EID3 antibody
- Known as:
- EID3 (anti-)
- Catalog number:
- orb101586
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- EID3 antibody
Related genes to: EID3 antibody
- Gene:
- EID3 NIH gene
- Name:
- EP300 interacting inhibitor of differentiation 3
- Previous symbol:
- -
- Synonyms:
- FLJ25832, NSMCE4B, NSE4B
- Chromosome:
- 12q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-10-12
- Date modifiied:
- 2018-08-15
Related products to: EID3 antibody
Related articles to: EID3 antibody
- Mammalian spermatogenesis is a highly complex process of cell proliferation, meiosis, and differentiation. A series of genes are expressed in an orderly and precise manner to ensure spermatogenesis, with chromatin undergoing intricate changes throughout. EP300-interacting inhibitor of differentiation 3 (Eid3) is a testis-enriched gene, but its role in male reproduction remains unclear. - Source: PubMed
Publication date: 2024/11/17
Zhang PingZhang LongshengYu LiZhou XinliChen XuZhou YuchuanWang NinglingZhu Hui - Hepatocellular carcinoma (HCC) is associated with one of the highest mortality rates among cancers, rendering its early diagnosis clinically invaluable. Serum biomarkers, specifically alpha-fetoprotein (AFP), represent the most promising and widely used diagnostic biomarkers for HCC. However, its detection rate is low in the early stages of HCC progression, and distinguishing specific false positives for other liver-related diseases, such as cirrhosis and acute hepatitis, remains challenging. Therefore, this study was conducted to identify biomarkers for hepatitis B (HBV)-related liver diseases by screening differentially expressed autoantibodies against tumor-associated antigens (TAAbs). We designed a large-scale multistage investigation, encompassing initial screening, HCC-focused, and ELISA validation cohorts to identify potential TAAbs in HBV-related liver diseases, spanning from healthy control (HC) individuals to patients with chronic hepatitis B (CHB), hepatitis B-related cirrhosis (HBC), and HCC, using protein microarray technology. The differential biological characteristics of TAAbs were analyzed using bioinformatics analysis. Validation of tumor-specific biomarkers for HCC was performed using ELISA. In the screening cohort, 547 candidate TAAbs were identified in the HCC group compared to those in the HC group. In the HCC-focused cohort, 64, 61, and 65 candidate TAAbs were identified in the CHB, HBC, and HCC groups, respectively, compared to those in the HC group. Thirty-four proteins exhibited continuously elevated expression from HCs to patients with CHB, HBC, and HCC. Among these, nine were identified as cancer-specific proteins. In the validation cohort, UBE2Z, CNOT3, and EID3 were correlated with liver function indicators in patients with hepatitis B-related HCC. Overall, UBE2Z, CNOT3, and EID3 emerged as cancer-specific biomarkers for HBV-related liver disease, providing a scientific basis for clinical application. - Source: PubMed
Publication date: 2024/11/01
Hao WudiZhao DanyangMeng YuanYang MeiMa MeichenHu JingwenLiu JianhuaQin Xiaosong - Tinnitus, the perception of sound without any external sound source, is a prevalent hearing health concern. Mounting evidence suggests that a confluence of genetic, environmental, and lifestyle factors can influence the pathogenesis of tinnitus. We hypothesized that alteration in DNA methylation, an epigenetic modification that occurs at cytosines of cytosine-phosphate-guanine (CpG) dinucleotide sites, where a methyl group from S-adenyl methionine gets transferred to the fifth carbon of the cytosine, could contribute to tinnitus. DNA methylation patterns are tissue-specific, but the tissues involved in tinnitus are not easily accessible in humans. This pilot study used saliva as a surrogate tissue to identify differentially methylated CpG regions (DMRs) associated with tinnitus. The study was conducted on healthy young adults reporting bilateral continuous chronic tinnitus to limit the influence of age-related confounding factors and health-related comorbidities. - Source: PubMed
Publication date: 2024/08/15
Bhatt Ishan SunilkumarGaray Juan Antonio RaygozaTorkamani AliDias Raquel - - Source: PubMed
Yuan ChenfengHong HanhuiWang NanChen TongCao MaoshengZhao YunShen CaomeihuiChen XueLuo YuxinZhang BoqiZhou XuLi Chunjin - Exploring the molecular mechanisms of cell behaviors is beneficial for promoting periodontal ligament stem cell (PDLSC)-mediated tissue regeneration. This study intends to explore the regulatory effects of EID3 on cell proliferation, apoptosis, and osteogenic differentiation and to preliminarily explore the regulatory mechanism of EID3. Here, EID3 was overexpressed or knocked down in PDLSCs by recombinant lentivirus. Then, cell proliferation activity was analyzed by colony-forming assay, EdU assay, and cell cycle assay. Cell apoptosis was detected by flow cytometry. The osteo-differentiation potential was analyzed using ALP activity assay, ALP staining, alizarin red staining, and mRNA and protein assay of osteo-differentiation related genes. The results showed that when EID3 was knocked down, the proliferation activity and osteogenic differentiation potential of PDLSCs decreased, while they increased when EID3 was overexpressed. The cell apoptosis rate decreased in PDLSCs with EID3 knockdown but increased in PDLSCs with EID3 overexpression. Moreover, EID3 inhibited the transduction of the AKT/MTOR and ERK signaling pathway. In addition, TAZ negatively regulated the expression of EID3, and the overexpression of EID3 partially reversed the promotive effects of TAZ on the osteogenic differentiation of PDLSCs. Taken together, EID3 inhibits the proliferation and osteogenic differentiation while promoting the apoptosis of PDLSCs. EID3 inhibits the transduction of the AKT/MTOR and ERK signaling pathways and mediates the regulatory effect of TAZ on PDLSC osteogenic differentiation. - Source: PubMed
Publication date: 2024/01/10
Jia LingluTian HuiSun ShaoqingHao XingyaoWen Yong