AIG1 is a novel Pirh2-interacting protein that activates the NFAT signaling pathway.

Pirh2 is an E3 ligase that negatively regulates p53 through both direct physical interaction and ubiquitin-mediated proteolysis. Here, we identified a novel Pirh2-interacting protein, AIG1, by yeast two-hybrid screening and confirmed its interaction with p53 both in vitro and in vivo. Quantitative real-time reverse transcription-PCR analysis showed that AIG1 expression levels were reduced in 50 out of 79 (63%) human hepatocellular carcinomas (HCCs) when compared to matched, non-cancerous liver tissue; levels were significantly different between HCCs with or without lymph node metastasis.

System biology analysis of cell cycle pathway involved in hepatocellular carcinoma.

To investigate genetic mechanisms of hepatocarcinogenesis and identify potential anticancer targets in hepatocellular carcinoma (HCC), we analyzed microarray gene expression profiles between 33 HCCs and their corresponding noncancerous liver tissues. Functional analysis of differentially-expressed genes in HCC indicated that cell cycle dysregulation plays an important role in hepatocarcinogenesis. Based on 14 differentially-expressed genes involved in cell cycle in HCC, we applied Structural Equation Modeling (SEM) to establish a potential genetic network which could assist understanding of HCC molecular mechanisms.

Expression profile reveals novel prognostic biomarkers in hepatocellular carcinoma.

The purpose of this study was to identify and validate novel prognostic biomarkers in human hepatocellular carcinoma (HCC). We analyzed gene expression profiles not only between 33 HCCs and their corresponding noncancerous liver tissues, but also between 25 HCCs and pooled normal liver tissues using cDNA microarrays containing 12800 genes. Functional analysis of differentially expressed genes involved in HCC carcinogenesis and tumor progression revealed that up-regulated and down-regulated genes are mainly associated with cell cycle and immune response, respectively.

A novel hPirh2 splicing variant without ubiquitin protein ligase activity interacts with p53 and is down-regulated in hepatocellular carcinoma.

A novel splice variant of hPirh2, named hPirh2b, was isolated from human fetal liver cDNA library. hPirh2b has a 38-nucleotide deletion and encodes a 188-amino acid protein with a truncated RING-H2 domain. It shows no ubiquitin protein ligase activity.

SNP genotyping by multiplex amplification and microarrays assay for forensic application.

Objective: Research on the application feasibility of SNP genotyping for forensic identification by microarrays.

Methods: Oligonucleotide microarrays which could detect 34 different SNPs were used. After hybridization and washing, the arrays were scanned and fluorescence intensities analyzed using Microarray software.

LS-CAP: an algorithm for identifying cytogenetic aberrations in hepatocellular carcinoma using microarray data.

Biological techniques such as Array-Comparative genomic hybridization (CGH), fluorescent in situ hybridization (FISH) and affymetrix single nucleotide pleomorphism (SNP) array have been used to detect cytogenetic aberrations. However, on genomic scale, these techniques are labor intensive and time consuming. Comparative genomic microarray analysis (CGMA) has been used to identify cytogenetic changes in hepatocellular carcinoma (HCC) using gene expression microarray data.

[ABO genotyping by duplex amplification and oligonucleotide arrays assay].

Objective: ABO genotyping for forensic identification by oligonucleotide chip.

Methods: Oligonucleotide microarrays which could detect 3 different SNPs in exon 6 and exon 7 for ABO genotyping were used. Population studies on ABO was carried out in a sample of 115 unrelated Chinese Han individuals.

[Detecting genetic polymorphisms of CYP1 A1 and GSTM1 simultaneously with oligonucleotide microarray].

Cytochrome P4501A1 plays a major role in the bioactivation of a number of tobacco procarcinogens. Glutathione S-transferase( GSTM1), a member of the class of GST gene family, has been shown to be polymorphic because of gene deletion resulting in a failure to express the GSTM1 gene in 50% approximately 60% of individuals. Some CYP1 A1/GSTM1 null genotype combinations seem to predispose the lung, esophagus, and oral cavity of smokers to an even higher risk for cancer or DNA damage, requiring, however, confirmation.