D Site of Albumin Promoter Binding Protein (DBP) May Promote HematopoiesisBiology and Medicine (2011)
AbstractIt 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.
Publication DateSummer 2011
Citation InformationS.R. Sethu Narayanan. "D Site of Albumin Promoter Binding Protein (DBP) May Promote Hematopoiesis" Biology and Medicine Vol. 3 Iss. 3 (2011)
Available at: http://works.bepress.com/srsethunarayanan/2/