Ask about this productRelated genes to: KCTD15 Blocking Peptide
- Gene:
- KCTD15 NIH gene
- Name:
- potassium channel tetramerization domain containing 15
- Previous symbol:
- -
- Synonyms:
- MGC25497
- Chromosome:
- 19q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-05
- Date modifiied:
- 2019-02-21
Related products to: KCTD15 Blocking Peptide
Related articles to: KCTD15 Blocking Peptide
- Accumulating evidence strongly confirms that microRNAs (miRNAs) play a pivotal role in the development and progression of cardiovascular diseases. Specifically, miR-146a has been demonstrated to be implicated in the pathogenesis of multiple cardiac diseases. Nevertheless, the role of miR-146a in ischemic heart disease and its underlying molecular mechanism remains unclear. The expression levels of miR-146a during different stages of cardiac development were detected by quantitative polymerase chain reaction (qPCR). Gain-of-function and loss-of-function assays were conducted to evaluate the impact of miR-146a on cardiomyocyte (CM) proliferation. A myocardial infarction (MI) model was established, and M-mode echocardiography and Masson's trichrome staining were used to further investigate the effects of miR-146a on cardiac function recovery post-MI. Then, bioinformatics approaches, including RNA-seq, were utilized to predict Kctd15 as a potential target gene of miR-146a. Finally, a dual luciferase reporter assay and rescue experiment were used to verify miR-146a interactions with Kctd15. First, we found that miR-146a expression decreased with age. Then, overexpression of miR-146a inhibited CM proliferation, while miR-146a inhibition promoted CM proliferation in vitro. Similarly, overexpression of miR-146a was impaired in cardiac function recovery post-MI, whereas miR-146a deficiency improved post-MI cardiac function. Further, bioinformatics analysis suggested that miR-146a might regulate CM proliferation by targeting Kctd15, which was confirmed by overexpression of Kctd15 blocking the effect of miR-146a on CM proliferation. The current study demonstrates that miR-146a regulates CM proliferation through the miR-146a/Kctd15 mRNA/Kctd15 protein pathway, which may provide a potential molecular target for preventing and treating myocardial injury. KEY MESSAGES: Acute myocardial infarction (AMI) accounts for about 7 million deaths per year worldwide; the existing treatment methods such as thrombolysis and percutaneous coronary interventions cannot achieve a good prognosis. This study demonstrates that miR-146a is a negative regulator of CM proliferation and exerts its function through Kctd15. Kctd15 was first proposed to be related to CM proliferation. The study provides new support for endogenous CM proliferation and treatment in other cardiovascular diseases. - Source: PubMed
Publication date: 2026/03/29
Zhang ChenruiWei XuejiaoHe YongqinHu XingweiLi MengshaLi Bing - Polycystic ovary syndrome (PCOS), a common endocrine disorder, has been linked to environmental factors such as exposure to per- and polyfluoroalkyl substances (PFAS), which may induce disruptions in ovarian function. However, the molecular mechanisms underlying PFAS-PCOS interactions remain poorly understood. - Source: PubMed
Publication date: 2026/02/19
Jiang YuxiaoGe LiyingZhang ShanshanWang Mingming - Triple-negative breast cancer (TNBC) remains an aggressive malignancy with limited therapeutic options and poor prognosis, underscoring the critical need for novel therapeutic targets. This investigation elucidates the functional role of the potassium channel tetramerization domain 15 (KCTD15) in TNBC progression, providing mechanistic insights into its potential as a therapeutic target for this challenging disease. KCTD15 exhibited high expression in TNBC tissues, correlating with advanced grade and unfavorable prognosis. Functionally, KCTD15 knockdown in TNBC cell lines (BT-549/MDA-MB-231) markedly suppressed cellular proliferation, migration, and cancer stem cell properties, while concomitantly enhancing apoptosis. Mechanistically, KCTD15 directly interacted with KLF4, facilitating its nuclear translocation and subsequent activation of the β-catenin signaling cascade. Notably, KLF4 knockdown abrogated KCTD15-mediated stemness maintenance and β-catenin pathway activation. In vivo, KCTD15 silencing reduced xenograft tumor growth and downregulated Ki67, KLF4, and β-catenin protein expression in tumor tissues, confirming its oncogenic role through the KLF4/β-catenin axis. Our findings establish KCTD15 as a pivotal regulator of TNBC stemness through modulation of the KLF4/β-catenin signaling axis. These results provide a robust preclinical rationale for developing therapeutic strategies targeting this molecular axis in TNBC management. - Source: PubMed
Yao LiangSun WeiXing JunFeng Jing - Anthracyclines are a widely used and effective class of chemotherapy. However, a major limitation for their use is cardiotoxicity, manifesting as systolic dysfunction, congestive heart failure (HF) and arrhythmias. - Source: PubMed
Publication date: 2025/12/18
Reddy Joseph SPereyra MilagrosAbbas Mohammed TiseerArsanjani RezaPrah Isaac EBoddicker Nicholas JCerhan James RLarson Melissa CMwangi RaphaelHabermann Thomas MVillarraga Hector RVierkant Robert ALuehrs Tony CSicotte HuguesEgan Jan BLazaridis Konstantinos NMoossavi MaryamXu XiaoleiAdvani Pooja PAyoub ChadiNorton Nadine - The transcriptional regulation of skin appendage morphogenesis during development is poorly understood. We identified a previously unknown critical role of KCTD1/KCTD15 complexes in keratinocytes for the proper formation of skin appendages. Individuals with dominant-negative mutations in KCTD1/KCTD15 have sparse hair and anhidrosis, and mice lacking KCTD1 and KCTD15 in keratinocytes have diminished sweat glands and sebaceous glands as well as progressive hair sparseness. In this study, we show that these phenotypes are a consequence of the lack of the repressor function of KCTD1/KCTD15 complexes on AP-2α and AP-2β transcription factors in keratinocytes. Countering the derepression of AP-2α/AP-2β by heterozygosity for their genes rescues skin appendage defects in mice lacking KCTD1/KCTD15 in keratinocytes. Strikingly, loss of AP-2α and AP-2β in keratinocytes results in similar abnormalities, demonstrating that both an increase and a decrease in AP-2α/AP-2β activity impairs skin appendage development. In addition, we find that KCTD1/KCTD15-mediated repression of AP-2α/AP-2β in keratinocytes maintains epidermal homeostasis in the adult and that a dermatitis caused by deficiency of AP-2α in keratinocytes can be prevented by inactivation of KCTD1/KCTD15 complexes. Collectively, our findings identify a critical role of KCTD1/KCTD15 complexes in regulating skin appendage morphogenesis and epidermal homeostasis by repressing AP-2α/AP-2β transcription factors in keratinocytes. - Source: PubMed
Publication date: 2025/10/10
Senapati BillRaymundo Jackelyn RMakkar JassonDriskell Ryan RMarneros Alexander G