Table 2. Putative progenitor markers.

NK, natural killer cell; ERK1/2, extracellular signal–regulated kinase 1/2; DNAM-1, DNAX Accessory Molecule 1; BRCA1, Breast Cancer 1, Early Onset; MHC, major histocompatibility complex; MK, megakaryocyte; HSC, haematopoietic stem cell; CXCR4, C-X-C Motif Chemokine Receptor 4; MICB, MHC Class I Polypeptide-Related Sequence B; PVR, Poliovirus Receptor; ANXA1, Annexin A1; RHAMM, Receptor For Hyaluronan-Mediated Motility; VEGFR1, Vascular Endothelial Growth Factor Receptor 1.

Marker	Function
MICB	MHC class I–related protein (54) which binds to the NKG2D receptor on NKs or γδ T cells (55).
	Assembly is β2 microglobulin independent.
	Stress-associated marker (54), which can be secreted (56).
	Expression regulated by acetylation (57) of its heat shock element–containing promoter (54).
	Down-regulated in many cancers to evade the immune system (58).
PVR (CD155)	Transmembrane receptor that can also be secreted as a soluble factor (59). Involved in cell adhesion (60) via its role as a vitronectin receptor (61) as well as in the transendothelial migration of leukocytes (62).
	Binds to an NK receptor, DNAM-1 (63), which is expressed on platelets and is involved in MK and platelet adhesion to endothelial cells (64).
ANXA1	Induces HSC differentiation to granulocytes and macrophages (65).
CD168 (RHAMM)	Hyaluronic acid receptor (66) and also binds to mitotic spindle (67).
	Associates with BRCA1 and activates ERK1/2 downstream of CD44 (67).
	Expressed in actively cycling pre-HSCs from fetal liver (68).
	Cell cycle dependent and peaks in G2-M phase (69).
CD51	Expressed in fetal liver cells, which promote MK differentiation from HSCs (70).
	CD51+ perivascular cells promote platelet generation from MKs (71).
	CD41 expression replaces CD51 expression as HSCs differentiate (72).
VEGFR1	VEGF receptor expressed on monocytes, macrophages, HSCs, vascular smooth muscle cells, and leukemic cells (73).
	Increased expression in intermediates between HSCs and MKs (74).
	Activation leads to CXCR4 redistribution on MKs, movement toward vascular niche, and platelet production (75).