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IRF6 — S100A12

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Liu et al., Immunology 2000 : Using the reverse transcription-polymerase chain reaction ( RT-PCR ), we found that CGRP also decreased the LPS induced IL-12 p40 mRNA levels
Liu et al., Shock 2001 : We found that CGRP also increased the LPS induced iNOS mRNA levels by using reverse transcriptase-PCR method
Hou et al., J Neurosci Res 2001 (Neurogenic Inflammation) : In this work, we determined whether lipopolysaccharide (LPS) , an inflammatory stimulator, could trigger CGRP release from cultured DRG neurons and if so, which cellular signaling pathway was involved in this response ... These data suggest that LPS may stimulate CGRP release and [ Ca ( 2+ ) ] ( i ) elevation through PKC and PKA, but not PKG signaling pathway in DRG neurons of neonatal rats
Huang et al., Am J Respir Cell Mol Biol 2003 : Also, LPS caused significant increases in NEP mRNA, SP and CGRP levels, airway reactivity to capsaicin and SP, and neutrophil counts, but a significant decrease in macrophage count
Li et al., Stress 2009 : LPS , restraint and hypoglycaemia suppressed RAMP-1 mRNA, but not CL or CGRP mRNA expression in the mPOA
Sharma et al., Fertil Steril 2010 (Endometriosis...) : The endometrial-endometriotic stromal cells were isolated from ectopic ( group I ) and eutopic ( group II ) endometrium by established methods, cultured, and stimulated with LPS ( 1 µg/mL ), followed by atorvastatin treatment in a time- and dose dependent manner to investigate the effects of LPS on proliferation ( Ki-67 ) and expression of cyclooxygenase-2 (COX-2), vascular endothelial growth factor ( VEGF ), receptor for advanced glycation end products ( RAGE ), extracellular newly identified RAGE binding protein ( EN-RAGE ), peroxisome proliferator activated receptor-? ( PPAR-? ), and liver X receptor-a ( LXR-a ) genes in endometrial-endometriotic stromal cells and on levels of insulin-like growth factor binding protein-1 ( IGFBP-1 ) and 17ß-E ( 2 ) in endometrial-endometriotic stromal cell culture supernatant
Ma et al., Immunology 2010 : LPS induced inflammatory mediators such as nerve growth factor (NGF), interleukin-1beta (IL-1beta), IL-6, prostaglandin E ( 2 ) ( PGE ( 2 ) ) and nuclear factor-kappaB (NF-kappaB) signalling are involved in inducing CGRP, whereas the NGF receptor trkA and CGRP receptor signalling pathways are unexpectedly involved in suppressing LPS induced CGRP , which leads to the fine-tune regulation of CGRP release
McGillis et al., Cell Immunol 1993 : The inhibitory effect of CGRP on LPS induction of sIg appears to be mediated by a reduction in the expression of both mu and kappa mRNA
Hua et al., J Neurosci 1996 : This enhancement of the peptide release by LPS was blocked by IL-1beta tripeptide antagonist Lys-D-Pro-Thr ( 10 microM ) and mimicked by IL-1beta and TNF-alpha ( 10-100 pg/ml ), suggesting that the potentiating effect of LPS on CGRP release is mediated by generation of IL-1beta and TNF-alpha
McGillis et al., Can J Physiol Pharmacol 1995 : CGRP inhibits the lipopolysaccharide (LPS) induction of surface immunoglobulin ( sIg ) protein expression in 70Z/3 cells, an effect that is associated with a decrease in the steady-state levels of Ig heavy ( mu ) and light ( kappa ) chain mRNA
Torii et al., J Leukoc Biol 1997 : CGRP augmented the lipopolysaccharide (LPS) and granulocyte-macrophage colony stimulating factor ( GM-CSF ) -induced release of IL-10 protein and the induced expression of IL-10 mRNA in these cells