Category: 347174-05-4

Martin-Saiz, Lucia; Guerrero-Mauvecin, Juan; Martin-Sanchez, Diego; Fresnedo, Olatz; Gomez, Manuel J.; Carrasco, Susana; Cannata-Ortiz, Pablo; Ortiz, Alberto; Fernandez, Jose A.; Sanz, Ana B. published the artcile< Ferrostatin-1 modulates dysregulated kidney lipids in acute kidney injury>, Recommanded Product: Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is acute kidney injury ferrostatin1 lipidome lipid metabolism; Ferrostatin-1; acute kidney injury; ferroptosis; lipidomics; lyso-sulfatide; nephrotoxicity; phosphatidylethanolamine; phosphatidylinositol.

Ferroptosis, a form of regulated necrosis characterized by peroxidation of lipids such as arachidonic acid-containing phosphatidylethanolamine (PE), contributes to the pathogenesis of acute kidney injury (AKI). We have characterized the kidney lipidome in an exptl. nephrotoxic AKI induced in mice using folic acid and assessed the impact of the ferroptosis inhibitor Ferrostatin-1. Matrix-assisted laser desorption/ionization (MALDI) imaging mass spectrometry (IMS) was used to assess kidney lipidomics and it discriminated between glomeruli, medulla, and cortex in control kidneys, AKI kidneys, and AKI + Ferrostatin-1 kidneys. Out of 139 lipid species from 16 classes identified, 29 (20.5) showed significant differences between control and AKI at 48 h. Total PE and lyso-sulfatide species decreased, while phosphatidylinositol (PI) species increased in AKI. Dysregulated mRNA levels for Pemt, Pgs1, Cdipt, and Tamm41, relevant to lipid metabolism, were in line with the lipid changes observed Ferrostatin-1 prevented AKI and some AKI-associated changes in lipid levels, such as the decrease in PE and lyso-sulfatide species, without changing the gene expression of lipid metabolism enzymes. In conclusion, changes in the kidney lipid composition during nephrotoxic AKI are associated with differential gene expression of lipid metabolism enzymes and are partially prevented by Ferrostatin-1. 2022 The Pathol. Society of Great Britain and Ireland.

Journal of Pathology published new progress about Acute kidney injury. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Recommanded Product: Ethyl 3-amino-4-(cyclohexylamino)benzoate.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Lv, Min; Cai, Yuanzhen; Hou, Weikun; Peng, Kan; Xu, Ke; Lu, Chao; Yu, Wenxing; Zhang, Weisong; Liu, Lin published the artcile< The RNA-binding protein SND1 promotes the degradation of GPX4 by destabilizing the HSPA5 mRNA and suppressing HSPA5 expression, promoting ferroptosis in osteoarthritis chondrocytes>, HPLC of Formula: 347174-05-4, the main research area is ferroptosis osteoarthritis chondrocyte gene expression analysis; Chondrocyte; Ferroptosis; GPX4; HSPA5; Osteoarthritis; SND1.

Heat shock protein family A member 5 (HSPA5), a recently identified suppressor of ferroptosis, was reported to potentially regulating osteoarthritis. However, the exact role of HSPA5 and how its expression was regulated in osteoarthritis are largely unclear. Rat primary chondrocytes were treated with 10 ng/mL IL-1β for 24 h and incubated with ferrostatin-1 (a ferroptosis inhibitor). Cell viability, production of TNF-α, ROS and MDA, expression levels of collagen II, MMP13, GPX4, and SND1, and Fe2+ concentration were detected. Gain- and loss-of-function manipulations were performed to investigate the effect of HSPA5 on chondrocyte functions, and SND1 shRNA (sh-SND1) was transfected into IL-1β-treated primary chondrocytes alone or together with sh-HSPA5. Furthermore, the interaction between HSPA5 and GPX4 and the regulation of HSPA5 on GPX4 were explored. Finally, SND1 was knocked down in the rats with osteoarthritis, and the histopathol., expression of HSPA5-GPX4 axis, and levels of oxidative stress markers were evaluated. IL-1β treatment could enhance extracellular matrix (ECM) degradation (collagen II reduced and MMP13 increased), promote ferroptosis, manifested by decreased cell viability, increased levels of TNF-α, ROS, MDA, and Fe2+ concentrations, and decreased level of GPX4 protein, and increase SND1 expression in chondrocytes, which could be reversed by ferrostatin-1. Knockdown of SND1 enhanced ECM degradation and suppressed ferroptosis IL-1β-treated chondrocytes, which could be eliminated by knockdown of HSPA5. SND1 bound with HSPA5 at the 3’UTR and destabilized the HSPA5 mRNA. HSPA5 protein directly bound with GPX4 protein and pos. regulate its expression. HSPA5 overexpression suppressed IL-1β-induced chondrocyte ferroptosis, while this effect was counteracted by GPX4 silencing. Knockdown of SND1 upregulated HSPA5 and GPX4 in rat cartilage, inhibited inflammatory damage and ferroptosis, and alleviated OA progression. The RNA-binding protein SND1 promotes the degradation of GPX4 by destabilizing the HSPA5 mRNA and suppressing HSPA5 expression, promoting ferroptosis in osteoarthritis chondrocytes.

Inflammation Research published new progress about 3′-Untranslated region Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, HPLC of Formula: 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Xu, Yang; Li, Yuting; Li, Jiaxin; Chen, Wei published the artcile< Ethyl carbamate triggers ferroptosis in liver through inhibiting GSH synthesis and suppressing Nrf2 activation>, Product Details of C15H22N2O2, the main research area is ethyl carbamate GSH Nrf2 ferroptosis oxidative stress toxicity; Ethyl carbamate; Ferroptosis; GSH depletion; Lipid peroxidation; Nrf2.

Humans are inevitably exposed to Et carbamate (EC) via consumption of fermented food and beverages. EC, known as an environmental toxin, can cause oxidative stress-mediated severe toxicity, but the underlying mechanisms remain unveiled. Ferroptosis is a newly identified ROS-mediated non-apoptotic cell death characterized by iron accumulation and excessive lipid oxidation In this study, we first found that EC triggered ferroptosis in liver cells by detection of decreased cell viability, GSH, GPX4 and Ferritin levels, as well as increased iron and MDA contents. Ferroptosis inhibitor ferrostatin-1 (Fer-1) pretreatment rescued ferroptotic damage, indicating that ferroptosis was critical for EC-caused cell death. Furthermore, GSH synthesis precursor N-acetylcysteine displayed significant anti-ferroptotic properties and we suggested that GSH depletion might be the main cause of ferroptosis under EC exposure. EC-triggered GSH depletion mainly depended on suppressed GSH synthesis via inhibition of SLC7A11 and GCLC expressions. Notably, EC blocked Nrf2 activation by repression of phosphorylation modification and nuclear translocation, which further resulted in ferroptosis occurrence. We also observed EC-induced liver dysfunction and inflammation, accompanied with oxidative stress, ferroptosis and downregulated Nrf2 signaling in Balb/c mice, which could be effectively reversed by Fer-1 and tBHQ pretreatment. Together, our study indicated that ferroptosis is a new mechanism for EC-caused toxicity, which was attributed to Nrf2 inactivation and GSH depletion.

Redox Biology published new progress about Cell viability. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Product Details of C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Li, Jianchun; Yang, Jieke; Zhu, Bingwen; Fan, Junming; Hu, Qiongdan; Wang, Li published the artcile< Tectorigenin protects against unilateral ureteral obstruction by inhibiting Smad3-mediated ferroptosis and fibrosis>, Electric Literature of 347174-05-4, the main research area is tectorigenin Smad unilateral ureteral obstruction ferroptosis fibrosis; Smad3; ferroptosis; fibrosis; tectorigenin.

Renal tubular epithelial cell (TEC) injury and fibrosis are the key factors of the pathogenesis of chronic kidney disease. Here, we reported that tectorigenin is effectively protected against obstructive nephropathy established by unilateral ureteral obstruction (UUO). In vivo, tectorigenin administration significantly alleviated the deteriorations of renal functions including blood urea nitrogen and creatinine. Meanwhile, results from the histol. suggested that renal injury characterized by tubular cell damage and fibrosis lesions of kidneys in UUO group were markedly attenuated following tectorigenin treatment. Mechanistically, we found that tectorigenin treatment greatly inhibited Smad3 phosphorylation, and the transcription and protein level of Nox4, a newly identified direct downstream mol. of Smad3 and a modulator of ferroptosis, while it indirectly restored the expression of glutathione peroxidase 4, a neg. regulator of ferroptosis. Consistent with in vivo studies, treatment with tectorigenin also suppressed the ferroptosis induced by erastin/RSL3 and fibrosis stimulated by transforming growth factor β1 (TGF-β1) in primary renal TECs. What is more, treatment with ferroptosis inhibitor, ferrostatin-1, also impeded TGF-β1 stimulated the profibrotic effects in TECs, indicating that tectorigenin may relieve fibrosis by inhibiting ferroptosis in TECs. In addition, tectorigenin treatment exhibited a similar tendency, which inhibited Smad3 activation, and the docking anal. revealed that tectorigenin docked well into the Smad3 binding cavity with strong binding affinity (-7.9 kcal/mol). Thus, this study deciphers the protective effect of tectorigenin against obstructive nephropathy through inhibiting Smad3-mediated ferroptosis and fibrosis.

Phytotherapy Research published new progress about Blood urea nitrogen. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Electric Literature of 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Dang, Guohui; Li, Tianrun; Yang, Dongmin; Yang, Guangxin; Du, Xing; Yang, Juan; Miao, Yutong; Han, Lulu; Ma, Xiaolong; Song, Yuwei; Liu, Bo; Li, Xuan; Wang, Xian; Feng, Juan published the artcile< T lymphocyte-derived extracellular vesicles aggravate abdominal aortic aneurysm by promoting macrophage lipid peroxidation and migration via pyruvate kinase muscle isozyme 2>, Product Details of C15H22N2O2, the main research area is abdominal aorta aneurysmT lymphocyte macrophage dell migration glycolysis; Abdominal aortic aneurysm; Extracellular vesicles; Lipid peroxidation; Macrophage migration; Pyruvate kinase muscle isozyme 2.

T lymphocyte and macrophage infiltration in the aortic wall is critical for abdominal aortic aneurysm (AAA). However, how T lymphocytes interact with macrophages in the pathogenesis of AAA remains largely uncharacterized. In an elastase-induced murine AAA model, we first found that the expression of pyruvate kinase muscle isoenzyme 2 (PKM2), the last rate-limiting enzyme in glycolysis, was increased in infiltrated T lymphocytes of vascular lesions. T lymphocyte-specific PKM2 deficiency in mice (LckCrePKM2fl/fl) or i.p. administration of the sphingomyelinase inhibitor GW4869 caused a significant attenuation of the elastase-increased aortic diameter, AAA incidence, elastic fiber disruption, matrix metalloproteinases (MMPs) expression, and macrophage infiltration in the vascular adventitia compared with those in PKM2fl/fl mice. Mechanistically, extracellular vesicles (EVs) derived from PKM2-activated T lymphocytes elevated macrophage iron accumulation, lipid peroxidation, and migration in vitro, while macrophages treated with EVs from PKM2-null T lymphocytes or pretreated with the lipid peroxidation inhibitors ferrostatin-1 (Fer-1), liproxstatin-1 (Lip-1), or the iron chelating agent deferoxamine mesylate (DFOM) reversed these effects. In vascular lesions of elastase-induced LckCrePKM2fl/fl mice with AAA, the oxidant system weakened, with downregulated 4-hydroxynonenal (4-HNE) levels and strengthened antioxidant defense systems with upregulated glutathione peroxidase 4 (GPX4) and cystine/glutamate antiporter solute carrier family 7 member 11 (Slc7a11) expressions in macrophages. High-throughput metabolomics showed that EVs derived from PKM2-activated T lymphocytes contained increased levels of polyunsaturated fatty acid (PUFA)-containing phospholipids, which may provide abundant substrates for lipid peroxidation in target macrophages. More importantly, upregulated T lymphocyte PKM2 expression was also found in clin. AAA subjects, and EVs isolated from AAA patient plasma enhanced macrophage iron accumulation, lipid peroxidation, and migration ex vivo. Therefore, from cell-cell crosstalk and metabolic perspectives, the present study shows that PKM2-activated T lymphocyte-derived EVs may drive AAA progression by promoting macrophage redox imbalance and migration, and targeting the T lymphocyte-EV-macrophage axis may be a potential strategy for early warning and treating AAA.

Redox Biology published new progress about Abdominal aorta aneurysm. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Product Details of C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Ni, Haiwei; Ruan, Guojing; Sun, Cheng; Yang, Xuan; Miao, Zhenyan; Li, Jifei; Chen, Ying; Qin, Hai; Liu, Yichen; Zheng, Lufeng; Xing, Yingying; Xi, Tao; Li, Xiaoman published the artcile< Tanshinone IIA inhibits gastric cancer cell stemness through inducing ferroptosis>, Application In Synthesis of 347174-05-4, the main research area is tanshinone IIA gastric cancer cell stemness ferroptosis; SLC7A11; Tanshinone IIA; ferroptosis; gastric cancer; stemness.

Tanshinone IIA is the active constituent extracted from Salvia Miltiorrhza. Numerous studies have shown that Tanshinone IIA could inhibit tumor proliferation and metastasis, including gastric cancer. However, the effect of Tanshinone IIA on gastric cancer cell stemness stays unclear. Here, we found that Tanshinone IIA could reduce gastric cancer cell stemness through detecting spheroid-forming, flow cytometry anal., and the expression of stemness markers (OCT3/4, ALDH1A1, and CD44). Mechanistically, Tanshinone IIA increased the level of lipid peroxides and decreased glutathione level in gastric cancer cells, both of which are the markers of ferroptosis. Similarly, ferroptosis inducers (erastin, sulfasalazine, and sorafenib) reduced gastric cancer cell stemness. Addnl., the inhibitory effects of Tanshinone IIA on GC cell stemness were reversed by ferroptosis inhibitor (Fer-1) or overexpression of SLC7A11, which is a critical ferroptosis inhibitor. Therefore, we revealed that Tanshinone IIA inhibited the stemness of gastric cancer cells partly through inducing ferroptosis.

Environmental Toxicology published new progress about CD44 antigens Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Application In Synthesis of 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Lai, Xingrong; Sun, Yanhua; Zhang, Xuedi; Wang, Dan; Wang, Jialing; Wang, Haihua; Zhao, Yao; Liu, Xinling; Xu, Xin; Song, Haoran; Ping, Wenjia; Sun, Yanli; Hu, Zhenbo published the artcile< Honokiol induces ferroptosis by upregulating HMOX1 in acute myeloid leukemia cells>, Reference of 347174-05-4, the main research area is acute myeloid leukemia ferroptosis Honokiol HMOX1; AML; ferroptosis; heme oxygenase (HO)-1; honokiol; lipid peroxidation.

Acute myeloid leukemia (AML) is one of the malignant hematol. cancers with high mortality. Finding a more effective and readily available treatment is of the utmost importance. Here, we aimed to identify the anti-leukemia effect of a natural small mol. compound honokiol on a panel of AML cell lines, including THP-1, U-937, and SKM-1, and explored honokiol′s potential biol. pathways and mechanisms. The results showed that honokiol decreased the viability of the targeted AML cells, induced their cell cycle arrest at G0/G1 phase, and inhibited their colony-formation capacity. Honokiol also triggers a noncanonical ferroptosis pathway in THP-1 and U-937 cells by upregulating the level of intracellular lipid peroxide and HMOX1 significantly. Subsequent studies verified that HMOX1 was a critical target in honokiol-induced ferroptosis. These results reveal that honokiol is an effective anti-leukemia agent in AML cell lines and may be a potential ferroptosis activator in AML.

Frontiers in Pharmacology published new progress about Acute myeloid leukemia. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Reference of 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Yang, Wenchang; Wang, Yaxin; Zhang, Chenggang; Huang, Yongzhou; Yu, Jiaxian; Shi, Liang; Zhang, Peng; Yin, Yuping; Li, Ruidong; Tao, Kaixiong published the artcile< Maresin1 protect against ferroptosis-induced liver injury through ROS inhibition and Nrf2/HO-1/GPX4 activation>, Formula: C15H22N2O2, the main research area is liver injury maresin 1 ROS inhibition Nrf2 HO1 GPX4; Maresin1; Nrf2; ferroptosis; glutathione peroxidase 4; reactive oxygen species.

Drugs, viruses, and chem. poisons stimulating live in a short period of time can cause acute liver injury (ALI). ALI can further develop into serious liver diseases such as cirrhosis and liver cancer. Therefore, how to effectively prevent and treat ALI has become the focus of research. Numerous studies have reported Maresin1 (MaR1) has anti-inflammatory effect and protective functions on organs. In the present study, we used D-galactosamine/lipopolysaccharide (D-GalN/LPS) to establish an ALI model, explored the mechanism of liver cells death caused by D-GalN/LPS, and determined the effect of MaR1 on D-GalN/LPS-induced ALI. In vivo experiments, we found that MaR1 and ferrostatin-1 significantly alleviated D-GalN/LPSinduced ALI, reduced serum alanine transaminase and aspartate transaminase levels, and improved the survival rate of mice. Meanwhile, MaR1 inhibited hepatocyte death, inhibited tissue reactive oxygen species (ROS) expression, reduced malondialdehyde (MDA), reduced glutathione (GSH),GSH/oxidized glutathione (GSSG), and iron content induced byD-GalN/LPS in mice. In addition, MaR1 inhibited ferroptosis-induced liver injury through inhibiting the release of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and IL-6. Subsequently, western blot showed that MaR1 improved the expression of nuclear factor E2-related factor 2(Nrf2)/heme oxygenase-1 (HO-1)/glutathione peroxidase 4 (GPX4). In vitro experiments, we found that MaR1 inhibited LPS-induced and erastin-induced cell viability reduction Meanwhile, we found that MaR1 increased the MDA and GSH levels in cells. Western blot showed that MaR1 increased the expression level of Nrf2/HO-1/GPX4. Next, the Nrf2 was knocked down in HepG2 cells, and the results showed that the protective effect ofMaR1 significantly decreased. Finally, flow cytometry revealed that MaR1 inhibited ROS production and apoptosis. Overall, our study showed MaR1 inhibited ferroptosis-induced liver injury by inhibiting ROS production and Nrf2/HO-1/GPX4 activation.

Frontiers in Pharmacology published new progress about Apoptosis. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Formula: C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Sun, Lei; Wang, Hua; Yu, Shanshan; Zhang, Lin; Jiang, Jue; Zhou, Qi published the artcile< Herceptin induces ferroptosis and mitochondrial dysfunction in H9c2 cells>, Recommanded Product: Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is herceptin ferroptosis mitochondrial dysfunction heart failure; Herceptin; cardiotoxicity; ferroptosis; mitochondrial dysfunction.

Ferroptosis has been previously implicated in the pathol. progression of cardiomyopathy. Herceptin (trastuzumab), which targets HER2, is commonly applied for the treatment of HER2+ breast cancer. However, its clin. use is limited by its cardiotoxicity. Therefore, the present study aimed to investigate if targeting ferroptosis could protect against Herceptin-induced heart failure in an in vitro model of H9c2 cells after treatment of Herceptin, Herceptin + ferroptosis inhibitor ferrostatin-1 (Fer-1) or Herceptin + Deferoxamine. H9c2 cell viability was measured by MTT assay. Reactive oxygen species (ROS) levels were detected by measuring the fluorescence of DCFH-DA-A and MitoSOX Red. Glutathione (GSH)/oxidized glutathione (GSSG) ratio was measured using the GSH/GSSG Ratio Detection Assay kit. Mitochondrial membrane potential and ATP content were evaluated by JC-1 staining and bioluminescent assay kits, resp. Protein expressions of glutathione peroxidase 4, recombinant solute carrier family 7 member 11, mitochondrial optic atrophy1-1/2, mitofusin, Acyl-CoA synthetase long chain family member 4, cytochrome c, voltage-dependent anion-selective channel, dynamin-related protein, mitochondrial fission 1 protein and mitochondrial ferritin were evaluated by western blotting. It was found that Herceptin reduced H9c2 cell viability while increasing intracellular and mitochondrial ROS levels in a dose- and time-dependent manner. Furthermore, Herceptin decreased glutathione peroxidase (GPX) protein expression and the GSH/GSSG ratio in H9c2 cells in a dose- and time-dependent manner. The Fer-1 abolished this Herceptin-induced reduction in cell viability, GSH/GSSG ratio, mitochondrial membrane potential and ATP content. Fer-1 also reversed the suppressive effects of Herceptin on the protein expression levels of GPX4, recombinant solute carrier family 7 member 11, mitochondrial optic atrophy1-1/2 and mitofusin in H9c2 cells. Subsequently, Fer-1 was found to reverse the Herceptin-induced increase in mitochondrial ROS and iron levels in H9c2 cells, as well as the increased protein expression levels of Acyl-CoA synthetase long chain family member 4, cytochrome c, voltage-dependent anion-selective channel, dynamin-related protein, mitochondrial fission 1 protein and mitochondrial ferritin in H9c2 cells. However, compared with deferoxamine, an iron chelator, the effects of Fer-1 were less effective. Collectively, these findings provided insights into the pathogenic mechanism that underlie Herceptin-induced cardiomyopathy, which potentially provides a novel therapeutic target for the prevention of cardiotoxicity in HER2+ breast cancer treatment.

International Journal of Molecular Medicine published new progress about Antioxidant enzymes Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Recommanded Product: Ethyl 3-amino-4-(cyclohexylamino)benzoate.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Tsvetkov, Peter; Coy, Shannon; Petrova, Boryana; Dreishpoon, Margaret; Verma, Ana; Abdusamad, Mai; Rossen, Jordan; Joesch-Cohen, Lena; Humeidi, Ranad; Spangler, Ryan D.; Eaton, John K.; Frenkel, Evgeni; Kocak, Mustafa; Corsello, Steven M.; Lutsenko, Svetlana; Kanarek, Naama; Santagata, Sandro; Golub, Todd R. published the artcile< Copper induces cell death by targeting lipoylated TCA cycle proteins>, COA of Formula: C15H22N2O2, the main research area is copper cell death TCA cycle mitochondrial respiration homeostasis PDHA1.

Copper is an essential cofactor for all organisms, and yet it becomes toxic if concentrations exceed a threshold maintained by evolutionarily conserved homeostatic mechanisms. How excess copper induces cell death, however, is unknown. Here, we show in human cells that copper-dependent, regulated cell death is distinct from known death mechanisms and is dependent on mitochondrial respiration. We show that copper-dependent death occurs by means of direct binding of copper to lipoylated components of the tricarboxylic acid (TCA) cycle. This results in lipoylated protein aggregation and subsequent iron-sulfur cluster protein loss, which leads to proteotoxic stress and ultimately cell death. These findings may explain the need for ancient copper homeostatic mechanisms.

Science (Washington, DC, United States) published new progress about Animal gene Role: BSU (Biological Study, Unclassified), BIOL (Biological Study) (DBT). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, COA of Formula: C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics