Titlebook: High Performance Computing; ISC High Performance Amanda Bienz,Michèle Weiland,Carola Kruse Conference proceedings 2023 The Editor(s) (if ap

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Dominik Huber,Martin Schreiber,Martin Schulzulin diversity, which give rise to antigen binding heterodimers capable of responding to a wide spectrum of MHC-presented peptides. However, in this differentiation process only a small number of cells reach the mature state, as most are deleted by a process called negative selection (von . et al. 1

Cantankerous

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Jean-Baptiste Besnard,Ahmad Tarraf,Clément Barthélemy,Alberto Cascajo,Emmanuel Jeannot,Sameer Shende immune response and the onset of opportunistic infections and neoplasms. The mechanism responsible of CD4 T-cell depletion is mainly the induction of apoptosis, which can be activated by HIV through various pathways. In this chapter direct and indirect mechanisms of HIV-induced apoptosis in infecte

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Pcos971

resulting from a reciprocal t(9;22) translocation characterized by the formation of a shortened chromosome, named Philadelphia chromosome (Ph), in which the tyrosine kinase of c-ABL is constitutively activated. This chromosomal translocation generates . fusion genes which can be translated in three

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青石板

Jonatan Baumgartner,Christophe Lillo,Sébastien Rumleyof metastasis can be conceptually broken down into a series of sequential steps: acquisition of an invasive phenotype, intravasation, travel through the circulatory system, arrest at a secondary site, and extravasation and colonization at that site. The metastatic cell must be able to escape cell de

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ARIA

Vincenzo De Maio,Ivona Brandicdamage response. The phosphorylation of H2AX on Ser 139, named γH2AX, is an early response to the generation of DNA DSBs and extends along megabase-long domains, both sites of the lesion, supporting amplification of signal transduction pathways. In parallel, 53BP1 accumulates on damaged chromatin to

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Fotis Nikolaidis,Antony Chazapis,Manolis Marazakis,Angelos Bilass macromolecules and organelles. During the last decade, progress made in our understanding of the molecular controls of autophagy has uncovered the importance of tumor suppressor molecules in the stimulation of autophagy. Downexpression of autophagy is an early event during tumorigenesis. However,