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HDC — IRF6

Text-mined interactions from Literome

Endo et al., Br J Pharmacol 1999 (Bone Resorption) : However, Cl2MBP did not inhibit the increase in HDC activity induced by lipopolysaccharide (LPS)
Yamaguchi et al., Br J Pharmacol 2000 (Inflammation) : In this study, we also obtained a result suggesting that IL-1-deficiency might be compensated by a second, unidentified, mechanism serving to induce HDC in response to LPS when IL-1 is lacking
Sogawa et al., Life Sci 2001 : Previously, we reported that Ceph enhanced lipopolysaccharide (LPS) induced histidine decarboxylase (HDC) activity in mice spleens by consecutive pre-administration
Nakano et al., Nihon Yakurigaku Zasshi 2001 : Among the cytokines tested, GM-CSF or IL-3 specifically augmented the LPS dependent HDC induction by M phi
Endo et al., Br J Pharmacol 1992 (Drug-Induced Liver Injury) : 6. The induction of HDC in the liver by LPS , IL-1 or TNF was not suppressed by GalN and, at high doses, the response to LPS was enhanced
Wu et al., Int Immunopharmacol 2004 : To examine the contribution of mast cells to HDC induction in mice given LPS or IL-1, we examined the effects of LPS and IL-1 on HDC activity and/or histamine content in various organs ( liver, lung, spleen or bone marrow ) in mast cell-deficient mice ( W/Wv ), their normal littermates ( +/+ ) and BALB/c mice deficient in IL-1alpha, IL-1beta and tumor necrosis factor (TNF)-alpha ( IL-1alpha beta/TNFalphaKO mice ) ... The LPS stimulated increase in HDC activity in a given organ was similar between +/+ and W/W ( v ) mice, and between IL-1alpha beta/TNFalphaKO BALB/c and control BALB/c mice, and led to increases in histamine ... These results suggest that ( i ) in liver, lung and spleen, either the major cells supplying histamine via HDC induction in response to LPS and IL-1 are not mast cells, or mast cells are not a prerequisite for the induction of HDC ; ( ii ) the cells in which HDC is induced by LPS and IL-1 are similar or identical in a given organ ; and ( iii ) neither IL-1 nor TNF-alpha is a prerequisite for the induction of HDC by LPS
Deng et al., Toxicol Appl Pharmacol 2006 : We reported previously that in mice, ( i ) the inflammatory actions of N-BPs depend on IL-1, ( ii ) N-BP pretreatment augments both LPS stimulated IL-1 production and HDC induction, and ( iii ) the co-administration of clodronate ( a non-N-BP ) with an N-BP inhibits the latter 's inflammatory actions ( including HDC induction )
Shoji et al., Arch Oral Biol 2006 : Since mast cells are known to produce histamine through a difference mechanism than HDC induction, we compared LPS induced HDC activity in dental pulp and gingiva to that in ear skin ( a tissue rich in mast cells ) and liver ( a tissues lacking in mast cells ) ... LPS also induced a marked increase in the HDC activity in liver and ear skin at 6 h after LPS injection ... Still, the relative increase in LPS induced HDC activity in dental pulp and gingiva were much greater than that in ear skin
Hirasawa et al., Biochem Biophys Res Commun 2006 : Mithramycin A, an inhibitor of the binding of the Sp family to the GC box, reduced the LPS induced increase in the levels of HDC mRNA at 4 h and HDC protein at 8 h in a concentration dependent manner ... These results suggested that Sp1 is one of the transcription factors that regulate the LPS induced expression of HDC in RAW 264 cells
Hirasawa et al., Life Sci 2006 : The MAP kinase-Erk kinase 1 inhibitor U0126 ( 0.1-10 microM ) suppressed the LPS induced phosphorylation of p44/42 MAP kinase, and inhibited the LPS induced production of histamine and expression of the HDC mRNA and 74-kDa HDC protein in a concentration dependent manner ... These findings suggest that LPS increases histamine production in RAW 264 cells by inducing the expression of the 74-kDa HDC protein, and that the LPS induced expression of HDC is up-regulated at the transcriptional level by MAP kinases, especially p44 MAP kinase and JNK
Suzuki et al., Biochem Biophys Res Commun 2009 : We found that ( - ) -DHMEQ, an NF-kappaB inhibitor, inhibited lipopolysaccharide (LPS) induced histamine production and HDC induction in mouse macrophage cell line RAW264.7
Okamoto et al., Immunology 1990 : The response of mouse peritoneal macrophages to Escherichia coli lipopolysaccharide (LPS) resulted in induction of histidine decarboxylase (HDC) and, consequently, of histamine production
Oh et al., Immunology 1988 : Co-culture with T or B cells enhanced the LPS dependent increase in HDC activity in macrophages
Suzuki et al., Biochem Pharmacol 1986 : Escherichia coli lipopolysaccharide (LPS) induced a strong secretion of corticosterone in C3H/HeN mice with a concomitant increase in the splenic histidine decarboxylase activity
Endo et al., Biochem Pharmacol 1983 (Inflammation) : Both LPS ( a B-cell mitogen ) and Con A ( a T-cell mitogen ) induced HDC also in nude mice that lack T-cells, indicating that T-cells are not required for HDC induction by mitogens
Endo et al., Biochem Pharmacol 1982 : In the brain and thymus the LPS induced ornithine decarboxylase, but not histidine decarboxylase
Endo et al., Br J Pharmacol 1995 : 3. In macrophage depleted mice, the induction of HDC by LPS , IL-1 alpha or TNF-alpha was not impaired in the liver, and was potentiated in the lung and bone marrow
Nakatsu et al., Nihon Yakurigaku Zasshi 1995 : Cepharanthin enhanced LPS induced HDC activity in normal mice spleens and also enhanced it in genetically T cell-deficient nude mice spleens and T and B cell-deficient scid mice spleens
Niimi et al., J Neurochem 1997 : We investigated the effect of lipopolysaccharide (LPS) and various inflammatory cytokines on the histidine decarboxylase (HDC) activity in cultured cells of the rat embryonic brain ... In the adherent cell fraction of the cultured diencephalon cells, HDC activity was also enhanced by LPS and IL-1beta ... In a similar manner, LPS augmented HDC activity in the mixed primary culture of cerebral cortical cells and in its adherent cell fraction