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JOHN MILTON HAGEN BLOOD GROUP SYSTEM JMH BLOOD GROUP SYSTEM

Phenotype-Gene Relationships

Location

Phenotype

[Blood group, John-Milton-Hagen system]

TEXT

A number sign (#) is used with this entry because the John Milton Hagen (JMH) blood group system is based, at least partly, on variation in the gene encoding semaphorin-7A (SEMA7A; 607961) on chromosome 15q22.2-q23.

Description

JMH blood group antigens are carried by SEMA7A, a membrane- associated protein that plays important roles in the nervous system and immune responses. Three different JMH phenotypes have been identified based on the presence or absence of the high-frequency JMH (or JMH1) antigen: JMH-weak, JMH-negative, and JMH-variant. The JMH-weak and -negative phenotypes can be either acquired or inherited and are characterized by a reduction or complete loss of JMH expression on red blood cells (RBCs), often with concomitant occurrence of JMH antibodies. Acquired JMH-weak or -negative phenotypes are typically found in elderly persons and can be transient. The JMH antibodies present in the acquired phenotypes have autoimmune characteristics and are clinically irrelevant. The inherited JMH-negative phenotype has been found in only 1 family. Mechanisms underlying the JMH-weak and -negative phenotypes have yet to be identified. Individuals with the JMH-variant phenotype are usually JMH-positive and have alloantibodies compatible with JMH-negative RBCs. The JMH-variant phenotype results from rare missense mutations in the SEMA7A gene (summary by Seltsam et al. (2007) and Richard et al.

JOHN MILTON HAGEN BLOOD GROUP SYSTEM JMH BLOOD GROUP SYSTEM Phenotype-Gene Relationships Location <a href=15q24.1 Phenotype [Blood group, John-Milton-Hagen system] TEXT A number sign (#) is used with this entry because the John Milton Hagen (JMH) blood group system is based, at least partly, on variation in the gene encoding semaphorin-7A (SEMA7A; 607961 ) on chromosome 15q22.2-q23. Description JMH blood group antigens are carried by SEMA7A, a membrane- associated protein that plays important roles in the nervous system and immune responses. Three different JMH phenotypes have been identified based on the presence or absence of the high-frequency JMH (or JMH1) antigen: JMH-weak, JMH-negative, and JMH-variant. The JMH-weak and -negative phenotypes can be either acquired or inherited and are characterized by a reduction or complete loss of JMH expression on red blood cells (RBCs), often with concomitant occurrence of JMH antibodies. Acquired JMH-weak or -negative phenotypes are typically found in elderly persons and can be transient. The JMH antibodies present in the acquired phenotypes have autoimmune characteristics and are clinically irrelevant. The inherited JMH-negative phenotype has been found in only 1 family. Mechanisms underlying the JMH-weak and -negative phenotypes have yet to be identified. Individuals with the JMH-variant phenotype are usually JMH-positive and have alloantibodies compatible with JMH-negative RBCs. The JMH-variant phenotype results from rare missense mutations in the SEMA7A gene (summary by Seltsam et al. (2007) and Richard et al. (2011) ) . Clinical Features Seltsam et al. (2007) identified 3 different RBC phenotypes with unusual " id="pdf-obj-0-34" src="pdf-obj-0-34.jpg">

Clinical Features

Seltsam et al. (2007) identified 3 different RBC phenotypes with unusual

JMH expression in 33 of 44 individuals with abnormal JMH blood groups and their family members. Eleven individuals had a JMH-variant phenotype lacking single JMH epitopes, 18 individuals had a JMH- negative phenotype, and 4 individuals had a JMH-weak phenotype. In most cases, these JMH phenotypes were associated with the presence of JMH or JMH-like antibodies in serum. The 11 remaining individuals, who were family members of individuals with JMH-variant or JMH-negative phenotypes, had normal JHM blood groups.

JMH expression in 33 of 44 individuals with abnormal JMH blood groups and their family members.Seltsam et al. (2007) identified 5 propositi with JMH-variant phenotype from Canada, Germany, Japan, Poland, and the U.S. The JMH-variant phenotype was also present in 6 of 14 family members of the propositi. Determination of variant JMH status was based on variably positive or negative reactions of RBCs with anti-JMH serum samples. JMH-like antibodies were only present in the serum of the propositi, which reacted positive with all but JMH-negative RBCs, the propositus's own RBCs, and RBCs of compatible JMH-positive sibs. JMH-Negative Phenotype Seltsam et al. (2007) identified 18 individuals with JMH-negative phenotype from Canada, Germany, Israel, Sweden, Switzerland, and the U.S. The ages of the RBH-negative individuals, as far as known, ranged from 54 to 82 years. The JMH-negative phenotype was identified by negative reaction of the individuals' RBCs with JMH antisera from immunized patients. In addition, no JMH antigen was detected on the surface of JMH-negative RBCs by flow cytometric and immunoblot analyses. JMH antibodies were detected in 14 of the JMH-negative individuals. Four JMH-negative individuals belonged to an apparently healthy family in which the JMH-negative phenotype had been detected in 3 generations. The other JMH-negative individuals were unrelated and information about inheritance was not available. However, in 2 of these individuals, who were apparently healthy, JMH-negative status had remained stable over decades, excluding the transient JMH-negative " id="pdf-obj-1-4" src="pdf-obj-1-4.jpg">

JMH-Variant Phenotype

Seltsam et al. (2007) identified 5 propositi with JMH-variant phenotype from Canada, Germany, Japan, Poland, and the U.S. The JMH-variant phenotype was also present in 6 of 14 family members of the propositi. Determination of variant JMH status was based on variably positive or negative reactions of RBCs with anti-JMH serum samples. JMH-like antibodies were only present in the serum of the propositi, which reacted positive with all but JMH-negative RBCs, the propositus's own RBCs, and RBCs of compatible JMH-positive sibs.

JMH expression in 33 of 44 individuals with abnormal JMH blood groups and their family members.Seltsam et al. (2007) identified 5 propositi with JMH-variant phenotype from Canada, Germany, Japan, Poland, and the U.S. The JMH-variant phenotype was also present in 6 of 14 family members of the propositi. Determination of variant JMH status was based on variably positive or negative reactions of RBCs with anti-JMH serum samples. JMH-like antibodies were only present in the serum of the propositi, which reacted positive with all but JMH-negative RBCs, the propositus's own RBCs, and RBCs of compatible JMH-positive sibs. JMH-Negative Phenotype Seltsam et al. (2007) identified 18 individuals with JMH-negative phenotype from Canada, Germany, Israel, Sweden, Switzerland, and the U.S. The ages of the RBH-negative individuals, as far as known, ranged from 54 to 82 years. The JMH-negative phenotype was identified by negative reaction of the individuals' RBCs with JMH antisera from immunized patients. In addition, no JMH antigen was detected on the surface of JMH-negative RBCs by flow cytometric and immunoblot analyses. JMH antibodies were detected in 14 of the JMH-negative individuals. Four JMH-negative individuals belonged to an apparently healthy family in which the JMH-negative phenotype had been detected in 3 generations. The other JMH-negative individuals were unrelated and information about inheritance was not available. However, in 2 of these individuals, who were apparently healthy, JMH-negative status had remained stable over decades, excluding the transient JMH-negative " id="pdf-obj-1-11" src="pdf-obj-1-11.jpg">

JMH-Negative Phenotype

Seltsam et al. (2007) identified 18 individuals with JMH-negative phenotype from Canada, Germany, Israel, Sweden, Switzerland, and the U.S. The ages of the RBH-negative individuals, as far as known, ranged from 54 to 82 years. The JMH-negative phenotype was identified by negative reaction of the individuals' RBCs with JMH antisera from immunized patients. In addition, no JMH antigen was detected on the surface of JMH-negative RBCs by flow cytometric and immunoblot analyses. JMH antibodies were detected in 14 of the JMH-negative individuals. Four JMH-negative individuals belonged to an apparently healthy family in which the JMH-negative phenotype had been detected in 3 generations. The other JMH-negative individuals were unrelated and information about inheritance was not available. However, in 2 of these individuals, who were apparently healthy, JMH-negative status had remained stable over decades, excluding the transient JMH-negative

phenotype. RT-PCR analysis of total mRNA from peripheral blood cells of JMH-negative individuals revealed normal expression of SEMA7A. Peripheral B lymphocytes from JMH-negative individuals could be stimulated to express normal levels of SEMA7A, and reticulocytes from JMH-negative individuals exhibited normal expression of SEMA7A. RBCs of JMH-negative individuals showed normal expression of other GPI- linked membrane proteins, excluding deficient biosynthesis of the GPI anchor as the basis for loss of SEMA7A on RBCs. Seltsam et al. (2007)concluded that the JMH-negative phenotype results from an autoimmune-related and/or RBC lineage-specific posttranscriptional or posttranslational mechanism.

phenotype. RT-PCR analysis of total mRNA from peripheral blood cells of JMH-negative individuals revealed normal expressionSeltsam et al. (2007) c oncluded that the JMH-negative phenotype results from an autoimmune-related and/or RBC lineage-specific posttranscriptional or posttranslational mechanism. JMH-Weak Phenotype Seltsam et al. (2007) identified 4 individuals with RBH-weak phenotype. RBCs from these individuals exhibited weak reactions with JMH antibodies, and JMH antibodies were present in serum samples. In 2 individuals, RBCs produced a weakly positive direct antiglobulin test. Three of the JMH-weak individuals were over 50 years of age, and the fourth was a 32-year-old pregnant woman. The pregnant woman displayed variable SEMA7A expression during pregnancy, and her baby was born without any symptoms of hemolytic disease of the fetus or newborn. Inheritance JMH-Variant Phenotype By family studies, including extended genomic sequencing, Seltsam et al. (2007) found that the JMH-variant phenotype was inherited in an autosomal recessive fashion in 5 families. JMH-Negative Phenotype Seltsam et al. (2007) noted that the JMH-negative phenotype, which is typically acquired rather than inherited, was present in 3 generations of an apparently healthy family. They confirmed this finding and concluded that autosomal dominant inheritance was likely. " id="pdf-obj-2-7" src="pdf-obj-2-7.jpg">

JMH-Weak Phenotype

Seltsam et al. (2007) identified 4 individuals with RBH-weak phenotype. RBCs from these individuals exhibited weak reactions with JMH antibodies, and JMH antibodies were present in serum samples. In 2 individuals, RBCs produced a weakly positive direct antiglobulin test. Three of the JMH-weak individuals were over 50 years of age, and the fourth was a 32-year-old pregnant woman. The pregnant woman displayed variable SEMA7A expression during pregnancy, and her baby was born without any symptoms of hemolytic disease of the fetus or newborn.

phenotype. RT-PCR analysis of total mRNA from peripheral blood cells of JMH-negative individuals revealed normal expressionSeltsam et al. (2007) c oncluded that the JMH-negative phenotype results from an autoimmune-related and/or RBC lineage-specific posttranscriptional or posttranslational mechanism. JMH-Weak Phenotype Seltsam et al. (2007) identified 4 individuals with RBH-weak phenotype. RBCs from these individuals exhibited weak reactions with JMH antibodies, and JMH antibodies were present in serum samples. In 2 individuals, RBCs produced a weakly positive direct antiglobulin test. Three of the JMH-weak individuals were over 50 years of age, and the fourth was a 32-year-old pregnant woman. The pregnant woman displayed variable SEMA7A expression during pregnancy, and her baby was born without any symptoms of hemolytic disease of the fetus or newborn. Inheritance JMH-Variant Phenotype By family studies, including extended genomic sequencing, Seltsam et al. (2007) found that the JMH-variant phenotype was inherited in an autosomal recessive fashion in 5 families. JMH-Negative Phenotype Seltsam et al. (2007) noted that the JMH-negative phenotype, which is typically acquired rather than inherited, was present in 3 generations of an apparently healthy family. They confirmed this finding and concluded that autosomal dominant inheritance was likely. " id="pdf-obj-2-14" src="pdf-obj-2-14.jpg">

Inheritance

JMH-Variant Phenotype

By family studies, including extended genomic sequencing, Seltsam et al. (2007) found that the JMH-variant phenotype was inherited in an autosomal recessive fashion in 5 families.

phenotype. RT-PCR analysis of total mRNA from peripheral blood cells of JMH-negative individuals revealed normal expressionSeltsam et al. (2007) c oncluded that the JMH-negative phenotype results from an autoimmune-related and/or RBC lineage-specific posttranscriptional or posttranslational mechanism. JMH-Weak Phenotype Seltsam et al. (2007) identified 4 individuals with RBH-weak phenotype. RBCs from these individuals exhibited weak reactions with JMH antibodies, and JMH antibodies were present in serum samples. In 2 individuals, RBCs produced a weakly positive direct antiglobulin test. Three of the JMH-weak individuals were over 50 years of age, and the fourth was a 32-year-old pregnant woman. The pregnant woman displayed variable SEMA7A expression during pregnancy, and her baby was born without any symptoms of hemolytic disease of the fetus or newborn. Inheritance JMH-Variant Phenotype By family studies, including extended genomic sequencing, Seltsam et al. (2007) found that the JMH-variant phenotype was inherited in an autosomal recessive fashion in 5 families. JMH-Negative Phenotype Seltsam et al. (2007) noted that the JMH-negative phenotype, which is typically acquired rather than inherited, was present in 3 generations of an apparently healthy family. They confirmed this finding and concluded that autosomal dominant inheritance was likely. " id="pdf-obj-2-24" src="pdf-obj-2-24.jpg">

JMH-Negative Phenotype

Seltsam et al. (2007) noted that the JMH-negative phenotype, which is typically acquired rather than inherited, was present in 3 generations of an apparently healthy family. They confirmed this finding and concluded that autosomal dominant inheritance was likely.

phenotype. RT-PCR analysis of total mRNA from peripheral blood cells of JMH-negative individuals revealed normal expressionSeltsam et al. (2007) c oncluded that the JMH-negative phenotype results from an autoimmune-related and/or RBC lineage-specific posttranscriptional or posttranslational mechanism. JMH-Weak Phenotype Seltsam et al. (2007) identified 4 individuals with RBH-weak phenotype. RBCs from these individuals exhibited weak reactions with JMH antibodies, and JMH antibodies were present in serum samples. In 2 individuals, RBCs produced a weakly positive direct antiglobulin test. Three of the JMH-weak individuals were over 50 years of age, and the fourth was a 32-year-old pregnant woman. The pregnant woman displayed variable SEMA7A expression during pregnancy, and her baby was born without any symptoms of hemolytic disease of the fetus or newborn. Inheritance JMH-Variant Phenotype By family studies, including extended genomic sequencing, Seltsam et al. (2007) found that the JMH-variant phenotype was inherited in an autosomal recessive fashion in 5 families. JMH-Negative Phenotype Seltsam et al. (2007) noted that the JMH-negative phenotype, which is typically acquired rather than inherited, was present in 3 generations of an apparently healthy family. They confirmed this finding and concluded that autosomal dominant inheritance was likely. " id="pdf-obj-2-31" src="pdf-obj-2-31.jpg">

Mapping

The SEMA7A gene, which encodes the protein carrying the JHM antigens, was mapped to chromosome 15q22.2-q23 by Lange et al. (1998).

Mapping The SEMA7A gene, which encodes the protein carrying the JHM antigens, was mapped to chromosomeLange et al. (1998) . Molecular Genetics JMH-Variant Phenotype In 5 unrelated individuals with JMH-variant phenotype from 5 different countries, Seltsam et al. (2007) identified 4 missense mutations in the SEMA7A gene ( 607961.0001 - 607961.0004 ) . These mutations were not detected in genomic DNA from 100 randomly selected individuals from Northern Germany. All 4 missense mutations occurred in the semaphorin domain of SEMA7A. Studies with JMH-variant RBCs and transfectants expressing membrane-anchored recombinant SEMA7A proteins showed that the variant SEMA7A proteins were of normal length and were expressed at levels equal to those of the wildtype protein. In inhibition studies with soluble recombinant wildtype and variant SEMA7A proteins, JMH-like alloantibodies of JMH-variant individuals did not react with the related recombinant variant SEMA7A protein, but they did react with the wildtype and unrelated variant SEMA7A proteins, indicating that expression of variant JMH antigen is based on the absence of certain SEMA7A epitopes. Serologic compatibility testing of JMH-variant blood samples confirmed these results. In 4 young Native American women with JMH-negative phenotype from a reservation northwest of Quebec City, Canada, Richard et al. (2011) i dentified a novel missense mutation in the SEMA7A gene ( 607961.0005 ) . At least 2 of the women were JHM-positive and their alloantibody was compatible with most JHM-negative RBCs tested; the other 2 women were not tested. Soluble forms of wildtype and R347L variant SEMA7A proteins were produced in vitro and demonstrated a specific alloantibody reaction with wildtype recombinant SEMA7A, but not with the R347L variant form. JMH-Negative Phenotype " id="pdf-obj-3-8" src="pdf-obj-3-8.jpg">

Molecular Genetics

JMH-Variant Phenotype

In 5 unrelated individuals with JMH-variant phenotype from 5 different countries, Seltsam et al. (2007) identified 4 missense mutations in the SEMA7A gene (607961.0001-607961.0004). These mutations were not detected in genomic DNA from 100 randomly selected individuals from Northern Germany. All 4 missense mutations occurred in the semaphorin domain of SEMA7A. Studies with JMH-variant RBCs and transfectants expressing membrane-anchored recombinant SEMA7A proteins showed that the variant SEMA7A proteins were of normal length and were expressed at levels equal to those of the wildtype protein. In inhibition studies with soluble recombinant wildtype and variant SEMA7A proteins, JMH-like alloantibodies of JMH-variant individuals did not react with the related recombinant variant SEMA7A protein, but they did react with the wildtype and unrelated variant SEMA7A proteins, indicating that expression of variant JMH antigen is based on the absence of certain SEMA7A epitopes. Serologic compatibility testing of JMH-variant blood samples confirmed these results.

Mapping The SEMA7A gene, which encodes the protein carrying the JHM antigens, was mapped to chromosomeLange et al. (1998) . Molecular Genetics JMH-Variant Phenotype In 5 unrelated individuals with JMH-variant phenotype from 5 different countries, Seltsam et al. (2007) identified 4 missense mutations in the SEMA7A gene ( 607961.0001 - 607961.0004 ) . These mutations were not detected in genomic DNA from 100 randomly selected individuals from Northern Germany. All 4 missense mutations occurred in the semaphorin domain of SEMA7A. Studies with JMH-variant RBCs and transfectants expressing membrane-anchored recombinant SEMA7A proteins showed that the variant SEMA7A proteins were of normal length and were expressed at levels equal to those of the wildtype protein. In inhibition studies with soluble recombinant wildtype and variant SEMA7A proteins, JMH-like alloantibodies of JMH-variant individuals did not react with the related recombinant variant SEMA7A protein, but they did react with the wildtype and unrelated variant SEMA7A proteins, indicating that expression of variant JMH antigen is based on the absence of certain SEMA7A epitopes. Serologic compatibility testing of JMH-variant blood samples confirmed these results. In 4 young Native American women with JMH-negative phenotype from a reservation northwest of Quebec City, Canada, Richard et al. (2011) i dentified a novel missense mutation in the SEMA7A gene ( 607961.0005 ) . At least 2 of the women were JHM-positive and their alloantibody was compatible with most JHM-negative RBCs tested; the other 2 women were not tested. Soluble forms of wildtype and R347L variant SEMA7A proteins were produced in vitro and demonstrated a specific alloantibody reaction with wildtype recombinant SEMA7A, but not with the R347L variant form. JMH-Negative Phenotype " id="pdf-obj-3-24" src="pdf-obj-3-24.jpg">

In 4 young Native American women with JMH-negative phenotype from a reservation northwest of Quebec City, Canada, Richard et al. (2011)identified a novel missense mutation in the SEMA7A gene (607961.0005). At least 2 of the women were JHM-positive and their alloantibody was compatible with most JHM-negative RBCs tested; the other 2 women were not tested. Soluble forms of wildtype and R347L variant SEMA7A proteins were produced in vitro and demonstrated a specific alloantibody reaction with wildtype recombinant SEMA7A, but not with the R347L variant form.

Mapping The SEMA7A gene, which encodes the protein carrying the JHM antigens, was mapped to chromosomeLange et al. (1998) . Molecular Genetics JMH-Variant Phenotype In 5 unrelated individuals with JMH-variant phenotype from 5 different countries, Seltsam et al. (2007) identified 4 missense mutations in the SEMA7A gene ( 607961.0001 - 607961.0004 ) . These mutations were not detected in genomic DNA from 100 randomly selected individuals from Northern Germany. All 4 missense mutations occurred in the semaphorin domain of SEMA7A. Studies with JMH-variant RBCs and transfectants expressing membrane-anchored recombinant SEMA7A proteins showed that the variant SEMA7A proteins were of normal length and were expressed at levels equal to those of the wildtype protein. In inhibition studies with soluble recombinant wildtype and variant SEMA7A proteins, JMH-like alloantibodies of JMH-variant individuals did not react with the related recombinant variant SEMA7A protein, but they did react with the wildtype and unrelated variant SEMA7A proteins, indicating that expression of variant JMH antigen is based on the absence of certain SEMA7A epitopes. Serologic compatibility testing of JMH-variant blood samples confirmed these results. In 4 young Native American women with JMH-negative phenotype from a reservation northwest of Quebec City, Canada, Richard et al. (2011) i dentified a novel missense mutation in the SEMA7A gene ( 607961.0005 ) . At least 2 of the women were JHM-positive and their alloantibody was compatible with most JHM-negative RBCs tested; the other 2 women were not tested. Soluble forms of wildtype and R347L variant SEMA7A proteins were produced in vitro and demonstrated a specific alloantibody reaction with wildtype recombinant SEMA7A, but not with the R347L variant form. JMH-Negative Phenotype " id="pdf-obj-3-35" src="pdf-obj-3-35.jpg">

JMH-Negative Phenotype

Seltsam et al. (2007) found that JMH-negative individuals lacked phenotypically relevant mutations in the coding region or promoter of the SEMA7A gene. They concluded that the JMH-negative phenotype does not result from variation in the SEMA7A gene.

<a href=Seltsam et al. (2007) found that JMH-negative individuals lacked phenotypically relevant mutations in the coding region or promoter of the SEMA7A gene. They concluded that the JMH-negative phenotype does not result from variation in the SEMA7A gene. JMH-Weak Phenotype Seltsam et al. (2007) found that JMH-weak individuals lacked phenotypically relevant mutations in the SEMA7A gene. They concluded that the JMH-weak phenotype does not result from variation in the SEMA7A gene. REFERENCES Lange, C., Liehr, T., Goen, M., Gebhart, E., Fleckenstein, B., Ensser, A. New eukaryotic semaphorins with close homology to semaphorins of DNA viruses. Genomics 51: 340-350, 1998. [PubMed: 9721204 , related 1. citations ] [ Full Text ] Richard, M., St-Laurent, J., Perreault, J., Long, A., St-Louis, M. A new SEMA7A variant found in Native Americans with alloantibody. Vox Sang. 100: 322-326, 2011. [PubMed: 20854351 , related citations ] [ Full 2. Text ] Seltsam, A., Strigens, S., Levene, C., Yahalom, V., Moulds, M., Moulds, J. J., Hustinx, H., Weisbach, V., Figueroa, D., Bade-Doeding, C., DeLuca, D. S., Blasczyk, R. The molecular diversity of Sema7A, the semaphorin that carries the JMH blood group antigens. Transfusion 47: 133-146, 3. 2007. [PubMed: 17207242 , related citations ] [ Full Text ] " id="pdf-obj-4-5" src="pdf-obj-4-5.jpg">

JMH-Weak Phenotype

Seltsam et al. (2007) found that JMH-weak individuals lacked phenotypically relevant mutations in the SEMA7A gene. They concluded that the JMH-weak phenotype does not result from variation in the SEMA7A gene.

<a href=Seltsam et al. (2007) found that JMH-negative individuals lacked phenotypically relevant mutations in the coding region or promoter of the SEMA7A gene. They concluded that the JMH-negative phenotype does not result from variation in the SEMA7A gene. JMH-Weak Phenotype Seltsam et al. (2007) found that JMH-weak individuals lacked phenotypically relevant mutations in the SEMA7A gene. They concluded that the JMH-weak phenotype does not result from variation in the SEMA7A gene. REFERENCES Lange, C., Liehr, T., Goen, M., Gebhart, E., Fleckenstein, B., Ensser, A. New eukaryotic semaphorins with close homology to semaphorins of DNA viruses. Genomics 51: 340-350, 1998. [PubMed: 9721204 , related 1. citations ] [ Full Text ] Richard, M., St-Laurent, J., Perreault, J., Long, A., St-Louis, M. A new SEMA7A variant found in Native Americans with alloantibody. Vox Sang. 100: 322-326, 2011. [PubMed: 20854351 , related citations ] [ Full 2. Text ] Seltsam, A., Strigens, S., Levene, C., Yahalom, V., Moulds, M., Moulds, J. J., Hustinx, H., Weisbach, V., Figueroa, D., Bade-Doeding, C., DeLuca, D. S., Blasczyk, R. The molecular diversity of Sema7A, the semaphorin that carries the JMH blood group antigens. Transfusion 47: 133-146, 3. 2007. [PubMed: 17207242 , related citations ] [ Full Text ] " id="pdf-obj-4-12" src="pdf-obj-4-12.jpg">

REFERENCES

Lange, C., Liehr, T., Goen, M., Gebhart, E., Fleckenstein, B., Ensser, A.New eukaryotic semaphorins with close homology to semaphorins of DNA viruses. Genomics 51: 340-350, 1998. [PubMed: 9721204, related

  • 1. citations] [Full Text] Richard, M., St-Laurent, J., Perreault, J., Long, A., St-Louis, M. A new SEMA7A variant found in Native Americans with alloantibody. Vox Sang. 100: 322-326, 2011. [PubMed: 20854351, related citations] [Full

  • 2. Text] Seltsam, A., Strigens, S., Levene, C., Yahalom, V., Moulds, M., Moulds, J. J., Hustinx, H., Weisbach, V., Figueroa, D., Bade-Doeding, C., DeLuca, D. S., Blasczyk, R. The molecular diversity of Sema7A, the semaphorin that carries the JMH blood group antigens. Transfusion 47: 133-146,