Ignet

Gene Information

Gene symbol: DEFB1

Gene name: defensin, beta 1

HGNC ID: 2766

Synonyms: HBD-1, DEFB-1, DEFB101, HBD1, BD1, MGC51822

Related Genes

#	Gene Symbol	Number of hits
1	APEX1	1 hits
2	CAMP	1 hits
3	CCL2	1 hits
4	CXCL1	1 hits
5	CXCL2	1 hits
6	DEFB110	1 hits
7	IFNG	1 hits
8	IL17D	1 hits
9	IL17F	1 hits
10	IL1B	1 hits
11	IL22	1 hits
12	IL6	1 hits
13	REG3G	1 hits
14	SLPI	1 hits

Related Sentences

#	PMID	Sentence
1	23668260	The infected mice displayed a significant up-regulation in the expression of chemokines (Cxcl1, Cxcl2 and Ccl2), numerous pro-inflammatory cytokines (Ifng, Il1b, Il6, and Il17f), as well as Il22 and a number of anti-microbial peptides (Defa1, Defa28, Defb1, Slpi and Reg3g) at the site(s) of infection.
2	23668260	However, CD4 T cells of the untreated and C. difficile-infected mice expressed similar levels of CD69 and CD25.
3	23668260	Neither tissue had up-regulated levels of Tbx21, Gata3 or Rorc.
4	23668260	They also displayed significantly higher phosphorylation of AKT and signal transducer and activator of transcription 3 (STAT3), an indication of pro-survival signalling.
5	23668260	These data underscore the local, innate, pro-inflammatory nature of the response to C. difficile and highlight eIF2α phosphorylation and the interleukin-22-pSTAT3-RegIIIγ axis as two of the pathways that could be used to contain and counteract the damage inflicted on the intestinal epithelium.
6	25815330	Our aim was to investigate the effects of hyperthermia, ultraviolet A rays (UVA), and ultraviolet C rays (UVC) as well as glucose and ascorbic acid (AA) on the regulation of human β-defensin 1 (DEFB1), cathelicidin (CAMP), and interferon-γ (IFNG) genes in normal human keratinocytes (NHK).
7	25815330	We found that AA is a more potent APE for DEFB1 than glucose in NHK.
8	25815330	Glucose but not AA is an APE for CAMP.
9	25815330	AA-dependent DEFB1 upregulation below 20 mM predicts in vitro antimicrobial activity as well as glucose- and AA-dependent CAMP and IFNG upregulation.
10	25815330	UVC upregulates CAMP and DEFB1 genes but UVA only upregulates the DEFB1 gene.
11	25815330	Our results suggest that glucose upregulates CAMP in an IFN-γ-independent manner.
12	25815330	Our aim was to investigate the effects of hyperthermia, ultraviolet A rays (UVA), and ultraviolet C rays (UVC) as well as glucose and ascorbic acid (AA) on the regulation of human β-defensin 1 (DEFB1), cathelicidin (CAMP), and interferon-γ (IFNG) genes in normal human keratinocytes (NHK).
13	25815330	We found that AA is a more potent APE for DEFB1 than glucose in NHK.
14	25815330	Glucose but not AA is an APE for CAMP.
15	25815330	AA-dependent DEFB1 upregulation below 20 mM predicts in vitro antimicrobial activity as well as glucose- and AA-dependent CAMP and IFNG upregulation.
16	25815330	UVC upregulates CAMP and DEFB1 genes but UVA only upregulates the DEFB1 gene.
17	25815330	Our results suggest that glucose upregulates CAMP in an IFN-γ-independent manner.
18	25815330	Our aim was to investigate the effects of hyperthermia, ultraviolet A rays (UVA), and ultraviolet C rays (UVC) as well as glucose and ascorbic acid (AA) on the regulation of human β-defensin 1 (DEFB1), cathelicidin (CAMP), and interferon-γ (IFNG) genes in normal human keratinocytes (NHK).
19	25815330	We found that AA is a more potent APE for DEFB1 than glucose in NHK.
20	25815330	Glucose but not AA is an APE for CAMP.
21	25815330	AA-dependent DEFB1 upregulation below 20 mM predicts in vitro antimicrobial activity as well as glucose- and AA-dependent CAMP and IFNG upregulation.
22	25815330	UVC upregulates CAMP and DEFB1 genes but UVA only upregulates the DEFB1 gene.
23	25815330	Our results suggest that glucose upregulates CAMP in an IFN-γ-independent manner.
24	25815330	Our aim was to investigate the effects of hyperthermia, ultraviolet A rays (UVA), and ultraviolet C rays (UVC) as well as glucose and ascorbic acid (AA) on the regulation of human β-defensin 1 (DEFB1), cathelicidin (CAMP), and interferon-γ (IFNG) genes in normal human keratinocytes (NHK).
25	25815330	We found that AA is a more potent APE for DEFB1 than glucose in NHK.
26	25815330	Glucose but not AA is an APE for CAMP.
27	25815330	AA-dependent DEFB1 upregulation below 20 mM predicts in vitro antimicrobial activity as well as glucose- and AA-dependent CAMP and IFNG upregulation.
28	25815330	UVC upregulates CAMP and DEFB1 genes but UVA only upregulates the DEFB1 gene.
29	25815330	Our results suggest that glucose upregulates CAMP in an IFN-γ-independent manner.
30	27179873	Genes that were differentially expressed over the transition period included those involved in neutrophil adhesion (SELL, ITGB2, and ITGBX), mediation of the immune response (TLR4, HLA-DRA, and CXCR2), maturation, cell cycle progression, apoptosis (MCL1, BCL2, FASLG, and RIPK1), and control of gene expression (PPARG, PPARD, and STAT3).
31	27179873	We noted reduced gene expression of proinflammatory cytokines (IFNG, TNF, IL12, and CCL2) on the day of calving, whereas anti-inflammatory cytokine gene expression (IL10) was upregulated.
32	27179873	Increased gene expression of antimicrobial peptides (BNBD4, DEFB10, and DEFB1) occurred on the day of calving.