Recombinant Human Non-Metastatic Cells 4 NME4
- Known as:
- Recombinant Human Non-Metastatic Cells 4 NME4
- Catalog number:
- pro-219
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Non-Metastatic Cells 4 NME4
Related genes to: Recombinant Human Non-Metastatic Cells 4 NME4
- 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: Recombinant Human Non-Metastatic Cells 4 NME4
Related articles to: Recombinant Human Non-Metastatic Cells 4 NME4
- Cardiolipin (CL), a dimeric phospholipid with four acyl chains and a small polar head group, is one of the most striking examples of evolutionary continuity in cell biology. Present in the plasma membrane of α-proteobacteria and retained without fundamental modification in the inner mitochondrial membrane (IMM) of every eukaryote examined, CL has persisted across roughly two billion years of evolution, a period over which the mitochondrion shed the great majority of its ancestral genes. This review develops, as an organizing hypothesis rather than an established fact, the proposal that CL acts as a programmable signaling hub: a lipid whose physical chemistry and membrane address allow it to nucleate distinct supramolecular platforms in response to discrete stress signals, each platform coupling a specific mitochondrial state to a defined cell fate outcome. Three CL-dependent platforms are examined, together with a fourth, emerging axis, and the evidence supporting each is explicitly graded. Platform 1, the catalytic peroxidase platform, converts the constitutive CL-cytochrome (cyt ) structural complex into an enzymatic reaction under oxidative stress, generating oxidized CL (oxCL) species that contribute to cyt release from the IMM; this platform is the best supported of the four. Platform 2, the receptor-like mitophagy platform, exploits NME4-dependent CL scramblase activity to translocate CL from the IMM to the outer mitochondrial membrane (OMM) surface upon membrane potential dissipation, creating an externalized "eat-me" signal recognized by LC3-II; the evidence here is moderate and largely cell-based. Platform 3, the caspase-8/BID activation platform, is proposed to assemble a CL microdomain scaffold at the OMM that recruits caspase-8, markedly accelerates BID cleavage, and couple extrinsic apoptotic signals to mitochondrial outer membrane permeabilization (MOMP); this model rests substantially on reconstituted systems and requires further validation in intact cells and in vivo. A fourth, still-debated axis links CL externalization to innate immune activation through NLRP3 recruitment, for which alternative membrane-recruitment models exist. The argument advanced here is that the conservation of CL is unlikely to be explained by its structural roles alone, although those roles are themselves sufficient to impose strong selection; disentangling structural from signaling contributions remains an open problem, and the comparative genomic work needed to do so has not yet been performed. - Source: PubMed
Publication date: 2026/07/31
Petit Patrice X - We report the synthesis of hexafluorophosphate (PF6-) salts directly from white phosphorus (P4) and simple fluorides MF (M = Li, Na, K, Cs, NMe4) in a single step. The utilization of p-quinones, such as 2,3-dichloro-4,5-dicyano-1,4-benzoquinone (DDQ) offers a selective fluorination pathway, which affords MPF6 salts in up to 95% yield in acetonitrile (MeCN). NMR investigations of the DDQ-mediated P4 fluorination reaction revealed the formation of PF3 and PF5·MeCN as key reaction intermediates. Donor-acceptor interactions between DDQ and fluoride are critical, effectively increasing the fluoride concentration and enabling efficient fluorination to PF6-. Tetraethylene glycol (TEG) selectively stops the reaction at the adduct K[PF5·TEG]. In contrast, noncoordinating dichloromethane (DCM) favors PF3 formation by suppressing EDA interactions through low fluoride solubility, possibly via the tris(hydroquinonyl)phosphite P(DDQH)3, 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 P4 fluorination. - Source: PubMed
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