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Nicolas Delaleu Heike Immervoll Janet Cornelius Roland Jonsson 《Arthritis research & therapy》2008,10(1):R22
Introduction
Sj?gren's syndrome (SS) is a systemic autoimmune disease that mainly targets the exocrine glands. The aim of this study was to investigate the involvement of 87 proteins measured in serum and 75 proteins analyzed in saliva in spontaneous experimental SS. In addition, we intended to compute a model of the immunological situation representing the overt disease stage of SS. 相似文献3.
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Bernadette Schreiner Heike Westerburg Ignasi Forné Axel Imhof Walter Neupert Dejana Mokranjac 《Molecular biology of the cell》2012,23(22):4335-4346
The vast majority of mitochondrial proteins are synthesized in the cytosol and transported into the organelle in a largely, if not completely, unfolded state. The proper function of mitochondria thus depends on folding of several hundreds of proteins in the various subcompartments of the organelle. Whereas folding of proteins in the mitochondrial matrix is supported by members of several chaperone families, very little is known about folding of proteins in the intermembrane space (IMS). We targeted dihydrofolate reductase (DHFR) as a model substrate to the IMS of yeast mitochondria and analyzed its folding. DHFR can fold in this compartment, and its aggregation upon heat shock can be prevented in an ATP-dependent manner. Yme1, an AAA (ATPases associated with diverse cellular activities) protease of the IMS, prevented aggregation of DHFR. Analysis of protein aggregates in mitochondria lacking Yme1 revealed the presence of a number of proteins involved in the establishment of mitochondrial ultrastructure, lipid metabolism, protein import, and respiratory growth. These findings explain the pleiotropic effects of deletion of YME1 and suggest an important role for Yme1 as a folding assistant, in addition to its proteolytic function, in the protein homeostasis of mitochondria 相似文献
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Christopher Boehlke Heike Janusch Christoph Hamann Christian Powelske Miriam Mergen Henriette Herbst Fruzsina Kotsis Roland Nitschke E. Wolfgang Kuehn 《PloS one》2015,10(10)
Ift88 is a central component of the intraflagellar transport (Ift) complex B, essential for the building of cilia and flagella from single cell organisms to mammals. Loss of Ift88 results in the absence of cilia and causes left-right asymmetry defects, disordered Hedgehog signaling, and polycystic kidney disease, all of which are explained by aberrant ciliary function. In addition, a number of extraciliary functions of Ift88 have been described that affect the cell-cycle, mitosis, and targeting of the T-cell receptor to the immunological synapse. Similarly, another essential ciliary molecule, the kinesin-2 subunit Kif3a, which transports Ift-B in the cilium, affects microtubule (MT) dynamics at the leading edge of migrating cells independently of cilia. We now show that loss of Ift88 impairs cell migration irrespective of cilia. Ift88 is required for the polarization of migrating MDCK cells, and Ift88 depleted cells have fewer MTs at the leading edge. Neither MT dynamics nor MT nucleation are dependent on Ift88. Our findings dissociate the function of Ift88 from Kif3a outside the cilium and suggest a novel extraciliary function for Ift88. Future studies need to address what unifying mechanism underlies the different extraciliary functions of Ift88. 相似文献
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Multidrug resistance (MDR) is a major problem in cancer chemotherapy. As P-glycoprotein is the key molecule in MDR, many investigators have constructed anti-P-glycoprotein monoclonal antibodies (MAbs). Those antibodies, including MRK16 and C219, were used for elucidation of the mechanism of MDR and for overcoming of MDR. This article describes the characterization of the antibodies against the P-glycoprotein and other proteins of multidrug-resistant tumor cells, and discusses the therapeutic implication of the antibodies.Abbreviation ADCC
antibody-dependent cell-mediated cytotoxicity 相似文献
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Predicted increases in atmospheric carbon dioxide (CO2) are widely anticipated to increase biomass accumulation by accelerating rates of photosynthesis in many plant taxa. Little, however, is known about how soil-borne plant antagonists might modify the effects of elevated CO2 (eCO2), with root-feeding insects being particularly understudied. Root damage by insects often reduces rates of photosynthesis by disrupting root function and imposing water deficits. These insects therefore have considerable potential for modifying plant responses to eCO2. We investigated how root damage by a soil-dwelling insect (Xylotrupes gideon australicus) modified the responses of Eucalyptus globulus to eCO2. eCO2 increased plant height when E. globulus were 14 weeks old and continued to do so at an accelerated rate compared to those grown at ambient CO2 (aCO2). Plants exposed to root-damaging insects showed a rapid decline in growth rates thereafter. In eCO2, shoot and root biomass increased by 46 and 35%, respectively, in insect-free plants but these effects were arrested when soil-dwelling insects were present so that plants were the same size as those grown at aCO2. Specific leaf mass increased by 29% under eCO2, but at eCO2 root damage caused it to decline by 16%, similar to values seen in plants at aCO2 without root damage. Leaf C:N ratio increased by >30% at eCO2 as a consequence of declining leaf N concentrations, but this change was also moderated by soil insects. Soil insects also reduced leaf water content by 9% at eCO2, which potentially arose through impaired water uptake by the roots. We hypothesise that this may have impaired photosynthetic activity to the extent that observed plant responses to eCO2 no longer occurred. In conclusion, soil-dwelling insects could modify plant responses to eCO2 predicted by climate change plant growth models. 相似文献
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