In this time, We are faced with a turning point of high school building. Corresponding to the change of social environment, the new movements about education reformation such as large enforcement of ...optional subject system, quicken the flexible operation of credit system and newly established synthetic course of study have already been started with the introduction of new curriculum. In this paper, we conducted investigation about disjoint condition of class and it's pattern in using the school rooms in order to obtain the planning concept of school rooms.
Phosphofructokinase 1 (PFK1) plays a critical role in glycolysis; however, its role and regulation in tumorigenesis are not well understood. Here, we demonstrate that PFK1 platelet isoform (PFKP) is ...the predominant PFK1 isoform in human glioblastoma cells and its expression correlates with total PFK activity. We show that PFKP is overexpressed in human glioblastoma specimens due to an increased stability, which is induced by AKT activation resulting from phosphatase and tensin homologue (PTEN) loss and EGFR-dependent PI3K activation. AKT binds to and phosphorylates PFKP at S386, and this phosphorylation inhibits the binding of TRIM21 E3 ligase to PFKP and the subsequent TRIM21-mediated polyubiquitylation and degradation of PFKP. PFKP S386 phosphorylation increases PFKP expression and promotes aerobic glycolysis, cell proliferation, and brain tumor growth. In addition, S386 phosphorylation in human glioblastoma specimens positively correlates with PFKP expression, AKT S473 phosphorylation, and poor prognosis. These findings underscore the potential role and regulation of PFKP in human glioblastoma development.Phosphofructokinase 1 (PFK1) plays a critical role in glycolysis. Here the authors show that PFK1 platelet isoform is upregulated in Glioblastoma and is required for tumor growth mechanistically, such upregulation is due to an increased stability induced by AKT activation via phosphorylation on residue S386.
Autophagy is crucial for maintaining cell homeostasis. However, the precise mechanism underlying autophagy initiation remains to be defined. Here, we demonstrate that glutamine deprivation and ...hypoxia result in inhibition of mTOR-mediated acetyl-transferase ARD1 S228 phosphorylation, leading to ARD1-dependent phosphoglycerate kinase 1 (PGK1) K388 acetylation and subsequent PGK1-mediated Beclin1 S30 phosphorylation. This phosphorylation enhances ATG14L-associated class III phosphatidylinositol 3-kinase VPS34 activity by increasing the binding of phosphatidylinositol to VPS34. ARD1-dependent PGK1 acetylation and PGK1-mediated Beclin1 S30 phosphorylation are required for glutamine deprivation- and hypoxia-induced autophagy and brain tumorigenesis. Furthermore, PGK1 K388 acetylation levels correlate with Beclin1 S30 phosphorylation levels and poor prognosis in glioblastoma patients. Our study unearths an important mechanism underlying cellular-stress-induced autophagy initiation in which the protein kinase activity of the metabolic enzyme PGK1 plays an instrumental role and reveals the significance of the mutual regulation of autophagy and cell metabolism in maintaining cell homeostasis.
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•Glutamine deprivation and hypoxia result in ARD1-dependent PGK1 K388 acetylation•PGK1 functioning as a protein kinase phosphorylates Beclin1 at S30•Beclin1 S30 phosphorylation enhances VPS34-Beclin1-ATG14L complex activity•Beclin1 S30 phosphorylation is required for autophagy initiation and tumorigenesis
Qian et al. demonstrate that glutamine deprivation and hypoxia inhibit mTOR and mTOR-dependent ARD1 S228 phosphorylation, which allows ARD1 to bind to PGK1 for PGK1 K388 acetylation. The acetylated PGK1 binds to and phosphorylates Beclin1 at S30, leading to activation of the VPS34-Beclin1 complex to initiate autophagosomal formation.
In this work, we investigate the performance of graphene-based Schottky junction thermophotovoltaic (TPV) devices in near-field conditions. Despite the low cost and excellent photoelectric properties ...of graphene, earlier studies have focused primarily on the contribution of the graphene layer to the photocurrent, assuming an internal quantum efficiency (IQE) of 100%. Our numerical model of a graphene/germanium Schottky junction TPV device reveals that the semiconductor layer predominates in the generation photocurrent, with an IQE of graphene less than 40%. We also evaluate the photocurrent densities generated by the semiconductor and graphene at an emitter temperature of 1000 K and a vacuum gap of 100 nm. Results show that using an indium tin oxide (ITO)-covered tungsten (W) emitter can increase photocurrents by a factor of around 10 and 11 for the semiconductor and graphene, respectively. Additionally, using a hyperbolic metamaterial (HMM) emitter can enhance photocurrents by around 4.7 and 5.2 times for the semiconductor and graphene, respectively. However, this comes at the cost of higher heat flux from the HMM emitter. Our findings will provide valuable insights for the design and optimization of TPV devices to improve their photocurrent and efficiency.
Thermophotonic cells in self-sustaining parallel circuits Yang, Zhimin; Song, Jaeman; Lee, Bong Jae
Journal of Quantitative Spectroscopy & Radiative Transfer/Journal of quantitative spectroscopy & radiative transfer,
January 2024, 2024-01-00, Volume:
312
Journal Article
Peer reviewed
Open access
•TPX system with different bandgaps in self-sustaining circuit is proposed.•Expressions of currents in the proposed system are clearly described.•Possibility of establishing self-sustaining circuit ...for proposed system is proven.•Impact of far-and near-field effect on the proposed system is analyzed.•Influence of near-field effect on TPX system with same bandgaps is discussed.
Thermophotonic (TPX) cells, which integrate a light-emitting diode (LED) and a photovoltaic (PV) cell, offer potential advantages over thermophotovoltaic (TPV) cells for low-grade waste heat utilization. While TPX cells traditionally operate in an independent circuit, which requires an external battery storage unit, the self-sustaining circuit presents an appealing alternative that eliminates the need for the storage unit. In this study, we conduct a comprehensive analysis of TPX cells operating in the self-sustaining circuit. We provide clear expressions for the electrical currents flowing through the LED and PV cell, considering the different bandgaps of the LED and the PV cell. Our results reveal that the bandgap energy of the LED must exceed that of the PV cell for the TPX cell to function in a self-sustaining parallel circuit. Furthermore, we demonstrate that the performance of the TPX cell in the self-sustaining circuit improves with a narrower bandgap energy for the PV cell and a wider bandgap energy for the LED, regardless of the far-field or near-field configurations. While near-field TPX cells exhibit higher power density, they also experience decreased energy efficiency compared to far-field TPX cells. Additionally, we explore the scenario where the bandgaps of the LED and PV cell are the same, analyzing the performance of a closed-structured self-sustaining parallel circuit with multiple LEDs and PV cells in the near-field configuration. We find that the near-field effect has a marginal impact on TPX cells with identical bandgaps, which means that the near-field TPX cell in the self-sustaining circuit will not be useful in practice. The insights gained from this work serve as valuable design guidelines for TPX cells operating in the self-sustaining parallel circuit, enabling practical operation without the need for an external battery storage unit.
EGFR activates phosphatidylinositide 3-kinase (PI3K), but the mechanism underlying this activation is not completely understood. We demonstrated here that EGFR activation resulted in lysine ...acetyltransferase 5 (KAT5)-mediated K395 acetylation of the platelet isoform of phosphofructokinase 1 (PFKP) and subsequent translocation of PFKP to the plasma membrane, where the PFKP was phosphorylated at Y64 by EGFR. Phosphorylated PFKP binds to the N-terminal SH2 domain of p85α, which is distinct from binding of Gab1 to the C-terminal SH2 domain of p85α, and recruited p85α to the plasma membrane resulting in PI3K activation. PI3K-dependent AKT activation results in enhanced phosphofructokinase 2 (PFK2) phosphorylation and production of fructose-2,6-bisphosphate, which in turn promotes PFK1 activation. PFKP Y64 phosphorylation–enhanced PI3K/AKT-dependent PFK1 activation and GLUT1 expression promoted the Warburg effect, tumor cell proliferation, and brain tumorigenesis. These findings underscore the instrumental role of PFKP in PI3K activation and enhanced glycolysis through PI3K/AKT-dependent positive-feedback regulation.
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•KAT5 acetylates PFKP at K395 and promotes the binding of PFKP to EGFR•EGFR-phosphorylated PFKP Y64 binds to p85α SH2 domain and activates PI3K•PFKP-activated AKT enhances GLUT1 expression and PFK2-mediated PFK1 activity•PFKP Y64 phosphorylation enhances the Warburg effect and tumorigenesis
Lee et al. demonstrate that KAT5-mediated PFKP acetylation and subsequent EGFR-phosphorylated PFKP bind to the N-terminal SH2 domain of p85α to activate PI3K, leading to enhanced AKT-dependent PFK2 activation, F-2,6-BP-production-dependent PFK1 activation, and GLUT1 expression. Non-metabolic function of PFKP promotes the Warburg effect through PI3K/AKT-dependent positive-feedback regulation.
Dietary fructose is primarily metabolized in the liver. Here we demonstrate that, compared with normal hepatocytes, hepatocellular carcinoma (HCC) cells markedly reduce the rate of fructose ...metabolism and the level of reactive oxygen species, as a result of a c-Myc-dependent and heterogeneous nuclear ribonucleoprotein (hnRNP) H1- and H2-mediated switch from expression of the high-activity fructokinase (KHK)-C to the low-activity KHK-A isoform. Importantly, KHK-A acts as a protein kinase, phosphorylating and activating phosphoribosyl pyrophosphate synthetase 1 (PRPS1) to promote pentose phosphate pathway-dependent de novo nucleic acid synthesis and HCC formation. Furthermore, c-Myc, hnRNPH1/2 and KHK-A expression levels and PRPS1 Thr225 phosphorylation levels correlate with each other in HCC specimens and are associated with poor prognosis for HCC. These findings reveal a pivotal mechanism underlying the distinct fructose metabolism between HCC cells and normal hepatocytes and highlight the instrumental role of KHK-A protein kinase activity in promoting de novo nucleic acid synthesis and HCC development.
Transposable elements or transposons are major players in genetic variability and genome evolution. Aberrant activation of long interspersed element-1 (LINE-1 or L1) retrotransposons is common in ...human cancers, yet their tumor-type-specific functions are poorly characterized. We identified MPHOSPH8/MPP8, a component of the human silencing hub (HUSH) complex, as an acute myeloid leukemia (AML)-selective dependency by epigenetic regulator-focused CRISPR screening. Although MPP8 is dispensable for steady-state hematopoiesis, MPP8 loss inhibits AML development by reactivating L1s to induce the DNA damage response and cell cycle exit. Activation of endogenous or ectopic L1s mimics the phenotype of MPP8 loss, whereas blocking retrotransposition abrogates MPP8-deficiency-induced phenotypes. Expression of AML oncogenic mutations promotes L1 suppression, and enhanced L1 silencing is associated with poor prognosis in human AML. Hence, while retrotransposons are commonly recognized for their cancer-promoting functions, we describe a tumor-suppressive role for L1 retrotransposons in myeloid leukemia.
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