Ask about this productRelated genes to: SYVN1 antibody
- Gene:
- SYVN1 NIH gene
- Name:
- synoviolin 1
- Previous symbol:
- -
- Synonyms:
- HRD1, DER3
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-28
- Date modifiied:
- 2016-06-21
Related products to: SYVN1 antibody
Related articles to: SYVN1 antibody
- Colorectal cancer (CRC) is a major global health burden with limited therapeutic efficacy, highlighting the need for novel pathogenic insights and therapeutic targets. Tissue Inhibitor of Metalloproteinase 1 (TIMP1) is overexpressed in CRC and correlates with poor prognosis, but its functional role and underlying mechanisms, particularly in relation to ferroptosis, remain unclear. - Source: PubMed
Publication date: 2026/04/16
Geng ChanghuiChen PengWang ZhihuiWang ShaokeLi Zheng'angBai Xuefeng - Aberrant cholesterol biosynthesis is a notable hallmark of cancers, supporting unlimited cell proliferation. Previously, we delineated that cholesterol synthases FDFT1 and SQLE promoted colorectal cancer (CRC) cell proliferation, while how these enzymes influence CRC metastasis and stemness remains unclear. This study demonstrates that suppress of FDFT1 or SQLE enhances CRC metastasis and stemness through impairing ER stress and degrading PDIA4 or SYVN1 individually. Additionally, the function of FDFT1 and SQLE on CRC metastasis relies on tryptophan. Tryptophan augments PDIA4-ACLY and SYVN1-SCD1 co-complex association to drive CRC metastasis and stemness. Consequently, the specific inhibitor of ACLY or SCD1 blocks FDFT1 or SQLE deficiency induced CRC metastasis using Male BALB/c nude mice. Besides, sub-cytotoxic concentrations of inhibitors targeting FDFT1 or SQLE generate the invasive feature in CRC cells. Overall, these findings indicate that cholesterol synthases impact ER homeostasis and fatty acid synthesis to regulate CRC metastasis and stemness, offering potential for combined targeted therapies in CRC. - Source: PubMed
Publication date: 2026/04/14
Li WenjieLin MoubinZhao YunTang YuqiChen YingHe Luwei - Osseointegration in patients with type 2 diabetes mellitus (T2DM) is poor, and overcoming osseointegration impairment safely and efficiently remains challenging. - Source: PubMed
Publication date: 2026/04/13
Wang LingxiaoDiao ZhanqiuWang WanqingHuang YishuLiu YangGao ZhenhuaMa PanShan ZhaochenLi JunFan Zhipeng - - Source: PubMed
Publication date: 2026/03/26
Zhu FupingLi WupingCao YinshengDai BingWu HangZhu YutongLiu Hui - Targeted protein degradation (TPD) technologies provide huge opportunities for drug discovery, but degrading transmembrane (TM) targets remains challenging. Since TM proteins are canonically folded on the endoplasmic reticulum (ER) membrane, we hypothesized that harnessing ER-associated degradation (ERAD) may enable efficient degradation of TM proteins. Here, we established a TPD technology hijacking ERAD and named it ERAD-engaging chimeras (ERADECs), capable of degrading TM targets with high efficacy. We identified desonide as a binder of SYVN1, an ER E3 ligase mediating ERAD. We designed ERADECs targeting programmed death-ligand 1 (PD-L1) by connecting desonide to a known PD-L1 ligand and observed SYVN1- and ERAD-dependent PD-L1 degradation with high efficacy. Functionally, these ERADECs exhibited stronger tumor suppression and PD-L1-lowering effects than a clinically used PD-L1 antibody in vivo. The concept of ERADECs is also expandable to other membrane targets. Collectively, we established a platform technology hijacking ERAD to selectively degrade TM targets with remarkable efficiency. - Source: PubMed
Song HaikunWang WeiMei TingfangZheng HuiwenNing KeniLiu XiaofanCheung SiulamCao ZhiyuanSheng DanqiMai XiaohanZhu HaoranGuo GuankaiLiu ShuaimengWei RongkaiWang QianCao YuDing YuFei YiyanLiu RuiHattori MotoyukiSheng ChunquanLu Boxun