Ask about this productRelated genes to: TADA3L antibody
- Gene:
- TADA3 NIH gene
- Name:
- transcriptional adaptor 3
- Previous symbol:
- TADA3L
- Synonyms:
- FLJ20221, FLJ21329, ADA3, hADA3, NGG1
- Chromosome:
- 3p25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-13
- Date modifiied:
- 2016-04-18
Related products to: TADA3L antibody
Related articles to: TADA3L antibody
- Mosquitoes, especially Aedes aegypti, transmit major human diseases such as dengue, Zika, and chikungunya. Epigenetic regulation, including histone acetylation, plays a key role in controlling Ae. aegypti development. However, the specific roles of histone acetyltransferases (HATs) and N-terminal acetyltransferases (NATs) in mosquito development remain poorly understood. In this study, we investigated 25 HAT/NAT genes functions by knocking them down via feeding Ae. aegypti larvae with dsRNA nanoformulations. Gene expression analysis confirmed that target gene expression was reduced by more than 50% in dsRNA-treated larvae. Knocking down 18 of these HATs/NATs resulted in over 50% mortality. Silencing KAT7, NATSCAN, NAT9, ATAT1, and TADA3 caused larval death, whereas knockdown of NAA80, NAA-Eco, GNPNAT1, HAT-B, and MCM3AP led to pupal mortality. Knockdown of NATSCAN, NF, TFIID, GNPNAT1, and NAA16 resulted in molting and metamorphic defects, characterized by untanned cuticles and failure to complete successful larval-pupal metamorphosis. Phylogenetic analysis of conserved domains of HATs and NATs revealed that evolutionarily conserved members cluster into distinct clades associated with larval- or pupal-specific functions. Developmental expression analysis showed stage-specific expression of these genes. Further, stage-specific expression analysis revealed that dynamic expression patterns of KAT7, RNACAT, NAT9, and NF are linked to larval growth and pupal metamorphosis. Treatment with 20-hydroxyecdysone (20E) or an ecdysone agonist increased mRNA levels of NAA30,NAA40,NAT9, and GNAT8, indicating hormonal control of histone acetylation. Ecdysone-induced HATs/NATs regulated the expression of primary ecdysone response genes: E75A and E93. These results demonstrate that HATs/NATs play key roles in Ae. aegypti development and therefore could serve as potential targets for mosquito control. - Source: PubMed
Publication date: 2026/04/27
Gaddelapati Sharath ChandraPalli Subba Reddy - Liver hepatocellular carcinoma (LIHC) is the most prevalent liver malignancy, often diagnosed at advanced stages, and resulting in a poor prognosis for patients. Ubiquitin-specific peptidase 22 (USP22) belongs to the ubiquitin-specific processing proteases (USPs) subfamily and has been identified as a gene signature associated with various cancer types in previous studies. However, the exact role of USP22 in LIHC remains to be fully elucidated. - Source: PubMed
Publication date: 2025/07/15
Xu KeminLu Yanjun - The high incidence of mutations and the crucial roles of KAT2A in cancer development have received increased attention. Nevertheless, a systematic comparison of the heterogeneity and dynamics across different cancer types has not been conducted. Hence, a deep analysis using public databases was performed to clarify the contributions of KAT2A and its correlation with tumorigenesis. The raw data regarding KAT2A expression in cancer patients and healthy controls were obtained from The Cancer Genome Atlas (TCGA). Sexually dimorphic manner, genomic alterations, and expression pattern of KAT2A, as well as the association of the KAT2A with survival, were retrieved from UALCAN, cBioportal, and TISIDB databases. Additionally, the Protein-Protein Interaction (PPI) analysis was conducted using the STRING database. The human protein atlas was used to obtain the staining results of protein levels in cancer and normal samples. The correlation between KAT2A and its potential target drugs was determined using TISIDB and HISTome2. Compared to the normal tissues, CHOL and TGCT tumors presented significantly high KAT2A expression, which was positively correlated with BLCA, BRCA, CESC, CHOL, COAD, ESCA, HNSC, KICH, KIRP, LIHC, LUAD, LUSC, READ, STAD, and THCA. However, no significant difference was detected between normal and tumor tissues for the sex difference pattern of KAT2A expression. The PPI analysis indicated that TADA3, CCDC101, TRRAP, SUPT3H, MYC, TADA2A, and USP22 levels were positively correlated with KAT2A expression, while TADA2B and ATXN7 were negatively correlated. A positive link of KAT2A with cancer isotypes and significant connections of the KAT2A expression to poor overall and disease-free survival were also observed. Further validation was conducted using immunohistochemistry (IHC) staining, qPCR, and Western blot. Some potential HAT inhibitory drugs of KAT2A were also determined, but more work and clinical trials are required before their application. - Source: PubMed
Li HuaLi ChunYang Lu-ZongLiu Ji - Transcriptional adaptor 3 (TADA3/ADA3) is a conserved transcriptional co-activator and is dysregulated in many aggressive tumors. However, the role of TADA3 in non-small cell lung cancer (NSCLC) remains unknown. It was previously demonstrated that TADA3 expression correlates with poor prognosis in patients with NSCLC. In the present study, the expression and function of TADA3 were investigated in cells in vitro and in vivo. TADA3 expression was evaluated in clinical specimens and cell lines using reverse transcription-quantitative PCR and western blot analysis. The TADA3 protein level was significantly higher in human NSCLC specimens compared with matched normal tissues. In human NSCLC cell lines, short hairpin RNA-mediated silencing of TADA3 suppressed their proliferative, migratory and invasive abilities in vitro, and delayed G1 to S phase progression through the cell cycle. Consistent with this, TADA3 silencing increased expression of the epithelial marker E-cadherin and reduced expression of the mesenchymal markers, N-cadherin, Vimentin, Snail, and Slug. To verify the effect of TADA3 on tumor formation and growth in vivo, a mouse tumor xenograft model was established. TADA3 silencing slowed the growth of NSCLC tumor xenografts in nude mice, and excised tumors showed a similarly altered pattern of epithelial-mesenchymal transition (EMT) marker expression. The present results demonstrated the significance of TADA3 in regulating the growth and metastasis of NSCLC and may provide a theoretical basis for early diagnosis and targeted therapy of NSCLC. - Source: PubMed
Publication date: 2023/03/30
Xu Li-QinZhang Shu-WenZhang RuiChen Jing-JingYuan Zai-XinFeng JianHuang Jian-An - The dysregulation of certain long non-coding RNAs (lncRNAs) has been considered to be involved in neuropsychiatric disorders such as depression, implying the vital role of these transcripts. We have previously identified many differentially expressed lncRNAs in chronic unpredictable mild stress (CUMS) induced mice. Among them, lncRNA Gm16638-201 was highly expressed in the hippocampus (HIP) of CUMS, but the specific role and the underlying mechanisms remain unclear. Here, we reported that lncRNA Gm16638-201 was highly expressed in the prefrontal cortex (PFC) of CUMS induced depressive mice. Bioinformatic analysis shows that Gm16638-201 is mainly located in the cytoplasm. Nine neurological-related genes (Elmo2, Satb1, Hnrnpul1, Sipa1l3, Mapt, Tada3, Sgip1, IL-16, and StarD5) were predicted to be regulated in cis or trans by Gm16638-201 and involved into the 14-3-3Ɛ neurotrophic signaling pathway. We further confirmed the down-regulation of 14-3-3Ɛ and the nine predicted target genes in the PFC of CUMS mice except for Sgip1 and IL-16. In addition, they were also down-regulated in the primary cortical cell cultures with overexpression of Gm16638-201 constructed using an adenoviral-medicated gene expression system. In conclusion, we found that overexpression of Gm16638-201 negatively regulated several target genes and inhibited the 14-3-3Ɛ pathway in the PFC of CUMS induced depressive mice. This promising result suggests that Gm16638-201 may be a potential novel therapeutic target for depression. - Source: PubMed
Zhang TingWang Wan LunLiu Tong JiaLu ShuangBian Yan ChaoXiao RuiZhang Chuan Ling