KCNG1 antibody - N-terminal region (ARP35469_P050)
- Known as:
- KCNG1 (anti-) - N-terminal region (ARP35469_P050)
- Catalog number:
- arp35469_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KCNG1 antibody - N-terminal region (ARP35469_P050)
Related genes to: KCNG1 antibody - N-terminal region (ARP35469_P050)
- Gene:
- KCNG1 NIH gene
- Name:
- potassium voltage-gated channel modifier subfamily G member 1
- Previous symbol:
- KCNG
- Synonyms:
- Kv6.1, kH2, K13
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-22
- Date modifiied:
- 2016-10-05
Related products to: KCNG1 antibody - N-terminal region (ARP35469_P050)
Related articles to: KCNG1 antibody - N-terminal region (ARP35469_P050)
- Physical activity is an established protective factor for colorectal cancer (CRC), but it is unclear if genetic variants modify this effect. To investigate this possibility, we conducted a genome-wide gene-physical activity interaction analysis. - Source: PubMed
Publication date: 2026/02/05
Peoples Anita RObón-Santacana MireiaKim Andre EKawaguchi Eric SFu YuboQu ConghuiMoratalla-Navarro FerranMorrison JohnLin YiArndt VolkerBerndt Sonja IBien Stephanie ABishop D TimothyBouras EmmanouilBrenner HermannBuchanan Daniel DCampbell Peter TChan Andrew TChang-Claude JennyConti David VCorley Douglas AcDevall Matthew ADimou NikiDrew David AGruber Stephen BGunter Marc JHarlid SophiaHarrison Tabitha AHoffmeister MichaelHsu LiHuyghe Jeroen RKeku Temitope OKundaje AnshulLewinger Juan PabloLi LiLynch Brigid MLe Marchand LoicMartín VicenteMurphy NeilNewton Christina COgino ShujiHardikar SheetalOse JenniferPai Rish KPalmer Julie RPapadimitriou NikosPardamean BensPellatt Andrew JPinchev MilaPlatz Elizabeth APotter John DRennert GadRuiz-Narvaez Edward ASakoda Lori CSchoen Robert EShcherbina AnnaStern Mariana CSu Yu-RuThomas Claire ETian YuTsilidis Konstantinos KUm Caroline Yvan Duijnhoven Franzel J BVan Guelpen BethanyVisvanathan KalaWang JunWhite EmilyWolk AlicjaWoods Michael OWu Anna HUlrich Cornelia MPeters UlrikeGauderman W JamesMoreno Victor - Physical activity (PA) is an established protective factor for colorectal cancer (CRC), but it is unclear if genetic variants modify this effect. To investigate this possibility, we conducted a genome-wide gene-PA interaction analysis. - Source: PubMed
Publication date: 2025/09/02
Peoples Anita RObón-Santacana MireiaKim Andre EKawaguchi Eric SFu YuboQu ConghuiMoratalla-Navarro FerranMorrison JohnLin YiArndt VolkerBerndt Sonja IBien Stephanie ABishop D TimothyBouras EmmanouilBrenner HermannBuchanan Daniel DCampbell Peter TChan Andrew TChang-Claude JennyConti David VCorley Douglas AcDevall Matthew ADimou NikiDrew David AGruber Stephen BGunter Marc JHarlid SophiaHarrison Tabitha AHoffmeister MichaelHsu LiHuyghe Jeroen RKeku Temitope OKundaje AnshulLewinger Juan PabloLi LiLynch Brigid MMarchand Loic LeMartín VicenteMurphy NeilNewton Christina COgino ShujiHardikar SheetalOse JenniferPai Rish KPalmer Julie RPapadimitriou NikosPardamean BensPellatt Andrew JPinchev MilaPlatz Elizabeth APotter John DRennert GadRuiz-Narvaez Edward ASakoda Lori CSchoen Robert EShcherbina AnnaStern Mariana CSu Yu-RuThomas Claire ETian YuTsilidis Konstantinos KUm Caroline Yvan Duijnhoven Franzel J Bvan Guelpen BethanyVisvanathan KalaWang JunWhite EmilyWolk AlicjaWoods Michael OWu Anna HUlrich Cornelia MPeters UlrikeGauderman W JamesMoreno Victor - The number of individuals diagnosed with opioid use disorder (OUD) has risen steeply because of increased prescribing of opioid drugs including oxycodone for chronic pain relief. When rats given extended access to oxycodone only a subset of animals self-administers more drug over time. Identifying the molecular mechanism associated with this behavior can introduce novel ways to combat OUD. Herein, we sought to identify the alteration in the expression of voltage gated and calcium activated potassium channels after extended access to oxycodone self-administration. - Source: PubMed
Publication date: 2025/08/11
Wabreha Ammanuel YAdjei NasserLadenheim BruceCadet Jean LudDaiwile Atul P - The energized structured water (ESW) concept supposes water can be imbued with energetic frequencies or vibrations, improving its quality and providing various health benefits. While some studies claim benefits, the mechanisms and effects of ESW are not well understood. This study investigates the impact of ESW on cellular bioenergetic function and oxidative stress in H9c2 cells. H9c2 cells were pretreated with ESW or control water (CW) at equivalent dilutions. Mitochondrial function was assessed using the Agilent Seahorse XF Pro Analyzer. Cell viability and reactive oxygen species (ROS) production were evaluated under HO-induced oxidative stress conditions. Differential gene expression analysis and Gene Ontology (GO) enrichment were conducted to identify significantly affected genes and biological processes in ESW-treated H9c2 cells. Results demonstrated that ESW pretreatment significantly increased maximal and spare respiratory capacity in H9c2 cells. In addition, ESW treatment increased the glycolytic ATP production without affecting mitochondrial and total ATP production. ESW treatment enhanced cell viability and reduced ROS production in cells exposed to HO-induced oxidative stress. Based on differential gene expression analysis, 717 genes including Myh1, Akr1b8, Hmox1, Kcng1, Ugt1a6, Clu, Gaa, Ftl1, Hspb7, and Gba1 were up-regulated and 422 genes including Hist1h2an, Slfn4, Rpl22l1, Polr2k, Il1rl1, Ndufb1, Atp5mkl1 were down-regulated by ESW compared to the controls. GO analysis indicated that ESW treatment significantly affects biological processes related to cellular stress response pathways. These findings suggest that ESW treatment may enhance cellular bioenergetics and stress resistance in H9c2 cells, potentially through modulation of gene expression related to stress responses and energy metabolism. - Source: PubMed
Publication date: 2025/08/05
Ranaweera Sachithra SZuniga-Hertz Juan PChitteti RamamurthyChernov Andrei VPatel Hemal H - KvS proteins are voltage-gated potassium channel subunits that form functional channels when assembled into heteromers with Kv2.1 () or Kv2.2 (). Mammals have 10 KvS subunits: Kv5.1 (), Kv6.1 (), Kv6.2 (), Kv6.3 (), Kv6.4 (), Kv8.1 (), Kv8.2 (), Kv9.1 (), Kv9.2 (), and Kv9.3 (). Electrically excitable cells broadly express channels containing Kv2 subunits and most neurons have substantial Kv2 conductance. However, whether KvS subunits contribute to these conductances has not been clear, leaving the physiological roles of KvS subunits poorly understood. Here, we identify that two potent Kv2 inhibitors, used in combination, can distinguish conductances of Kv2/KvS heteromers and Kv2-only channels. We find that Kv5, Kv6, Kv8, or Kv9-containing channels are resistant to the Kv2-selective pore-blocker RY785 yet remain sensitive to the Kv2-selective voltage sensor modulator guangxitoxin-1E (GxTX). Using these inhibitors in mouse superior cervical ganglion neurons, we find predominantly RY785-sensitive conductances consistent with channels composed entirely of Kv2 subunits. In contrast, RY785-resistant but GxTX-sensitive conductances consistent with Kv2/KvS heteromeric channels predominate in mouse and human dorsal root ganglion neurons. These results establish an approach to pharmacologically distinguish conductances of Kv2/KvS heteromers from Kv2-only channels, enabling investigation of the physiological roles of endogenous KvS subunits. These findings suggest that drugs which distinguish KvS subunits could modulate electrical activity of subsets of Kv2-expressing cell types. - Source: PubMed
Publication date: 2025/05/27
Stewart Robert GMarquis Matthew JamesJo SooyeonHarris Brandon JAberra Aman SCook VerityWhiddon ZacharyYarov-Yarovoy VladimirFerns MichaelSack Jon T