Ask about this productRelated genes to: KCTD10 Blocking Peptide
- Gene:
- KCTD10 NIH gene
- Name:
- potassium channel tetramerization domain containing 10
- Previous symbol:
- -
- Synonyms:
- MSTP028, BTBD28
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-28
- Date modifiied:
- 2019-02-21
Related products to: KCTD10 Blocking Peptide
Related articles to: KCTD10 Blocking Peptide
- Lung adenocarcinoma (LUAD) and chronic airway obstruction frequently coexist and are associated with poorer clinical outcomes. Although airway obstruction is recognized as a risk factor for adverse prognosis in LUAD, the molecular alterations associated with airway obstruction in LUAD remain incompletely understood. Most previous studies have been confounded by smoking-related molecular changes. - Source: PubMed
Publication date: 2026/07/19
Jiang ShutingXu QuanlinLiu DahongXuan KeweiShi WenyuChao XianzhenMan QuanqingLiu Yi - Co-directional (CD) transcription-replication conflicts (TRCs) arise when the DNA replication and transcription machineries progress along the same DNA template. Although generally considered less severe than head-on (HO) TRCs, CD TRCs are now recognized as frequent and actively regulated events that influence genome stability. The Cullin 3-Potassium channel tetramerization domain containing 10 (KCTD10) ubiquitin ligase complex functions as a bivalent sensor that detects CD collisions and directs the nonproteolytic ubiquitination of the elongation factor TCEA2, transiently remodeling RNA polymerase II to permit replisome bypass. This sensing-driven remodeling reframes CD TRCs as dynamic decision nodes where replication and transcription priorities are continuously negotiated, highlighting how conflict geometry, ubiquitin signaling, and genome maintenance are functionally integrated. - Source: PubMed
Publication date: 2026/05/13
Chen BinKloeber Jake AHuang JinzhouLou Zhenkun - IGF2BP1 stabilizes oncogenic mRNAs via m6A binding to drive lung adenocarcinoma (LUAD) progression, yet how this modification orchestrates immune evasion remains unclear. - Source: PubMed
Publication date: 2026/05/10
Xu YufenTan XiaoliLv XiaodongYang QiKe XingxingChen Wenyu - Transcription-replication conflicts (TRCs) are an increasingly recognized driver of genome instability in human cells. We recently identified the CUL3 adaptor KCTD10 as a sensor of co-directional TRCs, recruiting CUL3 to ubiquitinate transcriptional machinery and clear the path for replication forks. Here, we discuss the implications of this conflict-resolution pathway for human cancer. By integrating our mechanistic findings with large-scale functional genomics datasets, we identify oncogenic conditions that potentially create TRC-rich environments and render cells selectively dependent on KCTD10. These contexts reveal new mechanistic insights and potential therapeutic opportunities across a range of human cancers. - Source: PubMed
Publication date: 2026/03/04
Kloeber Jake AChen BinMutter RobertHuang JinzhouLou Zhenkun - Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of death worldwide, with plaque instability being a major culprit. Phenotypic switching of vascular smooth muscle cells (VSMCs) is a central event in atherosclerosis, driving both plaque progression and stability, yet the underlying mechanisms are incompletely understood, limiting drug development targeting this process. Kinesin family member 13B (KIF13B) has been implicated in vascular biology, but its function in VSMCs is unknown. Here, we demonstrate that VSMC-specific deletion of Kif13b in mice overexpressing proprotein convertase subtilisin/kexin type 9 (PCSK9) exacerbates lesion development and impairs plaque stability, characterized by thinner fibrous caps and increased inflammation. Mechanistically, we determined that KIF13B facilitated the ubiquitination and proteasomal degradation of Krüppel-like factor 4 (KLF4) through the potassium channel tetramerization domain-containing 10-dependent (KCTD10-dependent) pathway. This KIF13B/KCTD10 axis reduced KLF4 protein levels, thereby inhibiting the proinflammatory responses and fibroblast-like transition of VSMCs to preserve their contractile phenotype. Importantly, the adverse effects of Kif13b deficiency on atherogenesis were effectively rescued by the small-molecule KLF4 inhibitor Kenpaullone. Our results unveil a VSMC-specific atheroprotective role for KIF13B, define the KIF13B/KCTD10/KLF4 pathway as a key regulatory axis governing VSMC fate and plaque stability, and validate the therapeutic potential of KIF13B for treating advanced atherosclerosis. - Source: PubMed
Publication date: 2026/01/29
Miao GuolinHan YufeiChen JingxuanLiu YiranZhang GePei ShaotongZhao YinqiXu YitongZheng LiwenLi ZhaolingLiu XiangruShi SijingKang XuyaLiu YahanZhang LingHuang WeiWang YuhuiTang JunnanDong ErdanXian Xunde