By Harald Kropshofer, Anne B. Vogt
This novel, multidisciplinary instruction manual highlights contemporary proof that antigen featuring cells (APCs) should not in basic terms key avid gamers within the initiation or prevention of an antigen-specific T lymphocyte-mediated adaptive immune reaction, but in addition serious regulators and integrators within the interaction among our innate and adaptive immune system.Structured in a transparent approach to permit entry to a really vast readership, the ebook is written from the point of view of a biochemist, immunologist, and scientist with event in drug improvement. It covers all mobile varieties interested by antigen presentation, offering the most recent immunological proof with a spotlight on drug improvement. sponsored by means of a word list explaining all vital technical phrases, this brief yet complete reference covers easy introductory facets correct as much as information for complex experts.
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Extra resources for Antigen Presenting Cells: From Mechanisms to Drug Development
Abl initially phosphorylates Crk-accosiated substrate, CAS, at a single tyrosine residue (1) and at the same time binds to SH2 domain of adaptor protein Crk (CT10 regulator of kinase), contributing to additional phosphorylation of tyrosine residues of p130CAS (2). The Crk-based scaffold also provides a binding site for C3G, guanidine exchange factor protein. , 1998) leads to activation of JNK (c-jun N-terminal kinase) that, similar to ERK, can translocate to nucleus and induce transcription of c-jun gene.
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Pool sequencing of natural HLA-DR, DQ, and DP ligands reveals detailed peptide motifs, constraints of processing, and general rules. Immunogenetics 1994, 39, 230–242. 42 Nelson CA, Vidavsky I, Viner NJ, Gross ML, Unanue ER. Amino-terminal trimming of peptides for presentation on major histocompatibility complex class II molecules. Proc. Natl. Acad. Sci. A. 1997, 94, 628–633. 43 Jardetzky TS, Gorga JC, Busch R, Rothbard J, Strominger JL, Wiley DC. Peptide binding to HLA-DR1: a peptide with most residues substituted to alanine retains MHC binding.