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NumreringReferensOmslagsbildHitta
1011.
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1012.
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1013.
  • Sukonina, Valentina, et al. (författare)
  • FOXK1 and FOXK2 regulate aerobic glycolysis.
  • 2019
  • Ingår i: Nature. - 1476-4687. ; 566, s. 279-283
  • Tidskriftsartikel (refereegranskat)abstract
    • Adaptation to the environment and extraction of energy are essential for survival. Some species have found niches and specialized in using a particular source of energy, whereas others-including humans and several other mammals-have developed a high degree of flexibility1. A lot is known about the general metabolic fates of different substrates but we still lack a detailed mechanistic understanding of how cells adapt in their use of basic nutrients2. Here we show that the closely related fasting/starvation-induced forkhead transcription factors FOXK1 and FOXK2 induce aerobic glycolysis by upregulating the enzymatic machinery required for this (for example, hexokinase-2, phosphofructokinase, pyruvate kinase, and lactate dehydrogenase), while at the same time suppressing further oxidation of pyruvate in the mitochondria by increasing the activity of pyruvate dehydrogenase kinases 1 and 4. Together with suppression of the catalytic subunit of pyruvate dehydrogenase phosphatase 1 this leads to increased phosphorylation of the E1α regulatory subunit of the pyruvate dehydrogenase complex, which in turn inhibits further oxidation of pyruvate in the mitochondria-instead, pyruvate is reduced to lactate. Suppression of FOXK1 and FOXK2 induce the opposite phenotype. Both in vitro and in vivo experiments, including studies of primary human cells, show how FOXK1 and/or FOXK2 are likely to act as important regulators that reprogram cellular metabolism to induce aerobic glycolysis.
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1014.
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1015.
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1016.
  • Taga, A, et al. (författare)
  • Non-collinear states in magnetic sensors
  • 2000
  • Ingår i: NATURE. - : MACMILLAN PUBLISHERS LTD. - 0028-0836. ; 406:6793, s. 280-282 Language: English
  • Tidskriftsartikel (refereegranskat)abstract
    • Certain materials have an electrical conductivity that is extremely sensitive to an applied magnetic field; this phenomenon, termed 'giant magnetoresistance'(1-3), can be used in sensor applications. Typically, such a device comprises several ferromagneti
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1017.
  • Takala, Heikki, et al. (författare)
  • Signal amplification and transduction in phytochrome photosensors
  • 2014
  • Ingår i: Nature. - 0028-0836. ; 509:7499, s. 245-248
  • Tidskriftsartikel (refereegranskat)abstract
    • Sensory proteins must relay structural signals from the sensory site over large distances to regulatory output domains. Phytochromes are a major family of red-light-sensing kinases that control diverse cellular functions in plants, bacteria and fungi(1-9). Bacterial phytochromes consist of a photosensory core and a carboxy-terminal regulatory domain(10,11). Structures of photosensory cores are reported in the resting state(12-18) and conformational responses to light activation have been proposed in the vicinity of the chromophore(19-23). However, the structure of the signalling state and the mechanism of downstream signal relay through the photosensory core remain elusive. Here we report crystal and solution structures of the resting and activated states of the photosensory core of the bacteriophytochrome from Deinococcus radiodurans. The structures show an open and closed form of the dimeric protein for the activated and resting states, respectively. This nanometre-scale rearrangement is controlled by refolding of an evolutionarily conserved 'tongue', which is in contact with the chromophore. The findings reveal an unusual mechanism in which atomic-scale conformational changes around the chromophore are first amplified into ana angstrom-scale distance change in the tongue, and further grow into a nanometre-scale conformational signal. The structural mechanism is a blueprint for understanding how phytochromes connect to the cellular signalling network.
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1018.
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1019.
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1020.
  • Tammela, Tuomas, et al. (författare)
  • Blocking VEGFR-3 suppresses angiogenic sprouting and vascular network formation.
  • 2008
  • Ingår i: Nature. - 1476-4687. ; 454:7204, s. 656-60
  • Tidskriftsartikel (refereegranskat)abstract
    • Angiogenesis, the growth of new blood vessels from pre-existing vasculature, is a key process in several pathological conditions, including tumour growth and age-related macular degeneration. Vascular endothelial growth factors (VEGFs) stimulate angiogenesis and lymphangiogenesis by activating VEGF receptor (VEGFR) tyrosine kinases in endothelial cells. VEGFR-3 (also known as FLT-4) is present in all endothelia during development, and in the adult it becomes restricted to the lymphatic endothelium. However, VEGFR-3 is upregulated in the microvasculature of tumours and wounds. Here we demonstrate that VEGFR-3 is highly expressed in angiogenic sprouts, and genetic targeting of VEGFR-3 or blocking of VEGFR-3 signalling with monoclonal antibodies results in decreased sprouting, vascular density, vessel branching and endothelial cell proliferation in mouse angiogenesis models. Stimulation of VEGFR-3 augmented VEGF-induced angiogenesis and sustained angiogenesis even in the presence of VEGFR-2 (also known as KDR or FLK-1) inhibitors, whereas antibodies against VEGFR-3 and VEGFR-2 in combination resulted in additive inhibition of angiogenesis and tumour growth. Furthermore, genetic or pharmacological disruption of the Notch signalling pathway led to widespread endothelial VEGFR-3 expression and excessive sprouting, which was inhibited by blocking VEGFR-3 signals. Our results implicate VEGFR-3 as a regulator of vascular network formation. Targeting VEGFR-3 may provide additional efficacy for anti-angiogenic therapies, especially towards vessels that are resistant to VEGF or VEGFR-2 inhibitors.
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