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Defensin, beta 4A

hBD-2, beta-defensin-2
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 4, an antibiotic peptide which is locally regulated by inflammation. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Defensin, BDI, CAN, POLYMERASE, HAD
Papers on hBD-2
Association of High-Risk Human Papillomavirus with Genital Tract Mucosal Immune Factors in HIV-Infected Women.
Herold et al., United States. In Am J Reprod Immunol, Feb 2016
RESULTS: Compared to controls, HR-HPV groups had higher plasma viral loads (P = 0.004), lower CD4 cells (P = 0.02), more genital tract HIV RNA (P = 0.03), greater number of different HPV types (P < 0.001), higher cervicovaginal lavage (CVL) IL-1α (P = 0.03) and human beta-defensin 2 (HBD2) (P = 0.049), and less anti-HIVB al activity (P = 0.03).
Vaginal Inflammation: Association between Leukocyte Concentration and Levels of Immune Mediators.
Gonçalves et al., Campinas, Brazil. In Am J Reprod Immunol, Feb 2016
We correlated extracellular matrix metalloproteinase inducer (EMMPRIN), matrix metalloproteinase-8 (MMP-8), hyaluronan (HA), hyaluronidase-1 (Hyal-1), human β-defensin-2 (hBD2), and neutrophil gelatinase-associated lipocalin (NGAL) concentrations with the extent of leukocyte infiltration into the vagina and suggest their participation in vaginal inflammation.
Kinetic analysis and molecular modelling of the inhibition mechanism of roneparstat (SST0001) on human heparanase.
Giannini et al., Parma, Italy. In Glycobiology, Feb 2016
In particular, docking solutions were obtained in which i) a single roneparstat molecule interacts with both heparin-binding domains (HBD) of heparanase or ii) two fragments of roneparstat interact with either HBD-1 or HBD-2, consistent with the possibility of different inhibitor:enzyme binding stoichiometries.
MALT1 protease activity controls the expression of inflammatory genes in keratinocytes upon zymosan stimulation.
Hailfinger et al., Tübingen, Germany. In J Invest Dermatol, Feb 2016
Silencing or inhibition of MALT1 protease strongly decreased the expression of important inflammatory genes such as TNFα, IL17C, CXCL8 and HBD-2.
Oral administration of synthetic porcine beta-defensin-2 improves growth performance and cecal microbial flora and down-regulates the expression of intestinal toll-like receptor-4 and inflammatory cytokines in weaned piglets challenged with enterotoxigenic Escherichia coli.
Sun et al., Chongqing, China. In Anim Sci J, Jan 2016
UNASSIGNED: Synthetic porcine beta-defensin-2 (pBD-2) was tested as an alternative to antimicrobial growth-promoters in pig production.
Species-specific regulation of innate immunity by vitamin D signaling.
White et al., Montréal, Canada. In J Steroid Biochem Mol Biol, Oct 2015
Consistent with this, VDR target genes encoding AMPs human beta-defensin 2 (HBD2) and cathelicidin (CAMP) and the pattern recognition receptor NOD2 are induced by 1,25(OH)2D in human cells of epithelial or myeloid origin but not similarly regulated in mouse cells.
Two Cheers for Crohn's Disease and Periodontitis: Beta-Defensin-2 as an Actionable Target to Intervene on Two Clinically Distinct Diseases.
Gursoy et al., Turku, Finland. In Omics, Aug 2015
Furthermore, we propose a novel connector molecular target between these two ostensibly distinct diseases at a clinical level, human beta defensin (hBD)-2, and suggest pathways by which hBD-2 can conceivably connect Crohn's disease and periodontitis by virtue of regulating the innate-immune response.
Is variation in copy number of the human beta defensin gene cluster associated with preterm birth?
Peebles et al., London, United Kingdom. In Lancet, Mar 2015
The gene encoding HBD2, DEFB4A, is part of a defensin beta (DEFB) cluster on chromosome 8 that is variable in copy number.
Antimicrobial Peptides in Human Sepsis.
Schuerholz et al., Aachen, Germany. In Front Immunol, 2014
Recent studies have demonstrated higher levels of HNP 1-3 and HBD-2 in sepsis.
Human defensins facilitate local unfolding of thermodynamically unstable regions of bacterial protein toxins.
Kudryashov et al., Columbus, United States. In Immunity, 2014
HD5 and ?-defensin hBD2 shared similar toxin-unfolding effects with HNP1, albeit to different degrees.
Differential expression of human beta defensin 2 and 3 in gastric mucosa of Helicobacter pylori-infected individuals.
Malfertheiner et al., Berlin, Germany. In Helicobacter, 2013
Two major representatives, the human beta defensin 2 and 3 (hBD2 and hBD3), are both known to be regulated by, and to affect viability of, Helicobacter pylori.
The host and the flora.
Stange et al., Tübingen, Germany. In Dig Dis, 2012
Lactobacilli, the probiotic strain Escherichia coli Nissle and Salmonella enteritica stimulate HBD-2 expression, whereas Shigella flexneri downregulates the synthesis of HBD-1, HBD-3 and LL-37.
Specific-sized hyaluronan fragments promote expression of human β-defensin 2 in intestinal epithelium.
de la Motte et al., Cleveland, United States. In J Biol Chem, 2012
a highly size-specific, TLR4-dependent, innate defense response to fragmented HA contributes to intestinal epithelium barrier defense through the induction of intracellular HbetaD2 protein.
Andrographolide exerted its antimicrobial effects by upregulation of human β-defensin-2 induced through p38 MAPK and NF-κB pathway in human lung epithelial cells.
Li et al., Chengdu, China. In Can J Physiol Pharmacol, 2012
Andrographolide (1.0-10 micromol/L) can upregulate the expression of hBD-2 in a dose-dependent manner.
Extracellular HIV-1 Tat induces human beta-defensin-2 production via NF-kappaB/AP-1 dependent pathways in human B cells.
Park et al., South Korea. In Mol Cells, 2012
our results indicate that HIV-1 Tat can up-regulate the expression of hBD-2 via JNK-NF-kappaB/AP-1-dependent pathways in human B cells.
Genetic variability in beta-defensins is not associated with susceptibility to Staphylococcus aureus bacteremia.
Andersen et al., Copenhagen, Denmark. In Plos One, 2011
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
Beta defensin-2 is reduced in central but not in distal airways of smoker COPD patients.
Gjomarkaj et al., Palermo, Italy. In Plos One, 2011
The epithelial expression of TLR4 and of HBD2 was assessed in surgical specimens from current smokers COPD (s-COPD; n = 17), ex-smokers COPD (ex-s-COPD; n = 8), smokers without COPD (S; n = 12), and from non-smoker non-COPD subjects (C; n = 13).
IL-22 increases the innate immunity of tissues.
Sabat et al., Berlin, Germany. In Immunity, 2004
In these cells, IL-22 activated STAT3 and directly and transcriptionally increased the expression of beta-Defensin 2 and beta-Defensin 3. High levels of IL-22 were associated with strongly upregulated beta-Defensin expression in skin from patients with T cell-mediated dermatoses.
Multiple roles of antimicrobial defensins, cathelicidins, and eosinophil-derived neurotoxin in host defense.
Oppenheim et al., Frederick, United States. In Annu Rev Immunol, 2003
Beta-defensins interact with CCR6; murine beta-defensin-2 in addition activates TLR4.
Toll-like receptor 4-dependent activation of dendritic cells by beta-defensin 2.
Kwak et al., Bethesda, United States. In Science, 2002
acts directly on immature dendritic cells as an endogenous ligand for Toll-like receptor 4, inducing up-regulation of costimulatory molecules and dendritic cell maturation
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