Ask about this productRelated genes to: KCNK13 antibody
- Gene:
- KCNK13 NIH gene
- Name:
- potassium two pore domain channel subfamily K member 13
- Previous symbol:
- -
- Synonyms:
- K2p13.1, THIK-1, THIK1
- Chromosome:
- 14q32.11
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2016-02-04
Related products to: KCNK13 antibody
Related articles to: KCNK13 antibody
- Colorectal cancer (CRC) is among the lethal cancers, indicating the need for the identification of novel biomarkers for the detection of patients in earlier stages. RNA and microRNA sequencing were analyzed using bioinformatics and machine learning algorithms to identify differentially expressed genes (DEGs), followed by validation in CRC patients. - Source: PubMed
Publication date: 2024/11/05
Nazari ElhamKhalili-Tanha GhazalehPourali GhazalehKhojasteh-Leylakoohi FatemehAzari HaniehDashtiahangar MohammadFiuji HamidYousefli ZahraAsadnia AlirezaMaftooh MinaAkbarzade HamedNassiri MohammadrezaHassanian Seyed MahdiFerns Gordon APeters Godefridus JGiovannetti ElisaBatra JyotsnaKhazaei MajidAvan Amir - THIK-1 (KCNK13) is a halothane-inhibited and anionic-lipid-activated two-pore domain (K2P) K channel implicated in microglial activation and neuroinflammation, and a current target for the treatment of neurodegenerative disorders, for example Alzheimer's disease and amyothropic lateral sclerosis (ALS). However, compared to other K2P channels, little is known about the structural and functional properties of THIK-1. Here we present a 3.16-Å-resolution cryo-EM structure of human THIK-1 that reveals several distinct features, in particular, a tyrosine in M4 that contributes to a lower 'Y gate' that opens upon activation by physiologically relevant G-protein-coupled receptor and lipid signaling pathways. We demonstrate that linoleic acid bound within a modulatory pocket adjacent to the filter influences channel activity, and that halothane inhibition involves a binding site within the inner cavity, both resulting in conformational changes to the Y gate. Finally, the extracellular cap domain contains positively charged residues that line the ion exit pathway and contribute to the distinct biophysical properties of this channel. Overall, our results provide structural insights into THIK-1 function and identify distinct regulatory sites that expand its potential as a drug target for the modulation of microglial function. - Source: PubMed
Publication date: 2025/02/26
Rödström Karin E JEymsh BisherProks PeterHayre Mehtab SCordeiro SönkeMendez-Otalvaro EdwardMadry ChristianRowland AnnaKopec WojciechNewstead SimonBaukrowitz ThomasSchewe MarcusTucker Stephen J - The potassium (K) ion channel KCNK13 is specifically expressed in human microglia with elevated expression observed in post-mortem human brain tissue from patients with Alzheimer's disease. Modulation of KCNK13 activity by a small-molecule inhibitor is proposed as a potential treatment for neurodegenerative diseases. Herein, we describe the evolution of a series of KCNK13 inhibitors derived from a high-throughput screening campaign, resulting in , a potent, selective, and brain permeable clinical candidate molecule. demonstrated a concentration-dependent inhibition of the NLRP3-inflammasome mediated production of IL-1β from LPS-primed murine microglia. Cross-species pharmacokinetic data of are also disclosed. These findings support the advancement of in clinical trials. - Source: PubMed
Publication date: 2024/04/05
Bürli Roland WDoyle Kevin JDickson LouiseRowland AnnaMatthews KimStott Andrew JTeall MartinOssola BernardinoRussell Samuel GHarvey Jenna R MWu YimingNarayana LakshminarayanaBrice Nicola LCarlton MarkDawson Lee A - The trigeminal ganglion (TG) collects afferent sensory information from various tissues. Recent large-scale RNA sequencing of neurons of the TG and dorsal root ganglion has revealed a variety of functionally distinct neuronal subpopulations, but organ-specific information is lacking. - Source: PubMed
Publication date: 2024/01/18
Sotelo-Hitschfeld PamelaBernal LauraNazeri MasoudRenthal WilliamBrauchi SebastianRoza CarolinaZimmermann Katharina - Periparturient hypocalcemia is a complex metabolic disorder that occurs at the onset of lactation because of a sudden irreversible loss of Ca incorporated into colostrum and milk. Some cows are unable to quickly adapt to this demand and succumb to clinical hypocalcemia, commonly known as milk fever, whereas a larger proportion of cows develop subclinical hypocalcemia. The main goal of this study was to identify causative mutations and candidate genes affecting postpartum blood calcium concentration in Holstein cows. Data consisted of blood calcium concentration measured in 2513 Holstein cows on the first three days after parturition. All cows had genotypic information for 79 k SNP markers. Two consecutive rounds of imputation were performed: first, the 2513 Holstein cows were imputed from 79 k to 312 k SNP markers. This imputation was performed using a reference set of 17,131 proven Holstein bulls with 312 k SNP markers. Then, the 2513 Holstein cows were imputed from 312 k markers to whole-genome sequence data. This second round of imputation used 179 Holstein animals from the 1000 Bulls Genome Project as a reference set. Three alternative phenotypes were evaluated: (1) total calcium concentration in the first 24 h postpartum, (2) total calcium concentration in the first 72 h postpartum calculated as the area under the curve; and (3) the recovery of total calcium concentration calculated as the difference in total calcium concentration between 72 and 24 h. The identification of genetic variants associated with these traits was performed using a two-step mixed model-based approach implemented in the R package MixABEL. The most significant variants were located within or near genes involved in calcium homeostasis and vitamin D transport (GC), calcium and potassium channels (JPH3 and KCNK13), energy and lipid metabolism (CA5A, PRORP, and SREBP1), and immune response (IL12RB2 and CXCL8), among other functions. This work provides the foundation for the development of novel breeding and management tools for reducing the incidence of periparturient hypocalcemia in dairy cattle. - Source: PubMed
Publication date: 2023/12/11
Novo Larissa CPoindexter Michael BRezende Fernanda MSantos José E PNelson Corwin DHernandez Laura LKirkpatrick Brian WPeñagaricano Francisco