By A. Victor Hoffbrand, Daniel Catovsky, Edward G. D. Tuddenham

This can be a finished haematology textual content ebook. Very worthy for scientific and Lab haematologists, trainees and lab scientists

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The transcription factor GATA-1 is essential for maturation of erythroblasts; the absence of GATA-1 leads to apoptosis and a block in maturation. Some of the target genes regulated by GATA-1 are likely to be important for cell survival. Although many of the targets are unknown, it is clear that GATA-1 strongly induces expression of Bcl-XL and may therefore cooperate with EpoR signalling. In this way, Epo signalling, Fas-mediated signalling and GATA-1 converge on Bcl-XL, which represents a key target of the erythroid cell survival programme.

One principle that seems to be emerging is that factors affiliated with different lineages such as GATA-1 (erythroid) and PU1 (lymphocytes and granulocytes) are both present in uncommitted progenitors, reflecting the potential to develop along alternative different pathways (so-called multilineage priming). It is now known that GATA-1 and PU1 interact and cross-antagonize each other. Therefore, as cells differentiate, reinforcement of the transcriptional programme of one lineage may actively suppress an alternative lineage.

The full control of this system is complex and it should be noted that the EpoR pathway can also be activated by other mechanisms. For example, activation of c-Kit by its ligand, stem cell factor (SCF), causes tyrosine phosphorylation of the EpoR and a functional interaction between the two receptors is essential for normal erythropoiesis. Mechanisms for switching off the Epo–EpoR signalling pathway also exist. Specific phosphorylated tyrosines that occur on the Epo-stimulated dimerized EpoR provide docking sites for the SH2 domains of protein tyrosine phosphatases such as SHP1.

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