Ask about this productRelated genes to: HECTD1 antibody
- Gene:
- HECTD1 NIH gene
- Name:
- HECT domain E3 ubiquitin protein ligase 1
- Previous symbol:
- -
- Synonyms:
- KIAA1131
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-18
- Date modifiied:
- 2016-03-09
Related products to: HECTD1 antibody
Related articles to: HECTD1 antibody
- Acute ischemic stroke (AIS) is a leading cause of death and long-term disability globally, with current treatment options offering limited efficacy in improving neurological recovery. Building upon our earlier discovery, we previously characterized circHECTD1, a circular RNA generated from exons 23-24 of the HECTD1 gene, as a critical regulator of ischemic brain injury. Despite its therapeutic potential, targeted interventions against circHECTD1 have yet to be developed. In this work, we report a mannose-modified lipid nanoparticle for targeted delivery of si-circHECTD1 (si-circHECTD1@mLNP) to evaluate its therapeutic impact on neuroinflammation, infarct volume, and sensorimotor functions of stroke mice. In a murine transient middle cerebral artery occlusion (tMCAO) model, we found that nose-to-brain administration of si-circHECTD1@mLNPs selectively inhibited circHECTD1 expression, subsequently alleviated neuroinflammation, suppressed both astrocytic and microglial activation, reduced infarct volume, and ultimately improved functional recovery. Transcriptomic profiling further demonstrates not only downregulation of neuroinflammation-associated pathways but also upregulation of neuro-restorative programs. Our findings confirm circHECTD1 as a pathogenic mediator and therapeutic target in AIS, while establishing a versatile mLNP platform for RNA therapy to improve neurological outcomes of AIS. - Source: PubMed
Publication date: 2026/04/20
Ren HuiCai NingboSun YanLi GuanlongLi ZhuoyanShen LingYao HonghongHan BingHuang XinxinJia Yanpeng - Alveolar epithelial cells type 2 are lung progenitor and secretory cells capable of secreting four surfactant proteins, namely surfactant protein A (SFTPA), surfactant protein B (SFTPB), surfactant protein C (SFTPC), and surfactant protein D (SFTPD). Among these proteins, SFTPB not only participates in the composition of surfactant proteins but also has important immune functions. In occupational dust exposure, dust entering the bronchi and alveoli can come into direct contact and stimulate AT2. To investigate the expression of SFTPB in fibrotic lungs, we constructed a mouse pulmonary fibrosis model using silica and detected the spatial expression of SFTPB protein and SFTPB mRNA in lung sections. Herein, we observed an increase in SFTPB production from AT2 in SiO-exposed mice without a corresponding increase in mRNA levels in the lung sections. Pulmonary fibrosis continued to progress in mice on day 112 after modeling. During the progression of pulmonary fibrosis, the protein level of SFTPB was always higher than that of the control mice, accompanied by increased HECT domain E3 ubiquitin protein ligase 1 (HECTD1) and ubiquitin (Ub). HECTD1 knockdown can partially reverse the increase in SFTPB in AT2 induced by silica. Therefore, we concluded that HECTD1 mediated SFTPB overexpression in silica-induced fibrotic lungs. - Source: PubMed
Publication date: 2025/11/09
Chen MenglingFang Shencun - Retinoic acid (RA), a metabolite of vitamin A, exerts paradoxical effects in tissue repair, promoting regeneration in some contexts while driving fibrosis in others. However, the mechanisms governing this functional switch remain elusive. Here, we identify RA as a key paracrine signal that links tubular epithelial injury to fibroblast activation in renal fibrosis. Spatial metabolomics and single-cell transcriptomics reveal that ALDH1A2-mediated RA synthesis is upregulated in injured renal tubules, while RA receptor signaling is enriched in interstitial fibroblasts. RA stimulation induces fibroblast-to-myofibroblast transition (FMT) by upregulating RAI14, a cytoskeletal adaptor that binds and stabilizes TRIOBP, thereby preventing its HECTD1-mediated ubiquitination and degradation. This stabilization enhances F-actin assembly and cytoskeletal tension, leading to YAP nuclear translocation and activation of profibrotic transcriptional programs. Genetic ablation of RAI14 significantly attenuates renal fibrosis in vivo. Together, our findings uncover a tubule-derived RA-RAI14-TRIOBP-YAP axis that translates epithelial injury into fibroblast mechanotransduction, providing mechanistic insight into epithelial-mesenchymal communication and a potential therapeutic target for fibrotic kidney disease. - Source: PubMed
Publication date: 2025/11/14
Zhu JunWang MeixiaZhang YizhiWang XintaoDai LeiLi ZhuLi YangbingZhang XinxinWang HongjieZhao JieLi XiaozhouWang Hong-Hui - - Source: PubMed
Publication date: 2025/09/17
Li YapingHuang BaohuaYang HuaKan ShuangYao YanlingLiu XinPu ShimingHe GuozhangKhan Taj-MalookQi GuangyingZhou ZupingShu WeiChen Ming - Our goal is to leverage publicly available whole transcriptome and genome-wide CRISPR-Cas9 screen data to identify and prioritize novel breast cancer therapeutic targets. - Source: PubMed
Publication date: 2025/09/01
Lin Hao-KuenDai JiaweiPusztai Lajos