Ask about this productRelated genes to: HECTD3 antibody
- Gene:
- HECTD3 NIH gene
- Name:
- HECT domain E3 ubiquitin protein ligase 3
- Previous symbol:
- -
- Synonyms:
- FLJ21156
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-07
- Date modifiied:
- 2016-03-09
Related products to: HECTD3 antibody
Related articles to: HECTD3 antibody
- Thyroid hormone receptor-interacting protein 13 (TRIP13), an enzyme from the AAA-ATPase family, facilitates the assembly or disassembly of protein complexes and participates in various biological processes. However, its impact on cancer immune infiltration and pan-cancer prognosis remains largely unexplored. - Source: PubMed
Publication date: 2026/04/22
Zhao YuanqiaoZhao YongqiLiu RuilinLi JingWang Yinhuai - HECT E3 ligases regulate many cellular processes, yet how they recognise their substrates and synthesise specific types of poly-ubiquitin chains is still incompletely understood. HECTD3, a member of the "other HECT" family, is implicated in the regulation of inflammation, apoptosis, and infection and highly expressed in several cancers. These functions are largely attributed to its ligase activity and modification of diverse substrates with different types of ubiquitin chains. We present a detailed analysis of the ligase activity of HECTD3, including its ubiquitin linkage preferences, oligomeric state and substrate ubiquitination. Using cryo-EM, we provide the full-length structures of HECTD3 in both apo and ubiquitin-loaded forms, revealing key insights into its domain organisation, including discovery of a distinct fold of the N-terminal region, and mechanistic features. Some of these are shared with other HECT ligases, while others are unique to HECTD3 and contribute to differences in its catalytic mechanisms and functional diversity. - Source: PubMed
Publication date: 2026/02/14
Huber JessicaEsposito DiegoMaslen SarahChambers Dominic OSkehel J MarkRittinger Katrin - Upon infection, viral DNA/RNA is detected by cGAS/RIG-I-like receptors, triggering the adaptor MITA/STING- or VISA/MAVS-dependent innate antiviral immune response respectively. Both adaptors recruit the conserved TRAF3 and TRAF6 to activate TBK1-IRF3 and TAK1-NF-κB pathways respectively, leading to collaborative induction of antiviral effector genes. How the functions of TRAF3 and TRAF6 bifurcate in innate antiviral signaling remains enigmatic. We identified HTATSF1 as a positive regulator of virus-triggered innate antiviral response. Upon viral infection, HTATSF1 promotes HECTD3-catalyzed K63-linked polyubiquitination of TRAF3, leading to its recruitment of TBK1 and activation of IRF3. In contrast, HTATSF1 promotes recruitment of TAK1 to TRAF6 and activation of the TAK1-IKK-NF-κB axis independently of HECTD3. HTATSF1-deficiency impairs induction of downstream antiviral genes, and HTATSF1-deficient mice exhibit decreased cytokine production and increased mortality upon viral infection. Our findings demonstrate that HTATSF1 is an essential regulator of innate antiviral immune response by orchestrating the TRAF3-IRF3 and TRAF6-NF-κB pathways. - Source: PubMed
Publication date: 2025/11/26
Zeng Jia-QingRuan Zi-LunZhang QiYi Xue-MeiChen Yun-DaHu Ming-MingLi Shu - Carcass weight (CW) is a major determinant of beef yield and market value in Korea, yet the genetic basis of this trait remains largely unexplored in cattle from Jeju Island. In this study, we performed a genome-wide association study (GWAS) using both a mixed linear model (MLM) and the FarmCPU approach, followed by pathway and network analyses to identify loci and biological functions underlying CW variation. A total of 256 Jeju cattle (92 Jeju Black and 164 Jeju Black × Hanwoo crossbreds) were initially sampled. One crossbred sample failed genotyping, leaving 255 animals (92 Jeju Black and 163 crossbreds) for analysis. Animals were genotyped using the Illumina BovineSNP50 v3 BeadChip, and 39,055 high-quality single nucleotide polymorphisms (SNPs) were retained after quality control. The MLM analysis detected no genome-wide significant associations, whereas the FarmCPU analysis identified six significant loci on chromosomes 3, 5, 6, 10, and 13, each explaining 2.55-9.58% of the phenotypic variance. Candidate genes located near these loci included , , , , , and two uncharacterized protein-coding genes. Functional enrichment analysis identified biologically relevant pathways including lysine degradation, tryptophan metabolism, glycerolipid metabolism, fatty acid biosynthesis, extracellular matrix-receptor interaction, and signaling cascades such as PI3K-Akt and Rap1, although most pathways were not statistically significant after FDR correction. Protein-protein interaction (PPI) network analysis using STRING highlighted modules of signaling, extracellular matrix, and metabolic genes. These clusters suggest that coordinated interactions among these pathways contribute to carcass growth and development. These findings provide new insights into the molecular basis of CW in Jeju Black and Hanwoo × Jeju Black crossbred cattle and identify candidate genes and pathways that may be useful for genomic selection and the sustainable improvement of Jeju Black cattle populations. - Source: PubMed
Publication date: 2025/11/28
Won MiyoungLee JonganShin Sang-MinLee Seung-EunKim Won-JaeKim Eun-TaeKim Tae-HeePark Hee-BokShokrollahi Borhan - SLC7A11 (xCT) is a key subunit of the cysteine/glutamate transporter (system xc ), which is crucial for maintaining cellular redox homeostasis (especially glutathione synthesis) and regulating Ferroptosis. It is highly expressed in various malignant tumors and is a key factor leading to treatment resistance, making it an important anti-cancer target. This review systematically summarizes the complex multi-level regulatory network of SLC7A11: at the transcriptional level, key factors form precise regulatory hubs: the KEAP1/NRF2 pathway directly activates SLC7A11 transcription, endowing cancer cells with antioxidant and anti ferroptotic abilities; P53 acts as a core inhibitory factor, and its activity state (activated by STEAP3 iron overload or regulated by Gankyrin/DM2 degradation) directly determines the intensity of inhibition of SLC7A11; ATF4 integrates endoplasmic reticulum stress, oxidative damage, and epigenetic signals (such as SIRT3/KDM3B/KDM4A), and bidirectionally regulates SLC7A11 transcription. Epigenetic regulation involves RNA m6A modification (ALKBH5/FTO reduces stability, METTL3/IGF2BP3 enhances stability) and histone modification (BAP1/PRC1 inhibits through H2Aub). After translation, the stability of SLC7A11 protein is strictly regulated by ubiquitination (SOCS2/HECTD3 promotes degradation, OTUB1/TCF12 inhibits degradation) and palmitoylation (ZDHHC8/DUXAP8 antagonizes degradation). Of particular importance is that non coding RNAs indirectly release their inhibition of SLC7A11 mRNA by acting as "molecular sponges" to adsorb specific miRNAs, profoundly affecting tumor progression and resistance to ferroptosis. This study reveals how cancer cells abnormally upregulate SLC7A11 by hijacking multi-level mechanisms, gaining strong antioxidant/anti ferroptotic abilities, which are the core basis for their survival, proliferation, and resistance to treatment. This study also identified SLC7A11 as a convergence point for multiple key pathways, making it an ideal hub target for intervening in cancer and overcoming drug resistance. - Source: PubMed
Publication date: 2025/10/15
Zhang XizhengZhang YaoWei JiayuLi XuyanJiang AnqiShen YingHou YongzhongLiu Qian