NME4 (Human) Recombinant Protein (Q01)
- Known as:
- NME4 (Human) Recombinant Protein (Q01)
- Catalog number:
- H00004833-Q01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- NME4 (Human) Recombinant Protein (Q01)
Related genes to: NME4 (Human) Recombinant Protein (Q01)
- Gene:
- NME4 NIH gene
- Name:
- NME/NM23 nucleoside diphosphate kinase 4
- Previous symbol:
- -
- Synonyms:
- nm23-H4, NM23H4, NDPKD
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-19
- Date modifiied:
- 2016-07-15
Related products to: NME4 (Human) Recombinant Protein (Q01)
Related articles to: NME4 (Human) Recombinant Protein (Q01)
- We report the synthesis of hexafluorophosphate (PF) salts directly from white phosphorus (P) and simple fluorides MF (M = Li, Na, K, Cs, NMe) in a single step. The utilization of -quinones, such as 2,3-dichloro-4,5-dicyano-1,4-benzoquinone (DDQ) offers a selective fluorination pathway, which affords MPF salts in up to 95% yield in acetonitrile (MeCN). NMR investigations of the DDQ-mediated P fluorination reaction revealed the formation of PF and PF·MeCN as key reaction intermediates. Donor-acceptor interactions between DDQ and fluoride are critical, effectively increasing the fluoride concentration and enabling efficient fluorination to PF. Tetraethylene glycol (TEG) selectively stops the reaction at the adduct K[PF·TEG]. In contrast, noncoordinating dichloromethane (DCM) favors PF formation by suppressing EDA interactions through low fluoride solubility, possibly via the tris(hydroquinonyl)phosphite P(DDQH), underscoring the critical role of fluoride solubility. This work demonstrates that quinone-fluoride interactions can be exploited for oxidative fluorination chemistry, establishing a new conceptual framework for P fluorination. - Source: PubMed
Publication date: 2026/07/23
Falge BenjaminPhilipp MaximilianVilling TobiasGschwind Ruth MRodríguez-Lugo Rafael EWolf Robert - Mitochondrial dysfunction is increasingly recognized as a key factor in the development and progression of atrial fibrillation (AF). - Source: PubMed
Publication date: 2026/07/02
Miao QingXue WeiqiLu XinkaiLian FeihongJin Zheng - Vitrification is a vital tool for the long-term preservation of animal genetic resources, yet cryoinjury-manifesting as oxidative stress, structural damage, and metabolic disorders-severely compromises its efficacy. Here, we investigated the protective effects of melatonin (MT) supplementation on the cryotolerance of mouse morulae. First, mouse morulae were assigned to four groups treated with vitrification and thawing media containing MT (0, 10, 10, and 10 M) to determine optimal MT concentration. Subsequently, embryos treated with the optimal MT concentration were evaluated for developmental competence, oxidative stress, apoptosis, and mitochondrial function. Furthermore, transcriptome sequencing was performed to elucidate MT-regulated molecular pathways. The results demonstrated that MT supplementation at 10 M significantly enhanced developmental competence, as evidenced by increased blastocyst rate, hatched blastocyst rate, total cell number and the inner cell mass (ICM)-to-total cell ratio compared to the MT-free group ( < 0.05). Consequently, embryo transfer outcomes showed higher live births and weaned pups in the 10 M MT group versus those in controls ( < 0.05), achieving levels comparable to fresh embryos ( > 0.05). Mechanistically, MT reversed cryoinjury-induced mitochondrial dysfunction by elevating membrane potential(MMP) and Adenosine Triphosphate(ATP) production while reducing Reactive Oxygen Species (ROS) accumulation ( < 0.05). Transcriptomic analysis further revealed that vitrification perturbed metabolic pathways, including amino acid/fatty acid degradation and glucose/pyruvate metabolism. MT downregulated cryoinjury-induced overexpression of and , inhibiting excessive NF-κB activation and alleviating metabolic dysfunction. Additionally, MT restored expression of nucleotide synthesis genes (, , , , , ) critical for cell proliferation, and reversed downregulation of mitochondrial genes and , confirming restoration of mitochondrial homeostasis. In conclusion, melatonin alleviates vitrification-induced cryoinjury by restoring mitochondrial function, which rescues nucleotide synthesis and partially reverses associated metabolic dysfunction. These findings advance MT-mediated cryoprotection and underscore its translational value for embryo cryopreservation in animal genetic resource conservation. - Source: PubMed
Publication date: 2026/05/26
Ji PengyunMa WenkuiZhao MengmengYan LaiqingLiu YunjieYin DepengChen QianruChen BodaWu HaoGao ShuaiWang BingyuanZhang LuLiu Guoshi - Minimising methane (CH) emissions from livestock production is a global priority, and feed modifications, such as supplementing diets with microalgae, have previously been shown to help reducing enteric CH production. This study explored blood-derived host gene expression profiles from twenty lambs supplemented with increasing levels of microalgae oil to investigate their transcriptional responses associated with varying microalgae oil levels while also exploring the host systemic responses towards varied CH productions. - Source: PubMed
Publication date: 2026/06/23
Chacko Kaitholil Steffimol RoseMooney Mark HAubry AurélieCristobal-Carballo OmarHillis RichardRazban VahidYan TianhaiRezwan Faisal IMorrison StevenHuws SharonShirali Masoud - Gastric cancer (GC) exhibits marked epidemiological differences between European (EUR) and East Asian (EAS) populations, with significantly higher incidence rates in EAS. Circulating proteins represent promising drug targets; however, most proteomic studies have focused primarily on EUR ancestry, leaving EAS-specific targets largely underexplored. This study aims to identify ancestry-specific plasma protein targets for GC using Mendelian randomization (MR). - Source: PubMed
Publication date: 2026/05/01
Zhi PengCui YanXue GuanghuiQiao LingyuGeng JieChang ZhengyaoXu YinmeiYan JuanjuanWang YingliZhao Chenghui