Optimiranje podloge za uzgoj i sastava aminokiselina u miceliju gljive Pleurotus cornucopiae SD-01 obogaćenog kromom

Chromium(III) is an essential trace element for humans and animals. Pleutorus cornucopiae SD-01 is a nutritional and functional mushroom containing many kinds of bioactive ingredients. The aims of this work are to optimize the conditions of P. cornucopiae SD-01 cultivation with Cr enrichment in submerged culture by determining the dry cell mass, Cr content in mycelia and the rate of Cr enrichment, and to analyze the amino acid composition of Cr-enriched mycelia. The optimal medium contained (in g/L): potato 200, sucrose 25, yeast extract 4, KH2PO4 1 and MgSO4·7H2O 1. The optimum parameters of liquid culture were temperature 25 °C, cultivation time 6 days, the volume of the medium 100 mL, rotation speed 160 rpm and initial pH=6.5. Under the optimized conditions, the values of the dry cell mass, Cr content in mycelia and the rate of Cr enrichment were (6.63±0.35) g/L, (3670±211) μg/g and (12.15±1.01) % respectively, which were by (23.23±1.22), (18.19±1.06) and (45.68±2.67) % respectively, higher than those in the control. Chromium(III) in Cr-enriched mycelia was mainly combined with protein and polysaccharide. The contents of total amino acids and essential amino acids in Cr-enriched mycelia were increased by (31.25±0.58) and (44.26±0.76) %, respectively.Trovalentni je krom esencijalni element u tragovima, potreban za rast ljudi i životinja. Pleurotus cornucopiae SD-01 hranjiva je gljiva funkcionalnih svojstava, koja sadrži mnoge bioaktivne komponente. Svrha je ovoga rada bila optimirati uvjete uzgoja P. cornucopiae SD-01 u podlozi obogaćenoj kromom, i to određivanjem suhe stanične mase, udjela kroma u miceliju i stupnja obogaćivanja micelija, te analizirati aminokiselinski sastav micelija obogaćenog kromom. Optimalni sastav podloge bio je (u g/L): krumpir 200, saharoza 25, kvaščev ekstrakt 4, KH2PO4 1 i MgSO4·7H2O 1. Utvrđeni su optimalni parametri rasta: temperatura 25 °C, vrijeme uzgoja 6 dana, volumen podloge 100 mL, brzina rotacije 160 rpm i početni pH=6,5. U tim su uvjetima dobivene sljedeće vrijednosti: suha stanična masa od (6,63±0,35) g/L, veća za (23,23±1,22) %; udio kroma u miceliju od (3670±211) mg/g, veći za (18,19±1,06) % i stupanj obogaćivanja micelija kromom od (12,15±1,01) %, što je za (45,68±2,67) % više nego u kontrolnom uzorku. Utvrđeno je da se trovalentni krom u miceliju uglavnom veže za proteine i ugljikohidrate. Ukupni se udio aminokiselina u takvom obogaćenom miceliju povećao za (31,25±0,58) %, a udio esencijalnih aminokiselina za (44,26±0,76) %

Methyl 5-hy­droxy-3-phenyl-1,2-oxazolidine-5-carboxyl­ate

In the title compound, C11H13NO4, the isoxazolidine ring has an envelope conformation with the O atom as the flap. In the crystal, mol­ecules are liked via N—H⋯O and bifurcated O—H⋯(O,N) hydrogen bonds forming chains propagating along [010]. There are also C—H⋯O inter­actions present

Circular RNA circNOL10 Inhibits Lung Cancer Development by Promoting SCLM1-Mediated Transcriptional Regulation of the Humanin Polypeptide Family

circNOL10 is a circular RNA expressed at low levels in lung cancer, though its functions in lung cancer remain unknown. Here, the function and molecular mechanism of circNOL10 in lung cancer development are investigated using in vitro and in vivo studies, and it is shown that circNOL10 significantly inhibits the development of lung cancer and that circNOL10 expression is co‐regulated by methylation of its parental gene Pre‐NOL10 and by splicing factor epithelial splicing regulatory protein 1 (ESRP1). circNOL10 promotes the expression of transcription factor sex comb on midleg‐like 1 (SCML1) by inhibiting transcription factor ubiquitination and thus also affects regulation of the humanin (HN) polypeptide family by SCML1. circNOL10 also affects mitochondrial function through regulating the humanin polypeptide family and affecting multiple signaling pathways, ultimately inhibiting cell proliferation and cell cycle progression, and promoting the apoptosis of lung cancer cells, thereby inhibiting lung cancer development. This study investigates the functions and molecular mechanisms of circNOL10 in the development of lung cancer and reveals its involvement in the transcriptional regulation of the HN polypeptide family by SCML1. The results also demonstrate the inhibitory effect of HN on lung cancer cells growth. These findings may identify novel targets for the molecular therapy of lung cancer

Deletion of heat shock protein 60 in adult mouse cardiomyocytes perturbs mitochondrial protein homeostasis and causes heart failure.

To maintain healthy mitochondrial enzyme content and function, mitochondria possess a complex protein quality control system, which is composed of different endogenous sets of chaperones and proteases. Heat shock protein 60 (HSP60) is one of these mitochondrial molecular chaperones and has been proposed to play a pivotal role in the regulation of protein folding and the prevention of protein aggregation. However, the physiological function of HSP60 in mammalian tissues is not fully understood. Here we generated an inducible cardiac-specific HSP60 knockout mouse model, and demonstrated that HSP60 deletion in adult mouse hearts altered mitochondrial complex activity, mitochondrial membrane potential, and ROS production, and eventually led to dilated cardiomyopathy, heart failure, and lethality. Proteomic analysis was performed in purified control and mutant mitochondria before mutant hearts developed obvious cardiac abnormalities, and revealed a list of mitochondrial-localized proteins that rely on HSP60 (HSP60-dependent) for correctly folding in mitochondria. We also utilized an in vitro system to assess the effects of HSP60 deletion on mitochondrial protein import and protein stability after import, and found that both HSP60-dependent and HSP60-independent mitochondrial proteins could be normally imported in mutant mitochondria. However, the former underwent degradation in mutant mitochondria after import, suggesting that the protein exhibited low stability in mutant mitochondria. Interestingly, the degradation could be almost fully rescued by a non-specific LONP1 and proteasome inhibitor, MG132, in mutant mitochondria. Therefore, our results demonstrated that HSP60 plays an essential role in maintaining normal cardiac morphology and function by regulating mitochondrial protein homeostasis and mitochondrial function