• Considering the tissue distribution of ferroportin, the hepcidin-ferroportin interaction explains the efferent arm of iron homeostasis because it can control the iron absorption in the duodenum, as well as the release of iron from macrophages and hepatocytes. (diff.org)
  • Hepcidin then binds to ferroportin-1 ( FPN1 ) on the surface of macrophages , enterocytes and hepatocytes . (diff.org)
  • Although hepatocytes are the main sources of hepcidin, and the simplest model would place the iron sensor there (Fig 1), it is not certain that iron sensing takes place in hepatocytes. (diff.org)
  • Thus hepcidin levels decrease, its inhibitory effects diminish, and more iron is made available from the diet and from the storage pool in macrophages and hepatocytes. (diff.org)
  • Here, we aimed to identify proliferative hepatocytes from HCC and para-carcinoma tissues, detect differentially expressed genes between the two types of proliferative hepatocytes, and investigate their potential roles in aberrant proliferation. (biomedcentral.com)
  • Two respective gene signatures for proliferative cells and hepatocytes were established and used to identify proliferative hepatocytes from HCC and para-carcinoma tissues based on scRNA-Seq data. (biomedcentral.com)
  • Gene expression profiles between the two types of proliferative hepatocytes were compared. (biomedcentral.com)
  • Overall, 40 genes were upregulated in proliferative hepatocytes from para-carcinoma tissue, whereas no upregulated genes were detected in those from HCC tissue. (biomedcentral.com)
  • The ability to distinguish proliferative hepatocytes from hepatocellular carcinoma (HCC) and normal liver tissues and comparison of their gene expression profiles will aid us in understanding the mechanisms underlying aberrant proliferative signaling in malignant cells. (biomedcentral.com)
  • In addition, since the gene encoding the A56 protein is non-essential, it can be used as an insertion point for foreign genes and has been deleted in some viruses that are in clinical development as oncolytic agents. (microbiologyresearch.org)
  • The protein encompassing the predicted MetT-PCP domains of HEV ORF1 was tested for deubiquitinating activity using fluorogenic substrates - ubiquitin-7-amino-4-methylcoumarin (AMC), IFN-stimulated gene 15 (ISG15)-AMC, Nedd8-AMC and SUMO-AMC. (microbiologyresearch.org)
  • It is suggested that HJV and soluble HJV (sHJV) modulates hepcidin expression through activating bone morphogenetic protein (BMP) signaling. (diff.org)
  • with Pubmed ID, gene symbol/accession number and viral interacting protein. (polygenicpathways.co.uk)
  • HMOX2 is constitutively expressed to encode a 36 kDa HO-2 protein, mainly functioning to maintain the basal heme metabolism and may also play a role in inflammatory responses [ 4 ] . (encyclopedia.pub)
  • The cellular response in signal transduction cascades involves alteration of the expression of effector genes or activation/inhibition of targeted proteins. (wikipedia.org)
  • It is suggested that hepcidin also decreases expression of proteins involved in intestinal iron absorption, such as duodenal cytochrome-b ( Dcytb ) and divalent metal transporter-1 ( DMT1 ), although the mechanism and extent of control is unknown. (diff.org)
  • However, the mechanism of hepcidin regulation by iron is turning out to be unexpectedly complex. (diff.org)
  • Perhaps the best clue about hepcidin regulation by iron comes from the studies of genes involved in hereditary hemochromatosis. (diff.org)
  • Twelve of the genes, including HAMP , were specifically expressed in the liver tissue. (biomedcentral.com)
  • To explore the underlying molecular events that are associated with the progression of PGD, we sampled Atlantic salmon from three different marine production sites in Scotland and examined the gill tissue at three different levels of organization: gross morphology with the use of PGD scores (macroscopic examination), whole transcriptome (gene expression by RNA-seq) and histopathology (microscopic examination). (frontiersin.org)
  • Our results strongly suggested that the changes in PGD scores of the gill tissue were not associated with the changes in gene expression or histopathology. (frontiersin.org)
  • We demonstrated that the gene expression patterns associated with multifactorial gill disease were dominated by two processes: a range of immune responses driven by pro-inflammatory cytokines and the events associated with tissue damage and repair, driven by caspases and angiogenin. (frontiersin.org)
  • Hepatitis C virus (HCV) alters gene expression epigenetically to rearrange the cellular microenvironment in a beneficial way for its life cycle. (bvsalud.org)
  • Hepcidin inhibits the cellular efflux of iron by binding to and inducing the degradation of ferroportin (FPN) , the sole iron exporter in iron-transporting cells, thereby blocking iron flow into plasma. (diff.org)
  • Infection and inflammation can result in cytokines, such as interleukin-6 ( IL-6 ) stimulating hepcidin expression through molecular pathways that could include binding of STAT3 to the hepcidin promoter. (diff.org)
  • Although the human hepcidin promoter contains several consensus binding sites for hypoxia-inducible factor , these are not typical and not conserved in other mammals, and the molecular pathways that regulate hepcidin in response to hypoxia are not known [T Ganz et al, 2006] . (diff.org)
  • In the first one, first messenger cross through the cell membrane, binding and activating intracellular receptors localized at nucleus or cytosol, which then act as transcriptional factors regulating directly gene expression. (wikipedia.org)
  • When iron levels are high, molecules such as the hemochromatosis gene product ( HFE ), hemojuvelin ( HJV ) and transferrin receptor 2 ( TfR2 ) increase hepatic hepcidin expression. (diff.org)
  • This in turn activates the SMAD signaling pathway to induce hepcidin expression. (diff.org)
  • However, the pathway by which HFE and TfR2 induce hepcidin expression is unclear. (diff.org)
  • By contrast, increased erythropoietic activity suppresses hepcidin expression, as do anemia and hypoxia. (diff.org)
  • How these three processes inhibit hepcidin expression is unclear, but they are closely related. (diff.org)
  • Gene expression profiles of individual cells in HCC and para-carcinoma tissues can be effectively obtained using the single-cell RNA sequencing (scRNA-Seq) technique. (biomedcentral.com)
  • In contrast, integration of the gill RNA-seq data with the gill histopathology enabled us to identify common gene expression patterns associated with multifactorial gill disease, independently from the origin of samples. (frontiersin.org)
  • Hepcidin induction by iron is homeostatic because increased plasma hepcidin would act to inhibit further intestinal iron absorption and iron release from stores. (diff.org)
  • We propose that in Huh7 cells hepcidin modulation leads to an unfavourable intracellular environment for HCV replication. (microbiologyresearch.org)
  • When studying the metabolism of iron in the liver tissues of patients with chronic hepatitis C, the authors found that the expression of the hepcidin gene (HAMP), a hormone regulator of iron export, is markedly reduced in hepatocytes under conditions of oxidative stress caused by viral infection. (bvsalud.org)
  • This study aimed to evaluate the role of interleukin (IL)-28B gene polymorphism and IL-12 levels as predictors for a response to sofosbuvir/ribavirin (SOF/RBV) with (triple-therapy) or without (dual-therapy) Peg-alpha-interferon. (bvsalud.org)