Ask about this productRelated genes to: KCTD16 antibody
- Gene:
- KCTD16 NIH gene
- Name:
- potassium channel tetramerization domain containing 16
- Previous symbol:
- -
- Synonyms:
- KIAA1317
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-19
- Date modifiied:
- 2018-11-16
Related products to: KCTD16 antibody
Related articles to: KCTD16 antibody
- Chronic pain affects nearly 10% of the global population and remains a major clinical challenge due to the limited efficacy and adverse effects of current therapies. In this study, we identify the potassium channel tetramerization domain protein KCTD16 as a key modulator of GABA receptor mediated inhibition of nociceptive transmission. Immunohistochemical analysis revealed prominent KCTD16 expression in dorsal horn and dorsal root ganglion (DRG) neurons, consistent with a role in spinal nociceptive processing. KCTD16 knockout (KO) mice exhibited increased mechanical thresholds relative to wild-type (WT) littermates, while thermal sensitivity remained unchanged; this phenotype persisted following carrageenan-induced inflammation. The GABA receptor agonist Baclofen produced strong analgesic effects in WT mice under both basal and inflammatory conditions, whereas its anti-allodynic efficacy was significantly reduced in KO animals. Whole-cell patch-clamp recordings from dorsal horn neurons showed comparable baseline miniature excitatory and lower inhibitory postsynaptic currents (mEPSCs and mIPSCs) for KCTD16. However, following inflammation, Baclofen-induced suppression of excitatory transmission was potentiated in WT but markedly attenuated in KO neurons. Light-evoked synaptic inhibitory currents and calcium imaging of cultured DRG neurons further demonstrated enhanced Baclofen sensitivity in WT cells. These findings indicate that KCTD16 plays a critical role in presynaptic modulation of inhibitory control in the spinal dorsal horn, affecting the balance between the excitation and inhibition in nociceptive circuits. Collectively, these results demonstrate that KCTD16 modulates GABA receptor-dependent inhibitory control of nociceptive signaling and highlight the GABA receptor-KCTD16 complex as a promising new molecular target for effective pain treatments. - Source: PubMed
Publication date: 2026/01/25
Vasconcelos DanielHeles MarioAdamek PavelBhattacharyya AnirbanMelichar AdolfTurecek RostislavPalecek Jiri - Ovarian cancer (OC) remains one of the most lethal gynecological malignancies, characterized by late-stage diagnosis and high recurrence rates. Despite advances in treatment, the overall survival rate for OC patients remains low due to the lack of reliable biomarkers for early detection and prognosis. Thus, there is an urgent need for novel diagnostic and prognostic biomarkers to improve patient outcomes. In this study, we explored the potential role of the KCTD (Potassium Channel Tetramerization Domain-containing) family genes in OC. - Source: PubMed
Zhang LingCheng ChongTang Bin - Anti-IgLON5 disease is an autoimmune encephalopathy that often leads to severe disability or death. The efficacy of immunotherapy remains unknown. - Source: PubMed
Grüter ThomasGaig CarlesCrijnen Yvette STitulaer Maarten JSabater LidiaHeidbreder AnnaDargvainiene JustinaTietz AnjaKovac StjepanaDik AndreErro María ElenaLewerenz JanKraft AndreaSeifert FrankHöftberger RomanaThaler Franziska Sde Azevedo LucieWickel Jonathande Vries Juna MBoon Agnita J Wvan Steenhoven Robin WGold RalfWandinger Klaus-PeterKuhlenbäumer GregorDalmau Josep OLeypoldt FrankGraus FrancescAyzenberg Ilya - A significant correlation between type 2 diabetes mellitus (T2DM) and mood has been reported. However, the specific mechanism of mood's role in T2DM is unclear. This study aims to discover mood-related biomarkers in T2DM and further elucidate their underlying molecular mechanisms. The GSE81965 and GSE55650 datasets were sourced from public databases, and mood-related genes (MRGs) were retrieved from previous literature. Initially, differentially expressed MRGs (DE-MRGs) were obtained by combining differential expression analysis and weighted gene co-expression network analysis (WGCNA). Subsequently, the DE-MRGs were incorporated into the LASSO and SVM to identify diagnostic biomarkers for T2DM. Four machine learning methods were utilized to construct the diagnostic models in T2DM, and the model with the optimal algorithm was screened. Further, based on biomarkers, functional enrichment, immune infiltration, and regulatory network analyses were conducted to excavate deeper into the pathogenesis of T2DM. In vivo experiments were used to validate the expression of the biomarkers. A total of 23 DE-MRGs were identified by overlapping 723 DEGs and 64 key modules, and there were strong positive correlations between these DE-MRGs. Afterward, KCTD16, SLC8A1, RAB11FIP1, and RASGEF1B were identified as biomarkers associated with mood in T2DM, and they had favorable diagnostic performance. Meanwhile, the RF diagnostic model constructed based on biomarkers was performed optimally and had high diagnostic accuracy for T2DM patients. Animal experiments indicated that expression levels of SLC8A1, RAB11FIP1, and RASGEF1B in T2DM were consistent with the microarray results. In conclusion, KCTD16, SLC8A1, RAB11FIP1, and RASGEF1B were identified as biomarkers related to mood in T2DM. - Source: PubMed
Publication date: 2025/02/07
Wang MenglongWang TongruiLiu YangZhou LurongYin YuanpingGu Feng - During GABAergic synaptic transmission, G protein-coupled GABA receptors (GBRs) activate K channels that prolong the duration of inhibitory postsynaptic potentials (IPSPs). We now show that KCTD16, an auxiliary GBR subunit, anchors hyperpolarization-activated cyclic nucleotide-gated (HCN) channels containing HCN2/HCN3 subunits to GBRs. In dopamine neurons of the VTA (DA neurons), this interaction facilitates activation of HCN channels via hyperpolarization during IPSPs, counteracting the GBR-mediated late phase of these IPSPs. Consequently, disruption of the GBR/HCN complex in KCTD16 mice leads to prolonged optogenetic inhibition of DA neuron firing. KCTD16 mice exhibit increased anxiety-like behavior in response to stress - a behavior replicated by CRISPR/Cas9-mediated KCTD16 ablation in DA neurons or by intra-VTA infusion of an HCN antagonist in wild-type mice. Our findings support that the retention of HCN channels at GABAergic synapses by GBRs in DA neurons provides a negative feedback mechanism that restricts IPSP duration and mitigates the development of anxiety. - Source: PubMed
Publication date: 2025/02/04
Pérez-Garci EnriquePysanenko KaterynaRizzi GiorgioStuder FlorianUlrich DanielFritzius ThorstenFrüh SimonPorcu AlessandraBesseyrias ValérieMelichar AdolfGassmann MartinBarkat Tania RinaldiTureček RostislavTan Kelly RBettler Bernhard