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D Site of Albumin Promoter Binding Protein (DBP) May Promote Hematopoiesis
Biology and Medicine (2011)
  • S.R. Sethu Narayanan, Dr., University of Utah
It is hypothesized that the various cyclic phenomena in hematopoiesis [circadian (24hrs) and cyclic hematopoiesis (7days in mice and 21days in human)] reflect the involvement of circadian and /or metabolic regulatory mechanisms in hematopoietic processes. It is further hypothesized that D-site albumin promoter binding protein (DBP), a (circadian) clock controlled gene (CCG) may play a role in coordinating such phenomena. It is found that DBP can both activate and inhibit the activity of transcriptional regulators such as HIF-1, NF-kB and AP-1 families. DBP itself appears to be a target for the signalling molecules proline-rich tyrosine kinase 2 (PYK2), and dual-specificity Yak1-related tyrosine kinase 3 (DYRK3). Further evidence indicates possible roles for serum-glucocorticoid regulated kinase-1 (SGK1), protein kinase C (PKC) and glycogen synthase kinase (GSK3) in the regulation of DBP activity. These observations would indeed be consistent with a potential role for DBP in the regulation of survival, proliferation and differentiation of hematopoietic progenitors.
  • hematopoiesis
Publication Date
Summer 2011
Citation Information
S.R. Sethu Narayanan. "D Site of Albumin Promoter Binding Protein (DBP) May Promote Hematopoiesis" Biology and Medicine Vol. 3 Iss. 3 (2011)
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