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D-site of albumin promoter binding protein (DBP) may regulate hematopoiesis
Biology and Medicine, Vol 3 (3): 32-69, 2011 (2011)
  • SR Sethu Narayanan

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.

  • DBP,
  • PYK2,
  • phorbol,
  • hypoxia,
  • progenitor,
  • FDCP-mix cells
Publication Date
Summer July 1, 2011
Citation Information
SR Sethu Narayanan, (2011) "D-site of albumin promoter binding protein (DBP) may regulate hematopoiesis" Biology and Medicine, Vol 3 (3): 32-69,