Autophagy is a process of self-degradation of cellular components in which double-membrane autophagosomes sequester organelles or portions of cytosol and fuse with lysosomes or vacuoles for breakdown by resident hydrolases. Autophagy is upregulated in response to extra- or intracellular stress and signals such as starvation, growth factor deprivation, ER stress, and pathogen infection. Defective autophagy plays a significant role in human pathologies, including cancer, neurodegeneration, and infectious diseases. We present our current knowledge on the key genes composing the autophagy machinery in eukaryotes from yeast to mammalian cells and the signaling pathways that sense the status of different types of stress and induce autophagy for cell survival and homeostasis. We also review the recent advances on the molecular mechanisms that regulate the autophagy machinery at various levels, from transcriptional activation to post-translational protein modification.

/pdf/regulation-mechanisms-and-signaling-pathways-of-autophagy-4ypu4iix6w.pdf

Regulation Mechanisms and Signaling Pathways of Autophagy

Toxoplasma gondii: from animals to humans

During the past two decades, nitric oxide (NO) has been recognized as one of the most versatile players in the immune system. It is involved in the pathogenesis and control of infectious diseases, tumors, autoimmune processes and chronic degenerative diseases. Because of its variety of reaction partners (DNA, proteins, low–molecular weight thiols, prosthetic groups, reactive oxygen intermediates), its widespread production (by three different NO synthases (NOS) and the fact that its activity is strongly influenced by its concentration, NO continues to surprise and perplex immunologists. Today, there is no simple, uniform picture of the function of NO in the immune system. Protective and toxic effects of NO are frequently seen in parallel. Its striking inter- and intracellular signaling capacity makes it extremely difficult to predict the effect of NOS inhibitors and NO donors, which still hampers therapeutic applications.

Nitric oxide and the immune response

Endocytic mechanisms control the lipid and protein composition of the plasma membrane, thereby regulating how cells interact with their environments. Here, we review what is known about mammalian endocytic mechanisms, with focus on the cellular proteins that control these events. We discuss the well-studied clathrin-mediated endocytic mechanisms and dissect endocytic pathways that proceed independently of clathrin. These clathrin-independent pathways include the CLIC/GEEC endocytic pathway, arf6-dependent endocytosis, flotillin-dependent endocytosis, macropinocytosis, circular doral ruffles, phagocytosis, and trans-endocytosis. We also critically review the role of caveolae and caveolin1 in endocytosis. We highlight the roles of lipids, membrane curvature-modulating proteins, small G proteins, actin, and dynamin in endocytic pathways. We discuss the functional relevance of distinct endocytic pathways and emphasize the importance of studying these pathways to understand human disease processes.

Mechanisms of Endocytosis

Carrier-Based Ion-Selective Electrodes and Bulk Optodes. 1. General Characteristics.

Toxoplasmosis: a history of clinical observations

Historic Perspective on the Microsporidia: Expanding Horizons Structure of the Microsporidia Development Morphology and Life Cycles of the Microsporidia Molecular Biology, Molecular Phylogeny, and Molecular Diagnostic Approaches to the Microsporidia Microsporidian Biochemistry and Physiology The Structure, Function, and Composition of the Microsporidian Polar Tube Host-Parasite Relationships in Microsporidiosis: Animal Models and Physiology Clinical Syndromes Associated with Microsporidiosis Ocular Microsporidiosis Laboratory Diagnosis of Microsporidiosis Culture and Propagation of Microsporidia Microsporidia in Higher Vertebrates Fish Microsporidia Microsporidia in Insects Epidemiology of Microsporidiosis

The Microsporidia And Microsporidiosis

Toxoplasma gondii: the model apicomplexan

Purpose of reviewMicrosporidiosis is an emerging and opportunistic infection associated with a wide range of clinical syndromes in humans. This review highlights the research on microsporidiosis in humans during the previous 2 years.Recent findingsThe reduced and compact microsporidian genome has ge

Louis M. Weiss

Papers

Toxoplasma gondii: from animals to humans

Toxoplasmosis: a history of clinical observations

The Microsporidia And Microsporidiosis

Toxoplasma gondii: the model apicomplexan

Microsporidiosis: current status.