Jak-Stat Signaling : From Basics to Disease by Thomas Decker, Mathias Müller

By Thomas Decker, Mathias Müller

JAK tyrosine kinases and STAT transcription components represent a signaling pathway, that is activated via cytokines. via activating gene transcription it regulates crucial organic responses to environmental cues. The Jak-Stat pathway is fascinated by the legislation of telephone improvement, differentiation, proliferation and apoptosis. mistaken functionality may possibly give a contribution to hematopoietic malignancies and melanoma. This e-book offers entire insights into the newest simple and medical advancements within the box. the 1st half studies contemporary findings and new applied sciences referring to fundamentals of Jak-Stat functionality. the second one half describes the evolution of Jak-Stat signaling and the function of the pathway in invertebrate organisms. The 3rd half specializes in Jak-Stat signaling in hematopoietic cells below either physiological and pathophysiological stipulations. eventually, chapters within the fourth part describe the connection of Jak-Stat signaling to varied states of disorder, fairly an infection, leukemias and stable cancers. The publication is meant for all scientists in molecular biology, biochemistry and telephone biology facing biomedical issues.

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Jak-Stat Signaling : From Basics to Disease

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One such example is Heterochromatin Protein 1 alpha (HP1a) that was recently shown to bind this region of H3 (Dawson et al. 2009; Lavigne et al. 2009). The HP1 family of proteins are relatively small heterochromatin associated proteins. In humans there are three highly similar isoforms, HP1a, HP1b and HP1g (Fanti and Pimpinelli 2008). Each family member consists of two conserved domains; a chromodomain (CD) and a chromoshadow domain (CSD) separated by a less conserved flexible hinge region. Generally speaking, the three HP1 isoforms have overlapping functions and similar, but not identical, chromosomal locations (Fanti and Pimpinelli 2008; Lomberk et al.

J Biol Chem 276(16):12530–12538 Karaghiosoff M, Neubauer H, Lassnig C, Kovarik P, Schindler H, Pircher H, McCoy B, Bogdan C, Decker T, Brem G, Pfeffer K, Muller M (2000) Partial impairment of cytokine responses in Tyk2-deficient mice. Immunity 13(4):549–560 Kohlhuber F, Rogers NC, Watling D, Feng J, Gushin D, Briscoe J, Witthuhn BA, Kotenko SV, Pestka S, Stark GR, Ihle JN, Kerr IM (1997) A JAK1/JAK2 chimera can sustain alpha and gamma interferon responses. Mol Cell Biol 17:695–706 Kovanen PE, Leonard WJ (2004) Cytokines and immunodeficiency diseases: critical roles of the gamma(c)-dependent cytokines interleukins 2, 4, 7, 9, 15, and 21, and their signaling pathways.

Thus, this represents a clear example of nuclear JAK2 directly regulating gene transcription (of an important oncogene) via phosphorylation of H3Y41 at the chromatin interface. g. Lmo2/Nanog/c-Myc) P Y41 ? Increased mitotic recombination ? Chromosomal dysjunction and aneuploidy Heterochromatic repression Supression of mitotic recombination Sister chromatid cohesion Oncogenesis / Self Renewal Fig. 1 Nuclear JAK2 phosphorylates histone H3Y41 and prevents the binding of heterochromatin protein 1a (HP1a) to a novel binding site on chromatin.

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