miRNAs are an class of small noncoding RNAs and about 21-25 nucleotides in length. miRNAs inhibit the translation or induce mRNA degradation by binding to the 3 UTR of target mRNAs and have been identified as the tumor promoters or suppressors regulating the progression of cancers. miR-429, which is a member of an evolutionarily conserved family of miRNAs that includes miR-200b, miR-200a, miR-200c and miR-141, is expressed in various epithelial tissues. Our goal is to search the possible target genes of miR-429 in human liver cancer cell line HCCLM3.
No associated publication
Specimen part, Cell line, Treatment
View SamplesWhole transcript expression analysis was performed on liver biopsy from wild mice,DEN model mice and cell-treated mice(2 mice per group)
Transplantation of periportal vessel stem cells promotes liver injury repair in cirrhotic mice
Age, Specimen part
View SamplesHsp27 can regulate multiply signaling pathway and protect HCC cells apoptosis by mediating interaction with its cochaperones
No associated publication
Cell line
View SamplesEffect of injury and Pseudomonas aeruginosa inoculation in Drosophila melanogaster
Involvement of skeletal muscle gene regulatory network in susceptibility to wound infection following trauma.
Sex, Time
View SamplesMacrophages from RA synovial fluids were compared to primary human monocyte-derived macrophages.
Interferon-γ Represses M2 Gene Expression in Human Macrophages by Disassembling Enhancers Bound by the Transcription Factor MAF.
Specimen part, Disease stage, Subject
View SamplesGene expression analysis of freshly isolated CD14+ human monocytes and monocytes cultured in the presence or absence of interferon (IFN) -gamma for 24 h and then stimulated with Pam3Cys, a Toll-like receptor (TLR) 2 ligand, for 6 h. Results provide insight into mechanisms by which IFN-gamma reprograms early macrophage differentiation and subsequent response to TLR ligands.
Integrated regulation of Toll-like receptor responses by Notch and interferon-gamma pathways.
No sample metadata fields
View SamplesComplement receptor 2negative (CR2/CD21) B cells have been found enriched in patients with autoimmune diseases and in common variable immunodeficiency (CVID) patients who are prone to autoimmunity. However, the physiology of CD21/lo B cells remains poorly characterized. We found that some rheumatoid arthritis (RA) patients also display an increased frequency of CD21/lo B cells in their blood. A majority of CD21/lo B cells from RA and CVID patients expressed germline autoreactive antibodies, which recognized nuclear and cytoplasmic structures. In addition, these B cells were unable to induce calcium flux, become activated, or proliferate in response to B-cell receptor and/or CD40 triggering, suggesting that these autoreactive B cells may be anergic. Moreover, gene array analyses of CD21/lo B cells revealed molecules specifically expressed in these B cells and that are likely to induce their unresponsive stage. Thus, CD21/lo B cells contain mostly autoreactive unresponsive clones, which express a specific set of molecules that may represent new biomarkers to identify anergic B cells in humans.
Complement receptor 2/CD21- human naive B cells contain mostly autoreactive unresponsive clones.
No sample metadata fields
View SamplesMacrophages from RA synovial fluids were compared to primary human blood-derived macrophages.
No associated publication
No sample metadata fields
View SamplesKLF7 null mice show profound axonal growth defects in the olfactory epithelium. The goal of this study was the identification of potential KLF7 target genes in olfactory sensory neurons.
Identification of genes regulated by transcription factor KLF7 in differentiating olfactory sensory neurons.
No sample metadata fields
View SamplesMost autoreactive B cells are normally counterselected during early B cell development. To determine whether Toll-like receptors (TLRs) regulate the removal of autoreactive B lymphocytes, we tested the reactivity of recombinant antibodies from single B cells isolated from patients deficient for IL-1R-associated kinase (IRAK)-4, myeloid differentiation factor 88 (MyD88) and UNC-93B. Indeed, all TLRs except TLR3 require IRAK-4 and MyD88 to signal and UNC-93B-deficient cells are unresponsive to TLR3, TLR7, TLR8 and TLR9. All patients suffered from defective central and peripheral B cell tolerance checkpoints resulting in the accumulation of large numbers of autoreactive mature nave B cells in their blood. Hence, TLR7, TLR8, and TLR9 may prevent the recruitment of developing autoreactive B cells in healthy donors. Paradoxically, IRAK-4-, MyD88- and UNC-93B-deficient patients did not display autoreactive antibodies in their serum nor developed autoimmune diseases, suggesting that IRAK-4, MyD88 and UNC-93B pathway blockade may thwart autoimmunity in humans.
IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans.
No sample metadata fields
View Samples