40 research outputs found

    Key signalling nodes in mammary gland development and cancer. Mitogen-activated protein kinase signalling in experimental models of breast cancer progression and in mammary gland development

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    Seven classes of mitogen-activated protein kinase (MAPK) intracellular signalling cascades exist, four of which are implicated in breast disease and function in mammary epithelial cells. These are the extracellular regulated kinase (ERK)1/2 pathway, the ERK5 pathway, the p38 pathway and the c-Jun N-terminal kinase (JNK) pathway. In some forms of human breast cancer and in many experimental models of breast cancer progression, signalling through the ERK1/2 pathway, in particular, has been implicated as being important. We review the influence of ERK1/2 activity on the organised three-dimensional association of mammary epithelial cells, and in models of breast cancer cell invasion. We assess the importance of epidermal growth factor receptor family signalling through ERK1/2 in models of breast cancer progression and the influence of ERK1/2 on its substrate, the oestrogen receptor, in this context. In parallel, we consider the importance of these MAPK-centred signalling cascades during the cycle of mammary gland development. Although less extensively studied, we highlight the instances of signalling through the p38, JNK and ERK5 pathways involved in breast cancer progression and mammary gland development

    Spatial and temporal trends of the Stockholm Convention POPs in mothers’ milk — a global review

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    The complete chloroplast genome of Torilis scabra

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    Regulation of Neuronal Survival Factor MEF2D by Chaperone-Mediated Autophagy

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    Chaperone-mediated autophagy controls the degradation of selective cytosolic proteins and may protect neurons against degeneration. In a neuronal cell line, we found that chaperone-mediated autophagy regulated the activity of myocyte enhancer factor 2D (MEF2D), a transcription factor required for neuronal survival. MEF2D was observed to continuously shuttle to the cytoplasm, interact with the chaperone Hsc70, and undergo degradation. Inhibition of chaperone-mediated autophagy caused accumulation of inactive MEF2D in the cytoplasm. MEF2D levels were increased in the brains of a-synuclein transgenic mice and patients with Parkinson's disease. Wild-type \u3b1-synuclein and a Parkinson's disease-associated mutant disrupted the MEF2D-Hsc70 binding and led to neuronal death. Thus, chaperone-mediated autophagy modulates the neuronal survival machinery, and dysregulation of this pathway is associated with Parkinson's diseas

    POWER DEPENDENCE OF THE RECOMBINATION PROCESSES IN THE INXGA1-XAS/GAAS SINGLE-QUANTUM-WELL

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    We have measured the power dependence of the photoluminesence spectra from a set of strained InxGa1-xAs/GaAs single quantum wells. The result shows that the excitation power has important effect on the carrier recombination processes. When the power increases from 0.5 to 14 mW, the photoluminescence from the barrier becomes more intense than that from the well and the trapping efficiency decreases. At high excitation level, the ratio of the radiative recombination rate to the nonradiative recombination rate of the barrier increases ten times than that at lower excitation level, while it only doubles for the well

    Design mitochondria-specific fluorescent turn-on probes targeting G-quadruplexes for live cell imaging and mitophagy monitoring study

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    202208 bcchNot applicableOthersNational Natural Science Foundation of China [81473082, 22077020 and 32050410289];Natural Science Foundation of Guangdong Province, China [2017A030313078, 2017A030313071, and 2019A1515011799];Health and Medical Research Fund (HMRF), Hong Kong SAR [19200231];PolyU Startup Fund [P0035712];PolyU SZRI fund [A0039278]Published24 month
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