Download PDF by Harald Schulze, Joseph Italiano: Molecular and Cellular Biology of Platelet Formation:

By Harald Schulze, Joseph Italiano

ISBN-10: 3319395602

ISBN-13: 9783319395609

ISBN-10: 3319395629

ISBN-13: 9783319395623

This publication provides a finished perception into platelet biogenesis, platelet sign transduction, involvement of platelets in affliction, using varied animal versions for platelet learn and destiny views in regard to platelet construction and gene treatment. Being written through foreign specialists, the e-book is a concise state-of-the paintings within the box of platelet biogenesis, biology and learn. It represents an essential software for examine scientists in biomedicine, vascular biology, hematopoiesis and hemostasis and particularly for scientists in platelet study, in addition to for clinicians within the box of hematology and transfusion medicine.​

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Extra info for Molecular and Cellular Biology of Platelet Formation: Implications in Health and Disease

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The chemokine CXCL12 (SDF1α) and growth factor FGF4 promote both MK migration and interaction with the BMECs, thereby promoting platelet production [22]. Interestingly, this interaction is enhanced by inflammatory cytokines, such as interleukin-­1 beta (IL-1B) [33, 34]. Furthermore, stimulation of the pro-inflammatory VEGFR1 pathway leads to an upregulation of the CXCL12 receptor CXCR4 and increased in vivo platelet formation [35]. These findings suggest that increased interaction between MKs and stimulated endothelium is responsible for the thrombocytosis often observed in inflammation [36].

As mentioned above, TAL1 binding in conjunction with GATA1 distinguishes active from repressed transcription sites. Furthermore, evolutionary conserved association of E-box and GATA motifs separated by 9–12 base pairs has been documented in regulatory regions of several erythroid/MK genes including GATA1 itself [67]. A study of TAL1-binding sites in primary mouse erythroid and MK cells has shown very distinctive patterns of binding, which is conferred by the state of the chromatin (active/inactive) and interactions with other TFs, particularly GATA1.

However, a stochastic cell fate decision might only appear to be so as a consequence of our current inability to look into the minute molecular details of each individual cell in order to identify the probabilistic outcome of cell differentiation. The orchestration of the outcome of differentiation is ultimately driven at the cellular level by the precise arrangement of TFs in a given progenitor which will trigger the expression of lineage-specific gene regulatory networks. This paradigm is illustrated by the bipotent MK-erythroid progenitors (MEPs) that can develop either into an erythroblast or an MK for which they need to switch on a completely different gene repertoire.

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Molecular and Cellular Biology of Platelet Formation: Implications in Health and Disease by Harald Schulze, Joseph Italiano


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