NKAIN4(Na+_K+ transporting ATPase interacting 4)
- Known as:
- NKAIN4(Na+_K+ transporting ATPase interacting 4)
- Catalog number:
- ARP53119_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- NKAIN4(+_K+ transporting ATPase interacting 4)
Related genes to: NKAIN4(Na+_K+ transporting ATPase interacting 4)
- Gene:
- MT-ATP6 NIH gene
- Name:
- mitochondrially encoded ATP synthase membrane subunit 6
- Previous symbol:
- MTATP6, RP
- Synonyms:
- ATP6, ATPase-6, Su6m
- Chromosome:
- mitochondria
- Locus Type:
- gene with protein product
- Date approved:
- 1989-10-12
- Date modifiied:
- 2017-11-22
Related products to: NKAIN4(Na+_K+ transporting ATPase interacting 4)
106 kDa O-GlcNAc transferase-interacting protein,Homo sapiens,Human,KIAA1042,OIP106,Trafficking kinesin-binding protein 1,TRAK1130 kDa retinoblastoma-associated protein,p130,PPAR-alpha-interacting complex protein 128,pRb2,PRIC128,Rat,Rattus norvegicus,Rbl2,RBR-2,Retinoblastoma-like protein 2,Retinoblastoma-related protein 215S Mg(2+)-ATPase p97 subunit,Bos taurus,Bovine,TER ATPase,Transitional endoplasmic reticulum ATPase,Valosin-containing protein,VCP,VCP15S Mg(2+)-ATPase p97 subunit,Homo sapiens,Human,TER ATPase,Transitional endoplasmic reticulum ATPase,Valosin-containing protein,VCP,VCP15S Mg(2+)-ATPase p97 subunit,Mouse,Mus musculus,TER ATPase,Transitional endoplasmic reticulum ATPase,Valosin-containing protein,VCP,Vcp15S Mg(2+)-ATPase p97 subunit,Pig,Sus scrofa,TER ATPase,Transitional endoplasmic reticulum ATPase,Valosin-containing protein,VCP,VCP15S Mg(2+)-ATPase p97 subunit,Rat,Rattus norvegicus,TER ATPase,Transitional endoplasmic reticulum ATPase,Valosin-containing protein,VCP,Vcp17 kDa membrane-associated protein,Homo sapiens,Human,MAP17,PDZK1-interacting protein 1,PDZK1IP1,Protein DD9617 kDa membrane-associated protein,Map17,Mouse,Mus musculus,PDZK1-interacting protein 1,Pdzk1ip117 kDa membrane-associated protein,MAP17,PDZK1-interacting protein 1,PDZK1IP1,Pig,Sus scrofa17 kDa membrane-associated protein,Map17,PDZK1-interacting protein 1,Pdzk1ip1,Rat,Rattus norvegicus190 kDa guanine nucleotide exchange factor,Kiaa1998,Mouse,Mus musculus,p190RhoGEF,p190-RhoGEF,Rgnef,Rho-guanine nucleotide exchange factor,Rho-interacting protein 2,Rhoip2,Rip220 kDa nuclear cap-binding protein,CBP20,CBP20,Cell proliferation-inducing gene 55 protein,Homo sapiens,Human,NCBP 20 kDa subunit,NCBP2,NCBP-interacting protein 1,NIP1,Nuclear cap-binding protein subu21 kDa pRb-associated protein,C15orf3,CREBBP_EP300 inhibitory protein 1,CRI1,E1A-like inhibitor of differentiation 1,EID1,EID-1,EP300-interacting inhibitor of differentiation 1,Homo sapiens,Human,PNAS23 kDa subunit of V-ATPase,Atp6f,Atp6v0b,Mouse,Mus musculus,Vacuolar proton pump 21 kDa proteolipid subunit,V-ATPase 21 kDa proteolipid subunit,V-type proton ATPase 21 kDa proteolipid subunit Related articles to: NKAIN4(Na+_K+ transporting ATPase interacting 4)
- Source: PubMed
- Cymbopogon citratus (DC.) Stapf is a medicinal and edible herb that is widely used for the treatment of gastric, nervous and hypertensive disorders. In this study, we investigated the cardioprotective effects and mechanisms of the essential oil, the main active ingredient of Cymbopogon citratus, on isoproterenol (ISO)-induced cardiomyocyte hypertrophy. - Source: PubMed
Publication date: 2024/04/19
Ding Xiao-YunZhang HaoQiu Yu-MeiXie Meng-DieWang HuXiong Zheng-YuLi Ting-TingHe Chun-NiDong WeiTang Xi-Lan - Peripheral neuropathies in mitochondrial disease are caused by mutations in nuclear genes encoding mitochondrial proteins, or in the mitochondrial genome. Whole exome or genome sequencing enable parallel testing of nuclear and mtDNA genes, and it has significantly advanced the genetic diagnosis of inherited diseases. Despite this, approximately 40% of all Charcot-Marie-Tooth (CMT) cases remain undiagnosed. - Source: PubMed
Publication date: 2024/03/28
Ferreira TomasPolavarapu KiranOlimpio CatarinaParamonov IdaLochmüller HannsHorvath Rita - Osteoarthritis (OA) progresses due to the excessive generation of reactive oxygen and nitrogen species (ROS/RNS) and abnormal ATP energy metabolism related to the oxidative phosphorylation pathway in the mitochondria. Highly active single-atom nanozymes (SAzymes) can help regulate the redox balance and have shown their potential in the treatment of inflammatory diseases. In this study, we innovatively utilised ligand-mediated strategies to chelate Pt with modified g-CN by π-π interaction to prepare g-CN-loaded Pt single-atom (Pt SA/CN) nanozymes that serve as superoxide dismutase (SOD)/catalase (CAT) mimics to scavenge ROS/RNS and regulate mitochondrial ATP production, ultimately delaying the progression of OA. Pt SA/CN exhibited a high loading of Pt single atoms (2.45 wt%), with an excellent photothermal conversion efficiency (54.71%), resulting in tunable catalytic activities under near-infrared light (NIR) irradiation. Interestingly, the Pt-N active centres in Pt SA/CN formed electron capture sites for electron holes, in which g-CN regulated the d-band centre of Pt, and the N-rich sites transferred electrons to Pt, leading to the enhanced adsorption of free radicals and thus higher SOD- and CAT-like activities compared with pure g-CN and g-CN-loaded Pt nanoparticles (Pt NPs/CN). Based on the use of HO-induced chondrocytes to simulate ROS-injured cartilage and an OA joint model , the results showed that Pt SA/CN could reduce oxidative stress-induced damage, protect mitochondrial function, inhibit inflammation progression, and rebuild the OA microenvironment, thereby delaying the progression of OA. In particular, under NIR light irradiation, Pt SA/CN could help reverse the oxidative stress-induced joint cartilage damage, bringing it closer to the state of the normal cartilage. Mechanistically, Pt SA/CN regulated the expression of mitochondrial respiratory chain complexes, mainly NDUFV2 of complex 1 and MT-ATP6 of ATP synthase, to reduce ROS/RNS and promote ATP production. This study provides novel insights into the design of artificial nanozymes for treating oxidative stress-induced inflammatory diseases. - Source: PubMed
Publication date: 2024/02/21
Xiang JianhuiYang XinTan ManliGuo JianfengYe YutingDeng JiejiaHuang ZhangruiWang HanjieSu WeiCheng JianwenZheng LiLiu SijiaZhong JingpingZhao Jinmin - Mitochondrial ATP synthase (Complex V) catalyzes the last step of oxidative phosphorylation and provides most of the energy (ATP) required by human cells. The mitochondrial genes and encode two subunits of the multi-subunit Complex V. Since the discovery of the first variant in the year 1990 as the cause of Neuropathy, Ataxia, and Retinitis Pigmentosa (NARP) syndrome, a large and continuously increasing number of inborn variants in the and genes have been identified as pathogenic. Variants in these genes correlate with various clinical phenotypes, which include several neurodegenerative and multisystemic disorders. In the present review, we report the pathogenic variants in mitochondrial ATP synthase genes and highlight the molecular mechanisms underlying ATP synthase deficiency that promote biochemical dysfunctions. We discuss the possible structural changes induced by the most common variants found in patients by considering the recent cryo-electron microscopy structure of human ATP synthase. Finally, we provide the state-of-the-art of all therapeutic proposals reported in the literature, including drug interventions targeting mitochondrial dysfunctions, allotopic gene expression- and nuclease-based strategies, and discuss their potential translation into clinical trials. - Source: PubMed
Publication date: 2024/02/13
Del Dotto ValentinaMusiani FrancescoBaracca AlessandraSolaini Giancarlo