpha production in a TLR9-dependent manner
Mapping of key residues in the interaction between human Beta-defensin 3 and CXCR4 reveals key defensin motifs involved in protein binding.
These results suggest an important role for hBD3 in inducing dendritic cell activation, migration, and polarization.
Using a large, unique cohort of pediatric CA-SAB, this study found no significant association between DEFB1 genetic variation or DEFB4/DEFB103 gene copy number and susceptibility for Staphylococcus aureus bacteremia
Human beta-defensin 3 exhibits further functions than antimicrobial peptide activity in cultured bone cells, including stimulation of proliferation and differentiation.
Data show that high-glucose conditions inhibited the BD3 expression of epidermal keratinocytes.
hBD-1 might function as a tumor suppressor gene in oral squamous cell carcinoma, while hBD-2 and -3 might be protooncogenes.
extraplacental membranes can react differentialy to the arrival of E. coli, secreting HBD2 and HBD3 mainly in the choriodecidua region.
PPARgamma regulates the 1,25D-induced hBD-3 and cathelicidin expression in keratinocytes through the regulation of AP-1 and p38 activity.
hBD3 represents a novel NF-kappaB-regulated mediator of CCR7 expression and anti-apoptotic pathways.
Inducibility of HBD3 influences the severity of Gram-positive skin infection in humans in vivo.
Data show that beta-defensin cluster (DEFB4, DEFB103 and DEFB104) varied between 2 and 9 copies per genome, and high copy numbers (>4) were underrepresented among patients, suggesting that increased copy numbers could protect from CD.
Human pulmonary cells produce hBD-3 upon L. pneumophila infection via a TLR-JNK-AP-1-dependent pathway which may contribute to an efficient innate immune defense.
The beta-defensin antimicrobial peptides hBD1, hBD2 and hBD3 were expressed by immature dendritic cells as well as gingival epithelial cells.
Defensins form a family of microbicidal and cytotoxic peptides made by neutrophils. Members of the defensin family are highly similar in protein sequence. This gene encodes defensin, beta 103B, which has broad spectrum antimicrobial activity and may play an important role in innate epithelial defense.
, beta-defensin 3
, defensin, beta 103
, defensin, beta 3
, defensin-like protein
, beta defensin 3
, beta-defensin 103A
, defensin, beta 103B
, defensin, beta 103A