Titlebook: Biochemical Roles of Eukaryotic Cell Surface Macromolecules; Abhijit Chakrabarti,Avadhesha Surolia Conference proceedings 2015 The Editor(

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Human-Specific Evolutionary Changes in the Biology of Siglecs,sion of Siglec-5 expression on adaptive immune cells, new expression of Siglec-5 on amniotic epithelium, and elimination of Siglec-13 and -17 from innate immune cells. The Siglec-13 and -17 inactivation events fixed in the ancestral population shortly before the common ancestor of modern humans 100–

transient-pain

Structural Changes of GPI Anchor After Its Attachment to Proteins: Functional Significance,remodeling of lipid and glycan moieties in the endoplasmic reticulum is critical for efficient recruitment of GPI-APs into ER-exit site and association with their cargo receptors. Fatty acid remodeling of GPI in the Golgi is important for homodimerization and raft association. These structure–functi

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Defects in Erythrocyte Membrane Skeletal Architecture, alterations induced by the malarial parasite, ., in the infected erythrocytes. This review article attests to the enormous progress in our understanding of the contribution of erythrocyte membrane skeletal proteins to human diseases.

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Immuno-Modulatory Role of Porins: Host Immune Responses, Signaling Mechanisms and Vaccine Potentialne. This review highlights the role of porins in various host immuno-modulatory processes, the signaling mechanisms by which they activate host immune cells and their use as vaccines against various gram-negative bacterial infections.

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New Vis-Tas in Lactosylceramide Research,utics for use humans and certain veterinary purposes. In particular, this article will focus on two areas: 1. Inflammation and the LacCer–phospholipase-A-2 (PLA2) connection and 2. Implications of LacCer modulation on cardiac hypertrophy.

white-matter

A Signal with a Difference: The Role of GPI Anchor Signal Sequence in Dictating Conformation and Fua predominantly alpha helical conformation, reducing adhesion and preventing it from forming β-aggregates as is expected of the functional Als5. We had proposed that this was due to an interaction between the SS and the amyloidogenic domain on Als5. In this paper, we develop this theme further. We d

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