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. Author manuscript; available in PMC: 2017 Oct 30.
Published in final edited form as: ISBT Sci Ser. 2016 Jun 27;11(2):118–122. doi: 10.1111/voxs.12280

Table 1.

New antigens added to blood group systems

Blood group system Antigen number Alt. name Prevalence Molecular basis Protein change
MNS MNS47 SARA Low GYPA c.240G>T p.Arg80Ser
MNS MNS48 KIPP Low GYP(B-A-B) hybrid p.Ser51a
GPB(1-26)-GPwB(27-54)-GPA(55-57)-Bs(58-103)
LU LU23 LUIT High LU c.469G>A, 1289C>T p.Gly157Arg, p.Thr430Ile
LU LU24 LUGA High LU c.212G>A p.Arg71His
DO DO9 DOLC High ART4 c.566C>T p.Thr189Met
DO DO10 DODE High ART4 c.405C>A p.Asp135Glu
GLOB GLOB2 PX2 Highb B3GALNT1 c
Vel VEL1 Vel High SMIM1 c.64_80delGTCAGCCTAGGGGCTGT p.Ser22Glnfs*270
CD59 CD59.1 High CD59 c.146delA p.Asp49Valfs*31
AUG AUG1 High ENT1 c.589 + 1G>C p.Ser197fs
AUG AUG2 Ata High ENT1 c.1171G>A p.Glu391Lys
a

Distinguishes this protein from other known GP(B-A-B) hybrids.

b

Although PX2 is a product of β1,3GalNAc-T1 and therefore present on RBCs of common phenotype, it is absent from RBCs of P1k and P2k phenotypes whilst highly expressed on RBCs of the p phenotype.

c

Thus, all mutations causing the of P1k and P2k phenotypes also cause lack of PX2.