RHD*01W.3 - RHD*weak D type 3
(ISBT table: Weak D and Del v5.0)

This entry is an RHD allele.

RHD(S3C), RHD*8C>G, RHD*8G, RHD*8G (weak D type 3), weak D type 3,
Download VCF file

Molecular data

Nucleotides: 8C>G;

Amino acids: S3C;

Hybrid allele encompassing at least one RHCE exon: no

Comments on the molecular basis:

  • intronic sequence established by long range PCR and NGS
  • no other mutation in RHD, RHCE and RHAG by sequencing
  • no additional mutation within RHD exons 1-10 and flanking intron regions

Extracellular position of one or more amino acid substitutions:

  • none of the mutations are predicted to affect an extracellular amino acid
  • membrane localization: IC

Splicing:

Unconventional prediction methods:

Phenotype

Main D phenotype: weak D (last update: Dec. 28, 2020)
Reports by D phenotype
Other RH phenotypes: RH:-2, -3, -4,
  • RH:-2 inferred from the reported RHCE phenotypes of the carriers
  • RH:-3 inferred from the reported RHCE phenotypes of the carriers
  • RH:-4 inferred from the reported RHCE phenotypes of the carriers
Serology with monoclonal anti-D
  • 0 monoclonal IgG anti-D non-reactive with variant, out of 60 monoclonal IgG anti 22 IgM anti-D tested
  • 0 monoclonal IgG anti-D non-reactive with variant, out of 22 monoclonal IgG tested (Table 2)
  • only a few anti-D tested
  • tested with Diagast Dscreen kit
  • tested with Diagast Dscreen kit and ID-Partial Rh D-Typing Set, results not detailed
  • results are not detailed per Ab or per variant
  • 0 monoclonal IgG anti-D non-reactive with variant, 1 sample tested with 2 panels of monoclonal anti-D (17 IgG, 4 IgM) (Table 3)
  • weak reactions (+ to ++), with a panel of 10 monoclonal anti-D
Antigen Density (Ag/RBC)
  • range: 1333 - 2650, median: 1948 Ag/RBC, with 6 IgG anti-D; 11 RH:1,2,-3,4,5 samples tested (table 3)
  • Ag/RBC, epitope density profile with 59 monoclonal IgG anti-D (Figure 1)
  • 1932 Ag/RBC, derived from the results obtained with 59 of the 59 monoclonal IgG anti-D tested
  • range: 1503 - 1920, median: 1712 Ag/RBC, 2 samples, median (range) with 11 IgG anti-D
  • 1876 Ag/RBC
  • mean: 2477 Ag/RBC, 8 samples
  • range: 554 - 1398, median 976 Ag/RBC, 2 R1r samples
  • 1117 Ag/RBC, with 4 monoclonal anti-D; 1 RH:1,2,-3,4,5 sample (S2)
  • median: 1505 Ag/RBC, 6 samples from Tyrol (Austria)
  • median: 1732 Ag/RBC, 13 samples from Northern Germany
  • median: 1768 Ag/RBC, 10 samples from Southwestern Germany
  • mean: 2368 Ag/RBC, 9 samples; Ag density estimated from a measure with a single monoclonal IgG anti-D, compared to a RH:1,2,3,4,5 control sample with an antigen density assumed to be about 27.500 Ag/RBC
More phenotype data
Rhesus Similarity Index

  • 0.77 (derived from the results obtained with 59 of the 59 monoclonal IgG anti-D tested)
  • 0.81

Haplotype

Main CcEe phenotype association: Ce is the most frequent association (last update: Jan. 8, 2021)
Number of samples reported by haplotype
ce Ce cE CE
ce 1 128 1 0
Ce 86 0 0
cE 0 0
CE 0
Reports by CcEe phenotype
  • with ce
    • 1 sample (haplotype given, not complete phenotype) (Table S2)
  • with Ccee
    • 1 sample (1 sample? used as control)
    2 samples (2 samples used as controls, may have been included in other studies)
    5 samples
    7 samples
    24 samples
    6 samples
    68 samples
    3 samples
    12 samples
  • with Ce
    • 1 sample (heterozygous with RHef00313) (sample heterozygous with RHef00238)
    7 samples (haplotype given, not complete phenotype)
    2 samples (haplotype given, not phenotype)
    5 samples (haplotype given, not complete phenotype)
    59 samples (haplotype given, not complete phenotype)
    9 samples (haplotype given, not complete phenotype)
    3 samples (haplotype given, not complete phenotype)
    0 samples (haplotype given, not complete phenotype; presented as a general association) (no sample count, listed as a general association)
  • with ccEe
    • 1 sample (typo between RHef00288 and RHef00301?)
Main allele association: RHCE*02
Reports by allele association
  • RHCE*01 or RHCE*02
    • 1 sample
  • RHCE*02 or RHCE*01
    • 1 sample

Alloimmunization

Antibodies in carriers
Antibody specificity: D (RH1)
Summary: not considered at risk for allo-anti-D despite exceptional anti-D descriptions (last update: Dec. 28, 2020)
Detailed information
    Denomme GA et al. Transfusion (2005)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-): 0
  • Number listed as allo-:
  • Number listed as auto-:
  • Number of carriers of the allele assessed:
  • DAT:
  • Autologuous control:
  • Elution:
  • Autoadsorption:
  • Titer:
  • Was anti-LW excluded?:
  • Other antibodies detected:
  • Cross matches (with Ab and RBCs from different partial types):
  • Transfusion history:
  • Pregnancy history:
  • Anti-D Ig history:
  • Context:
  • Hemolytic consequences:
  • Comment: lists exposures to standard D antigen and patient blood management for several carriers
    Pham BN et al. Immunohematology (2013)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-): 0
  • Number listed as allo-:
  • Number listed as auto-:
  • Number of carriers of the allele assessed: 6
  • DAT: NA
  • Autologuous control: NA
  • Elution: NA
  • Autoadsorption: NA
  • Titer: NA
  • Was anti-LW excluded?: NA
  • Other antibodies detected: NA
  • Cross matches (with Ab and RBCs from different partial types): NA
  • Transfusion history: ND
  • Pregnancy history:
  • Anti-D Ig history: ND
  • Context: NA
  • Hemolytic consequences: NA
  • Comment:
    L Castilho et al. Vox Sanguinis (2019)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-):
  • Number listed as allo-: 1
  • Number listed as auto-:
  • Number of carriers of the allele assessed:
  • DAT: negative
  • Autologuous control:
  • Elution:
  • Autoadsorption: "auto-anti-D (was) ruled out"
  • Titer:
  • Was anti-LW excluded?: "anti-LW (was) ruled out"
  • Other antibodies detected: ND
  • Cross matches (with Ab and RBCs from different partial types): ND
  • Transfusion history: D+ units transfused, anti-D was detected 3 weeks after the last transfusion
  • Pregnancy history:
  • Anti-D Ig history: ND, probably none
  • Context: 12 year-old Bzrazilian SCD patient
  • Hemolytic consequences: Positive monocyte monolayer assay >5% suggests that the anti-D is clinically significant
  • Comment: no other mutation by sequencing of RHD, RHCE and RHAG
    Daniels G et al. Br J Haematol (2013) (review)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-): no new case detailed
  • Number listed as allo-:
  • Number listed as auto-: ND
  • Number of carriers of the allele assessed: ND
  • DAT: ND
  • Autologuous control: ND
  • Elution: ND
  • Autoadsorption: ND
  • Titer: ND
  • Was anti-LW excluded?: ND
  • Other antibodies detected: ND
  • Cross matches (with Ab and RBCs from different partial types): ND
  • Transfusion history: ND
  • Pregnancy history:
  • Anti-D Ig history: ND
  • Context: ND
  • Hemolytic consequences: ND
  • Comment: "individuals with RHef00238, RHef00288, and RHef00301 make alloanti-D only extremely rarely, if at all"
    Flegel WA et al. Curr Opin Hematol (2006)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-): no new case detailed
  • Number listed as allo-:
  • Number listed as auto-:
  • Number of carriers of the allele assessed:
  • DAT: NA
  • Autologuous control: NA
  • Elution: NA
  • Autoadsorption: NA
  • Titer: NA
  • Was anti-LW excluded?: NA
  • Other antibodies detected: NA
  • Cross matches (with Ab and RBCs from different partial types): NA
  • Transfusion history: NA
  • Pregnancy history:
  • Anti-D Ig history: NA
  • Context: NA
  • Hemolytic consequences: NA
  • Comment: "reports of the Rhesus Immunization Registery as of June 2006"
    C Nixon et al. Transfusion (2016)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-):
  • Number listed as allo-: 1
  • Number listed as auto-:
  • Number of carriers of the allele assessed:
  • DAT: negative
  • Autologuous control: ND
  • Elution: ND
  • Autoadsorption: ND
  • Titer: weakly reactive anti-D, detected with ficin-treated test-RBCs
  • Was anti-LW excluded?: ND
  • Other antibodies detected: ND
  • Cross matches (with Ab and RBCs from different partial types): ND
  • Transfusion history: yes, number and phenotype ND
  • Pregnancy history:
  • Anti-D Ig history: ND, probably none
  • Context: 84 year-old female with digestive bleeding
  • Hemolytic consequences: ND
  • Comment: no additional mutation within RHD exons 1-10 and flanking intron regions; hemizygous
Antibodies in D negative recipients

Alloimmunization in recipients: expected to be possible, see phenotype data

Reports

Summary: common allele, mainly in individuals of Central European (Caucasian) descent or compatible with such descent (last update: Dec. 28, 2020)
Detailed reports
  • 7/161 random donors with weak D phenotype; DVI samples were excluded by serologic testing in the German population (Southwestern Germany), White (Table 5)
  • 3/99 donors with weak D phenotype Australian
  • 65/146 (+ 2 heterozygous with RHef00626 and RHef00238) donors with weak D phenotype White, in the Austrian (Tyrol) population
  • 45/270 donors with weak D phenotype White, in the German (Northern Germany) population
  • 3/168 among 168 samples referred for weak D phenotype and/or allo anti-D in D positive individuals, 137 were characterized in the study (70 by serology, 67 by molecular analysis, 31 could not be typed because serologic typing was inconclusive and molecular typing could not be performed) in the French population (Caucasian)
  • 0/250 250 donors with RH:1,2,–3,4,5 phenotype among 1000 donors screened for RHD molecular variants by several PCR-SSP and exon 5 sequencing of all samples (500 R0r, 250 R1R, 250 R2r) in the German population (southwestern Germany)
  • 1/55 55 discrepant or weak D phenotypes among 33864 multiethnic patients (of African, Asian, Indoasian and European extraction) in the Canadian (Toronto) population
  • 14/99 individuals with weak D phenotype Portuguese
  • 11/289 289 samples with ambiguous D phenotype (333 consecutive samples with ambiguous D phenotype studied but 44 were hybrid alleles, excluded from the study) in the French (Western France) population
  • 19/201 (16 donors and 3 patients) among 201 samples with weak D expression, unclear D phenotype, or request for RHD typing within 44,743 donors and 8,604 patients tested in the Austrian population, Upper Austria
  • 5/55162 among samples C or E positive and positive for "Du test" (55162 samples were typed; 314 were ddCcee, with 63 positive for "Du test" and 154 were ddccEe, with 30 positive for "Du test"; of the 93 "Du positive", 60 underwent molecular analysis) in the French population
  • 9/101 donors with weak D phenotype Danish
  • 4/141 donors and patients with ambiguous D phenotype in French population
  • 2/26 donors with "weak D or questionnable D status" explored by NGS to compare with Sanger sequencing in the Austrian population, Upper Austria
  • 77/167 discrepant D testing results (donors?) Croatian
  • 4/43 (prevalence among weak D) or 4/5707 (phenotypic prevalence in population) 43 patients with weak D phenotype were genotyped in a cohort of 5707 patients from a private laboratory Argentinean
  • 4/45 (prevalence among weak D phenotype) or 4/12672 (phenotypic prevalence in population) 45 patients wih weak D phenotype were genotyped in a cohort of 12672 patients from a public hospital Argentinean
  • 3/16 among 2007 unrelated donors, 16 had weak D phenotype in the Brazilian population (Sao Paulo, mainly racially mixed non-white skin color individuals)
  • 3/163 selected variants included for the development of a genotyping assay mainly in the Dutch population (samples may have been included in other studies)
  • 35/430 (1 heterozygous) among samples with ambigous D phenotype in the French population (Table S1)
  • 1/31200 consecutive donors with D negative phenotype tested for presence of RHD intron 4, exon 7 and/or exon 10 in the Polish population
  • 6/748 among 748 individuals with D anomaly (weak or discrepant D phenotype or anti-D in individuals with D positive phenotype), 459 had D variants "that could be named weak D" (including alleles RHef00313, RHef00317 and RHef00318, as well as RHef00197 and RHef00283), 138 had partial D, 65 had no variant, 86 were not persued further (two variant alleles or incomplete or pending analysis) in the French population
  • 59/360 donors with atypical D phenotype (discrepancies or reactivity weaker than 3+) Brazilian
  • 6/58 (one heterozygous with RHef00238) within a donor population of 38836, 4272 initially typed D negative and 58 of these were found to be weak D with different reagents Albanian
  • 0/2000 among 2000 random donors (1777 typed D positive), all donors were genotyped for 8G in the Tunisian population (study may overlap with 24014941)
  • 13/627 weak D typing (95% from patients, 5% from donors; 21,2% were identified as RHef00442 or RHef00446 by authors, "mostly (…) inconclusive serology consequent to recent transfusion") in the Belgian (Flanders) population
  • 0/45 among 763408 donors, after ruling out partial D phenotypes by using 5 monoclonal anti-D, 75 were considered weak D phenotype and 45 were genotyped Japanese (some samples in common with 27183894)
  • 0/226 226 donors considered weak D phenotype, after ruling out partial D phenotypes by using 5 monoclonal anti-D Japanese (1 sample in common with 26340140)
  • 5/400 among random blood and bone marrow donors genotyped for RHD in the Brazilian population (Parana state, Southern Brazil)
  • 49/351 (+ 5 heterozygous: 2 with RHef00301 and RHef00333, 3 for RHef00238 and RHef00301) out of 351 prenatal patients with discrepant D phenotyping results (population tested 608486 patients) Canadian
  • 8/100 donors with weak D phenotype Australian
  • 2/104 (prevalence among weak D) or 2/21353 (phenotypic prevalence in population) 104 with weak D phenotype were genotyped in a cohort of 21353 pregnant women admixed Brazilian
  • 32/32 samples with RHD c.8C>G mutation (typical of RHef00301), subtypes excluded in the French population (Western France)
  • 0/223 donors with D negative phenotype initially, found to have D antigen expression (67 of the 223 samples of the cohort) or samples referred with discrepant or weak D typing, or discrepancies with previous typings, or anti-D in D positive individuals (156 of the 223 samples of the cohort) in the Indian population
  • 1/26 26 samples with weak D phenotype, analyzed by NGS Caucasian, in the UK (Bristol) population
  • 1/23 donors with weak D phenotype (among 4458 random donors, 4028 types D positive including 19 weak D phenotype, 420 typed D negative including 4 showed to be weak D by further serological testing; in total 23 donors had weak D phenotype) in the Maroccan population
  • 50/85 donors with weak D phenotype Bosnia Herzegovinian
  • 19/61 donors with weak D phenotype Serbian
  • 1/92 donors with apparent D negative phenotype, with C and/or E Bosnia Herzegovinian
  • 8/64 among 175000 donors, 64 had weak D phenotype and underwent molecular identification in the Greek population
  • 26/231 231 donors with weak D phenotype in the Argentinean population (Northwestern Argentina)
  • 40/273 donors with weak D phenotype in the Brazilian population
  • 1/57 samples with ambiguous D phenotype among about 15,800 samples tested (22/5,800 donors and 35/10,000 patients had ambiguous D phenotype) presumed Caucasian, in the Danish population (91,4% Caucasian)
  • 21/353 samples referred for discrepant or weak D typing mainly Whites, in the USA population
  • 1/185 RH:–1,–4 or RH:–1,–5 recipients reported by a French lab
  • 1 sample SCD patient Brazilian
  • 6/94 donors with discreapancies in D typing Southeast Brazilian
  • 1/16,253 samples of pregnant women with D negative of weak D (2+ or less), screened for fetal RHD in the Finnish population
  • 1 hemizygote among 278 samples selected for the development of nonspecific quantitative next-generation sequencing. (non-random samples, may have been reported in other studies)
Allele or phenotype frequency
  • 1/3759 estimated allele frequency in the German population (Southwestern Germany), White
  • less than 1/371 estimated allele frequency by testing random donor samples for D antigen density, those in the lower range of antigen density were genotyped German
  • 0.000219 estimated prevalence in the German population
  • 1/31200(CI: 1/6577 - 1/608187) estimated allele frequency in individuals with D negative phenotype in the Polish population
  • 1/12945 (CI: 1/35336 - 1/5948) estimated allele frequency Albanian
  • 0.052 allele frequency in 58 patients with weak D phenotype Brazilian (mixed origin, mainly between African and European descent)
  • 0.0047 allele frequency in 106 donors with weak D phenotype Brazilian (mixed origin, mainly between African and European descent)
  • 0.006 calculated in 16,253 samples of pregnant women with D negative of weak D (2+ or less), screened for fetal RHD in the Finnish population

2D diagram

generated using Protter extraintra Met1 Met1 Ser2 Ser2 Ser3 Ser3 Lys4 Lys4 Tyr5 Tyr5 Pro6 Pro6 Arg7 Arg7 Ser8 Ser8 Val9 Val9 Arg10 Arg10 10Arg11 Arg11 Cys12 Cys12 Leu13 Leu13 Pro14 Pro14 Leu15 Leu15 Trp16 Trp16 Ala17 Ala17 Leu18 Leu18 Thr19 Thr19 Leu20 Leu20 20Glu21 Glu21 Ala22 Ala22 Ala23 Ala23 Leu24 Leu24 Ile25 Ile25 Leu26 Leu26 Leu27 Leu27 Phe28 Phe28 Tyr29 Tyr29 Phe30 Phe30 30Phe31 Phe31 Thr32 Thr32 His33 His33 Tyr34 Tyr34 Asp35 Asp35 Ala36 Ala36 Ser37 Ser37 Leu38 Leu38 Glu39 Glu39 Asp40 Asp40 40Gln41 Gln41 Lys42 Lys42 Gly43 Gly43 Leu44 Leu44 Val45 Val45 Ala46 Ala46 Ser47 Ser47 Tyr48 Tyr48 Gln49 Gln49 Val50 Val50 50Gly51 Gly51 Gln52 Gln52 Asp53 Asp53 Leu54 Leu54 Thr55 Thr55 Val56 Val56 Met57 Met57 Ala58 Ala58 Ala59 Ala59 Ile60 Ile60 60Gly61 Gly61 Leu62 Leu62 Gly63 Gly63 Phe64 Phe64 Leu65 Leu65 Thr66 Thr66 Ser67 Ser67 Ser68 Ser68 Phe69 Phe69 Arg70 Arg70 70Arg71 Arg71 His72 His72 Ser73 Ser73 Trp74 Trp74 Ser75 Ser75 Ser76 Ser76 Val77 Val77 Ala78 Ala78 Phe79 Phe79 Asn80 Asn80 80Leu81 Leu81 Phe82 Phe82 Met83 Met83 Leu84 Leu84 Ala85 Ala85 Leu86 Leu86 Gly87 Gly87 Val88 Val88 Gln89 Gln89 Trp90 Trp90 90Ala91 Ala91 Ile92 Ile92 Leu93 Leu93 Leu94 Leu94 Asp95 Asp95 Gly96 Gly96 Phe97 Phe97 Leu98 Leu98 Ser99 Ser99 Gln100 Gln100 100Phe101 Phe101 Pro102 Pro102 Ser103 Ser103 Gly104 Gly104 Lys105 Lys105 Val106 Val106 Val107 Val107 Ile108 Ile108 Thr109 Thr109 Leu110 Leu110 110Phe111 Phe111 Ser112 Ser112 Ile113 Ile113 Arg114 Arg114 Leu115 Leu115 Ala116 Ala116 Thr117 Thr117 Met118 Met118 Ser119 Ser119 Ala120 Ala120 120Leu121 Leu121 Ser122 Ser122 Val123 Val123 Leu124 Leu124 Ile125 Ile125 Ser126 Ser126 Val127 Val127 Asp128 Asp128 Ala129 Ala129 Val130 Val130 130Leu131 Leu131 Gly132 Gly132 Lys133 Lys133 Val134 Val134 Asn135 Asn135 Leu136 Leu136 Ala137 Ala137 Gln138 Gln138 Leu139 Leu139 Val140 Val140 140Val141 Val141 Met142 Met142 Val143 Val143 Leu144 Leu144 Val145 Val145 Glu146 Glu146 Val147 Val147 Thr148 Thr148 Ala149 Ala149 Leu150 Leu150 150Gly151 Gly151 Asn152 Asn152 Leu153 Leu153 Arg154 Arg154 Met155 Met155 Val156 Val156 Ile157 Ile157 Ser158 Ser158 Asn159 Asn159 Ile160 Ile160 160Phe161 Phe161 Asn162 Asn162 Thr163 Thr163 Asp164 Asp164 Tyr165 Tyr165 His166 His166 Met167 Met167 Asn168 Asn168 Met169 Met169 Met170 Met170 170His171 His171 Ile172 Ile172 Tyr173 Tyr173 Val174 Val174 Phe175 Phe175 Ala176 Ala176 Ala177 Ala177 Tyr178 Tyr178 Phe179 Phe179 Gly180 Gly180 180Leu181 Leu181 Ser182 Ser182 Val183 Val183 Ala184 Ala184 Trp185 Trp185 Cys186 Cys186 Leu187 Leu187 Pro188 Pro188 Lys189 Lys189 Pro190 Pro190 190Leu191 Leu191 Pro192 Pro192 Glu193 Glu193 Gly194 Gly194 Thr195 Thr195 Glu196 Glu196 Asp197 Asp197 Lys198 Lys198 Asp199 Asp199 Gln200 Gln200 200Thr201 Thr201 Ala202 Ala202 Thr203 Thr203 Ile204 Ile204 Pro205 Pro205 Ser206 Ser206 Leu207 Leu207 Ser208 Ser208 Ala209 Ala209 Met210 Met210 210Leu211 Leu211 Gly212 Gly212 Ala213 Ala213 Leu214 Leu214 Phe215 Phe215 Leu216 Leu216 Trp217 Trp217 Met218 Met218 Phe219 Phe219 Trp220 Trp220 220Pro221 Pro221 Ser222 Ser222 Phe223 Phe223 Asn224 Asn224 Ser225 Ser225 Ala226 Ala226 Leu227 Leu227 Leu228 Leu228 Arg229 Arg229 Ser230 Ser230 230Pro231 Pro231 Ile232 Ile232 Glu233 Glu233 Arg234 Arg234 Lys235 Lys235 Asn236 Asn236 Ala237 Ala237 Val238 Val238 Phe239 Phe239 Asn240 Asn240 240Thr241 Thr241 Tyr242 Tyr242 Tyr243 Tyr243 Ala244 Ala244 Val245 Val245 Ala246 Ala246 Val247 Val247 Ser248 Ser248 Val249 Val249 Val250 Val250 250Thr251 Thr251 Ala252 Ala252 Ile253 Ile253 Ser254 Ser254 Gly255 Gly255 Ser256 Ser256 Ser257 Ser257 Leu258 Leu258 Ala259 Ala259 His260 His260 260Pro261 Pro261 Gln262 Gln262 Gly263 Gly263 Lys264 Lys264 Ile265 Ile265 Ser266 Ser266 Lys267 Lys267 Thr268 Thr268 Tyr269 Tyr269 Val270 Val270 270His271 His271 Ser272 Ser272 Ala273 Ala273 Val274 Val274 Leu275 Leu275 Ala276 Ala276 Gly277 Gly277 Gly278 Gly278 Val279 Val279 Ala280 Ala280 280Val281 Val281 Gly282 Gly282 Thr283 Thr283 Ser284 Ser284 Cys285 Cys285 His286 His286 Leu287 Leu287 Ile288 Ile288 Pro289 Pro289 Ser290 Ser290 290Pro291 Pro291 Trp292 Trp292 Leu293 Leu293 Ala294 Ala294 Met295 Met295 Val296 Val296 Leu297 Leu297 Gly298 Gly298 Leu299 Leu299 Val300 Val300 300Ala301 Ala301 Gly302 Gly302 Leu303 Leu303 Ile304 Ile304 Ser305 Ser305 Val306 Val306 Gly307 Gly307 Gly308 Gly308 Ala309 Ala309 Lys310 Lys310 310Tyr311 Tyr311 Leu312 Leu312 Pro313 Pro313 Gly314 Gly314 Cys315 Cys315 Cys316 Cys316 Asn317 Asn317 Arg318 Arg318 Val319 Val319 Leu320 Leu320 320Gly321 Gly321 Ile322 Ile322 Pro323 Pro323 His324 His324 Ser325 Ser325 Ser326 Ser326 Ile327 Ile327 Met328 Met328 Gly329 Gly329 Tyr330 Tyr330 330Asn331 Asn331 Phe332 Phe332 Ser333 Ser333 Leu334 Leu334 Leu335 Leu335 Gly336 Gly336 Leu337 Leu337 Leu338 Leu338 Gly339 Gly339 Glu340 Glu340 340Ile341 Ile341 Ile342 Ile342 Tyr343 Tyr343 Ile344 Ile344 Val345 Val345 Leu346 Leu346 Leu347 Leu347 Val348 Val348 Leu349 Leu349 Asp350 Asp350 350Thr351 Thr351 Val352 Val352 Gly353 Gly353 Ala354 Ala354 Gly355 Gly355 Asn356 Asn356 Gly357 Gly357 Met358 Met358 Ile359 Ile359 Gly360 Gly360 360Phe361 Phe361 Gln362 Gln362 Val363 Val363 Leu364 Leu364 Leu365 Leu365 Ser366 Ser366 Ile367 Ile367 Gly368 Gly368 Glu369 Glu369 Leu370 Leu370 370Ser371 Ser371 Leu372 Leu372 Ala373 Ala373 Ile374 Ile374 Val375 Val375 Ile376 Ile376 Ala377 Ala377 Leu378 Leu378 Met379 Met379 Ser380 Ser380 380Gly381 Gly381 Leu382 Leu382 Leu383 Leu383 Thr384 Thr384 Gly385 Gly385 Leu386 Leu386 Leu387 Leu387 Leu388 Leu388 Asn389 Asn389 Leu390 Leu390 390Lys391 Lys391 Ile392 Ile392 Trp393 Trp393 Lys394 Lys394 Ala395 Ala395 Pro396 Pro396 His397 His397 Glu398 Glu398 Ala399 Ala399 Lys400 Lys400 400Tyr401 Tyr401 Phe402 Phe402 Asp403 Asp403 Asp404 Asp404 Gln405 Gln405 Val406 Val406 Phe407 Phe407 Trp408 Trp408 Lys409 Lys409 Phe410 Phe410 410Pro411 Pro411 His412 His412 Leu413 Leu413 Ala414 Ala414 Val415 Val415 Gly416 Gly416 Phe417 Phe417 417 MSSKYPRSVRRCLPLWALTLEAALILLFYFFTHYDASLEDQKGLVASYQVGQDLTVMAAIGLGFLTSSFRRHSWSSVAFNLFMLALGVQWAILLDGFLSQFPSGKVVITLFSIRLATMSALSVLISVDAVLGKVNLAQLVVMVLVEVTALGNLRMVISNIFNTDYHMNMMHIYVFAAYFGLSVAWCLPKPLPEGTEDKDQTATIPSLSAMLGALFLWMFWPSFNSALLRSPIERKNAVFNTYYAVAVSVVTAISGSSLAHPQGKISKTYVHSAVLAGGVAVGTSCHLIPSPWLAMVLGLVAGLISVGGAKYLPGCCNRVLGIPHSSIMGYNFSLLGLLGEIIYIVLLVLDTVGAGNGMIGFQVLLSIGELSLAIVIALMSGLLTGLLLNLKIWKAPHEAKYFDDQVFWKFPHLAVGF MSSKYPRSVRRCLPLWALTLEAALILLFYFFTHYDASLEDQKGLVASYQVGQDLTVMAAIGLGFLTSSFRRHSWSSVAFNLFMLALGVQWAILLDGFLSQFPSGKVVITLFSIRLATMSALSVLISVDAVLGKVNLAQLVVMVLVEVTALGNLRMVISNIFNTDYHMNMMHIYVFAAYFGLSVAWCLPKPLPEGTEDKDQTATIPSLSAMLGALFLWMFWPSFNSALLRSPIERKNAVFNTYYAVAVSVVTAISGSSLAHPQGKISKTYVHSAVLAGGVAVGTSCHLIPSPWLAMVLGLVAGLISVGGAKYLPGCCNRVLGIPHSSIMGYNFSLLGLLGEIIYIVLLVLDTVGAGNGMIGFQVLLSIGELSLAIVIALMSGLLTGLLLNLKIWKAPHEAKYFDDQVFWKFPHLAVGF MSSKYPRSVRRCLPLWALTLEAALILLFYFFTHYDASLEDQKGLVASYQVGQDLTVMAAIGLGFLTSSFRRHSWSSVAFNLFMLALGVQWAILLDGFLSQFPSGKVVITLFSIRLATMSALSVLISVDAVLGKVNLAQLVVMVLVEVTALGNLRMVISNIFNTDYHMNMMHIYVFAAYFGLSVAWCLPKPLPEGTEDKDQTATIPSLSAMLGALFLWMFWPSFNSALLRSPIERKNAVFNTYYAVAVSVVTAISGSSLAHPQGKISKTYVHSAVLAGGVAVGTSCHLIPSPWLAMVLGLVAGLISVGGAKYLPGCCNRVLGIPHSSIMGYNFSLLGLLGEIIYIVLLVLDTVGAGNGMIGFQVLLSIGELSLAIVIALMSGLLTGLLLNLKIWKAPHEAKYFDDQVFWKFPHLAVGF MSSKYPRSVRRCLPLWALTLEAALILLFYFFTHYDASLEDQKGLVASYQVGQDLTVMAAIGLGFLTSSFRRHSWSSVAFNLFMLALGVQWAILLDGFLSQFPSGKVVITLFSIRLATMSALSVLISVDAVLGKVNLAQLVVMVLVEVTALGNLRMVISNIFNTDYHMNMMHIYVFAAYFGLSVAWCLPKPLPEGTEDKDQTATIPSLSAMLGALFLWMFWPSFNSALLRSPIERKNAVFNTYYAVAVSVVTAISGSSLAHPQGKISKTYVHSAVLAGGVAVGTSCHLIPSPWLAMVLGLVAGLISVGGAKYLPGCCNRVLGIPHSSIMGYNFSLLGLLGEIIYIVLLVLDTVGAGNGMIGFQVLLSIGELSLAIVIALMSGLLTGLLLNLKIWKAPHEAKYFDDQVFWKFPHLAVGF

Structure mapping

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Links

The Human RhesusBase
Genbank: KF680198
Erythrogene

References

  1. International Society of Blood Transfusion et al. International Society of Blood Transfusion (ISBT) allele table Online ressource, 1935. — Online ressource — [RHeference]
  2. Wagner FF et al. Molecular basis of weak D phenotypes. Blood, 1999. [Citation] [RHeference]
  3. Wagner FF et al. Weak D alleles express distinct phenotypes. Blood, 2000. [Citation] [RHeference]
  4. Cowley NM et al. RHD gene mutations and the weak D phenotype: an Australian blood donor study. Vox Sang, 2000. [Citation] [RHeference]
  5. Müller TH et al. PCR screening for common weak D types shows different distributions in three Central European populations. Transfusion, 2001. [Citation] [RHeference]
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Last update: Jan. 8, 2021