This chapter outlines the translocation of proteins into mitochondria. Most mitochondrial proteins are synthesized in the cytosol and subsequently imported into the organelle. According to the ...“conservative sorting” model, the precursor protein is first imported into the matrix, then cleaved by MPP, re-exported as an intermediate form into the inner membrane and finally cleaved to the mature protein by the inner membrane peptidase. Numerous mitochondrial preproteins, however, do not carry cleavable presequences, but contain internal targeting signals in the mature protein part. The signaling information for the specific targeting of preproteins to mitochondria is only contained in the targeting sequences of the preproteins and is decoded by membrane-bound receptors of the mitochondria. The binding chain thus serves as a guiding system to direct preproteins across the mitochondrial outer membrane and to the inner membrane. This chapter also highlights that a pressing issue will be the elucidation of the structural organization of the translocases, of receptors and channels. This is yet to be explored and to know which energy sources drive the translocation of preproteins across the outer membrane and how the import motor of mtHsp70 and Tim44 functions at a molecular level.
1. Most proteins of cell organelles are synthesized as precursor proteins on cytosolic polysomes and are directed by signal sequences into the correct compartments. 2. In this review, the ...characteristics of mitochondrial protein uptake will be described, including the specific recognition, membrane translocation, proteolytic processing and folding of nuclear-encoded precursor proteins. 3. Recent studies indicate that a proteinaceous machinery located in the mitochondrial membranes and matrix performs these key steps of protein import.
Even nowadays and at specialized centers, one of the leading causes of death is exsanguination. Trauma-induced coagulopathy (TIC) occuring with massive blood loss primarily results from loss of ...coagualtion factors and platelets and is aggravated by hemodilution. In addition, hyperfibrinolysis, hypothermia, acidosis and hypocalcaemia also contribute to the development of severe haemostatic derangement. During the past few years new insights into the pathophysiology of TIC and the widespread use of viscoelastic coagulation monitoring provoked the development of alternative treatment concepts. As for the previously recommended standard therapy using fresh frozen plasma and platelet concentrates also for alternative strategies no data from large prospective randomized studies are available until now, however, the evidence is growing favoring the use of coagulation factor concentrates guided by viscoelastic measurements.
Two driving mechanisms, one powered by membrane potential and the other a combination of pulling and trapping, seem to be involved in protein import into mitochondria.
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