Ask about this productRelated genes to: PYHIN1 antibody
- Gene:
- PYHIN1 NIH gene
- Name:
- pyrin and HIN domain family member 1
- Previous symbol:
- -
- Synonyms:
- IFIX, MGC23885
- Chromosome:
- 1q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-24
- Date modifiied:
- 2017-03-24
Related products to: PYHIN1 antibody
Related articles to: PYHIN1 antibody
- Dysfunctions within the liver system are intricately linked to the progression of diabetic retinopathy (DR) and non-alcoholic fatty liver disease (NAFLD). This study leverages systematic analysis to elucidate the complex cross-talk and communication pathways among diverse cell populations implicated in the pathogenesis of DR and NAFLD. - Source: PubMed
Publication date: 2025/02/26
Zhang ShuyanWu JiajunWang LeileiZhang ChengZhang YinjianFeng Yibin - Tobacco smoke is known to contain numerous harmful chemicals, and epidemiological evidence has firmly established smoking as a potent risk factor for hypertension and myocardial infarction (MI). However, the precise mechanisms by which smoking contributes to cardiovascular disease are not fully understood. The aim of this study is to identify common molecular signatures in blood that link smoking to acute MI (AMI). We extracted transcriptome data from seven blood microarray datasets in the Gene Expression Omnibus (GEO) database, encompassing a total of 403 patients. Employing both individual dataset analysis and a combined meta-analysis approach, we conducted a thorough examination of blood transcriptome profiles associated with AMI and smoking, uncovering numerous differentially expressed genes (DEGs). Functional enrichment analysis indicated that DEGs associated with AMI and smoking were significantly enriched in overlapping biological processes, such as immune response and inflammation. Moreover, three genes-PTGDR, PYHIN1, and PRSS23-were consistently altered in both conditions and were validated as dysregulated in AMI using an independent GEO dataset. Furthermore, quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) validation further confirmed the differential expression of PYHIN1 and PRSS23 in AMI patients. Our findings suggest that gene expression changes induced by smoking in blood may contribute to the heightened risk of AMI. These identified genes are likely to play critical roles in the pathogenesis of AMI. Given the accessibility of peripheral blood samples, the expression levels of these genes could potentially serve as biomarkers for assessing cardiovascular health, particularly in individuals with a history of long-term exposure to cigarette smoke. - Source: PubMed
Publication date: 2025/01/15
Liu Fang-FangYan Yi-XuanZhang Hong-FengLi Ke - Patients diagnosed with cancer face an increased risk of cardiovascular events in the short term, while those experiencing acute myocardial infarction (AMI) have a higher incidence of cancer. Given limitations in clinical resources, identifying shared biomarkers offers a cost-effective approach to risk assessment by minimizing the need for multiple tests and screenings. Hence, it is crucial to identify common biomarkers for both cancer survival and AMI prediction. Our study suggests that monocyte-derived biomarkers, specifically WEE1, PYHIN1, SEC61A2, and HAL, hold potential as predictors for cancer prognosis and AMI. We employed a novel formula to analyze mRNA levels in clinical samples from patients with AMI and cancer, resulting in the development of a new risk score based on expression profiles. By categorizing patients into high-risk and low-risk groups based on the median risk score, we observed significantly poorer overall survival among high-risk patients in cancer cohorts using Kaplan-Meier analysis. Furthermore, calibration curves, decision curve analysis (DCA), and clinical impact curve analyses provided additional evidence supporting the robust diagnostic capacity of the risk score for AMI. Noteworthy is the shared activation of the Notch Signaling pathway, which may shed light on common high-risk factors underlying both AMI and cancer. Additionally, we validated the differential expression of these genes in cell lines and clinical samples, respectively, reinforcing their potential as meaningful biomarkers. In conclusion, our study demonstrates the promise of mRNA levels as biomarkers and emphasizes the significance of further research for validation and refinement. - Source: PubMed
Publication date: 2023/09/14
Yuan NaPan Hai-HuaLiang Yan-ShanHu Hui-LinZhai Chang-LinWang Bo - Treatment-resistant depression (TRD) is a severe form of major depressive disorder (MDD) with substantial public health impact and poor treatment outcome. Treatment outcome in MDD is significantly heritable, but genome-wide association studies have failed to identify replicable common marker alleles, suggesting a potential role for uncommon variants. Here we investigated the hypothesis that uncommon, putatively functional genetic variants are associated with TRD. Whole-exome sequencing data was obtained from 182 TRD cases and 2021 psychiatrically healthy controls. After quality control, the remaining 149 TRD cases and 1976 controls were analyzed with tests designed to detect excess burdens of uncommon variants. At the gene level, 5 genes, ZNF248, PRKRA, PYHIN1, SLC7A8, and STK19 each carried exome-wide significant excess burdens of variants in TRD cases (q < 0.05). Analysis of 41 pre-selected gene sets suggested an excess of uncommon, functional variants among genes involved in lithium response. Among the genes identified in previous TRD studies, ZDHHC3 was also significant in this sample after multiple test correction. ZNF248 and STK19 are involved in transcriptional regulation, PHYIN1 and PRKRA are involved in immune response, SLC7A8 is associated with thyroid hormone transporter activity, and ZDHHC3 regulates synaptic clustering of GABA and glutamate receptors. These results implicate uncommon, functional alleles in TRD and suggest promising novel targets for future research. - Source: PubMed
Publication date: 2023/08/01
Shah Shrey BPeddada Teja NSong ChristopherMensah MaameSung HeejongYavi ManiYuan PeixiongZarate Carlos AMickey Brian JBurmeister MargitAkula NirmalaMcMahon Francis J - This study aims to clarify host factors of IFN treatment in the treatment of chronic hepatitis B (CHB) patients by screening the differentially expressed genes of IFN pathway CHB patients with different response to interferon (IFN) therapy. Three cases were randomly selected in IFN-responding CHB patients (Rs), non-responding CHB patients (NRs) and healthy participants, respectively. The human type I IFN response RT profiler PCR array was used to detect the expression levels of IFN-related genes in peripheral blood monocytes (PBMCs) from healthy participants and CHB patients before and after Peg-IFN-α 2a treatment. The results showed that more differentially expressed genes appeared in Rs group than NRs group after IFN treatment. Comparing with healthy participants, IFNG, IL7R, IRF1, and IRF8 were downregulated in both Rs and NRs group before IFN treatment; CXCL10, IFIT1, and IFITM1 were upregulated in the Rs; IL13RA1 and IFI35 were upregulated in the NRs, while IFRD2, IL11RA, IL4R, IRF3, IRF4, PYHIN1, and ADAR were downregulated. The expression of IL15, IFI35 and IFI44 was downregulated by 4.09 ( = 10.58, < 0.001), 5.59 ( = 3.37, = 0.028) and 10.83 ( = 2.8, = 0.049) fold in the Rs group compared with the NRs group, respectively. In conclusion, IFN-response-related gene array is able to evaluate IFN treatment response by detecting IFN-related genes levels in PBMC. High expression of CXCL10, IFIT1 and IFITM1 before treatment may suggest satisfied IFN efficacy, while high expression of IL13RA1, IL15, IFI35 and IFI44 molecules and low expression of IFRD2, IL11RA, IL4R, IRF3, IRF4, PYHIN1 and ADAR molecules may be associated with poor IFN efficacy. - Source: PubMed
Wang JiayiLu JiajieZhou ChenDu LingyaoTang Hong