10 research outputs found

    The N-Terminal Amphipathic Helix of the Topological Specificity Factor MinE Is Associated with Shaping Membrane Curvature

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    Pole-to-pole oscillations of the Min proteins in Escherichia coli are required for the proper placement of the division septum. Direct interaction of MinE with the cell membrane is critical for the dynamic behavior of the Min system. In vitro, this MinE-membrane interaction led to membrane deformation; however, the underlying mechanism remained unclear. Here we report that MinE-induced membrane deformation involves the formation of an amphipathic helix of MinE2–9, which, together with the adjacent basic residues, function as membrane anchors. Biochemical evidence suggested that the membrane association induces formation of the helix, with the helical face, consisting of A2, L3, and F6, inserted into the membrane. Insertion of this helix into the cell membrane can influence local membrane curvature and lead to drastic changes in membrane topology. Accordingly, MinE showed characteristic features of protein-induced membrane tubulation and lipid clustering in in vitro reconstituted systems. In conclusion, MinE shares common protein signatures with a group of membrane trafficking proteins in eukaryotic cells. These MinE signatures appear to affect membrane curvature

    Non-Hfe iron overload: Is Phlebotomy the answer?

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    Iron is an essential factor for life, however a physiologically optimal balance is critical. In this article we explore the role of iron as a co-factor in a range of chronic liver diseases and how it may contribute to the development of liver injury, fibrosis, cirrhosis and ultimately hepatocellular carcinoma. Whilst iron depletion therapy through phlebotomy is the most effective method of reducing iron stores, it is unclear whether this offers utility in the therapy of liver diseases in which iron is not the primary insult resulting in tissue injury. Here we examine the emerging evidence in the field of non-HFE hereditary haemochromatosis conditions associated with iron overload – is phlebotomy the answer

    Lynch syndrome-associated breast cancers do not overexpress chromosome 11-encoded mucins

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    Mismatch repair-deficient breast cancers may be identified in Lynch syndrome mutation carriers, and have clinicopathological features in common with mismatch repair-deficient colorectal and endometrial cancers such as tumour-infiltrating lymphocytes and poor differentiation. Mismatch repair-deficient colorectal cancers frequently show mucinous differentiation associated with upregulation of chromosome 11 mucins. The aim of this study was to compare the protein expression of these mucins in mismatch repair-deficient and -proficient breast cancers. Cases of breast cancer (n=100) were identified from families where (1) both breast and colon cancer co-occurred and (2) families met either modified Amsterdam criteria or had at least one early-onset

    Oxidative Stress, Antioxidant Status, and Redox Signaling in Carcinogenesis

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