We are analyzing https://link.springer.com/article/10.1007/s12026-008-8084-3.

Title:
Mutations of the Wiskott–Aldrich Syndrome Protein affect protein expression and dictate the clinical phenotypes | Immunologic Research
Description:
Mutations of the Wiskott–Aldrich Syndrome Protein (WASP) are responsible for classic Wiskott–Aldrich Syndrome (WAS), X-linked thrombocytopenia (XLT), and in rare instances congenital X-linked neutropenia (XLN). WASP is a regulator of actin polymerization in hematopoietic cells with well-defined functional domains that are involved in cell signaling and cell locomotion, immune synapse formation, and apoptosis. Mutations of WASP are located throughout the gene and either inhibit or disregulate normal WASP function. Analysis of a large patient population demonstrates a strong phenotype–genotype correlation. Classic WAS occurs when WASP is absent, XLT when mutated WASP is expressed and XLN when missense mutations occur in the Cdc42-binding site. However, because there are exceptions to this rule it is difficult to predict the long-term prognosis of a given affected boy solely based on the analysis of WASP expression.
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Topics {✒️}

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Familiärer, angeborener Morbus Werihofii?

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         headline:Mutations of the Wiskott–Aldrich Syndrome Protein affect protein expression and dictate the clinical phenotypes
         description:Mutations of the Wiskott–Aldrich Syndrome Protein (WASP) are responsible for classic Wiskott–Aldrich Syndrome (WAS), X-linked thrombocytopenia (XLT), and in rare instances congenital X-linked neutropenia (XLN). WASP is a regulator of actin polymerization in hematopoietic cells with well-defined functional domains that are involved in cell signaling and cell locomotion, immune synapse formation, and apoptosis. Mutations of WASP are located throughout the gene and either inhibit or disregulate normal WASP function. Analysis of a large patient population demonstrates a strong phenotype–genotype correlation. Classic WAS occurs when WASP is absent, XLT when mutated WASP is expressed and XLN when missense mutations occur in the Cdc42-binding site. However, because there are exceptions to this rule it is difficult to predict the long-term prognosis of a given affected boy solely based on the analysis of WASP expression.
         datePublished:2008-12-11T00:00:00Z
         dateModified:2008-12-11T00:00:00Z
         pageStart:84
         pageEnd:88
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            Wiskott–Aldrich Syndrome
            X-linked thrombocytopenia
            X-linked neutropenia
             WASP gene
            Mutation analysis
            Genotype–phenotype correlation
            Immunology
            Allergology
            Medicine/Public Health
            general
            Internal Medicine
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      headline:Mutations of the Wiskott–Aldrich Syndrome Protein affect protein expression and dictate the clinical phenotypes
      description:Mutations of the Wiskott–Aldrich Syndrome Protein (WASP) are responsible for classic Wiskott–Aldrich Syndrome (WAS), X-linked thrombocytopenia (XLT), and in rare instances congenital X-linked neutropenia (XLN). WASP is a regulator of actin polymerization in hematopoietic cells with well-defined functional domains that are involved in cell signaling and cell locomotion, immune synapse formation, and apoptosis. Mutations of WASP are located throughout the gene and either inhibit or disregulate normal WASP function. Analysis of a large patient population demonstrates a strong phenotype–genotype correlation. Classic WAS occurs when WASP is absent, XLT when mutated WASP is expressed and XLN when missense mutations occur in the Cdc42-binding site. However, because there are exceptions to this rule it is difficult to predict the long-term prognosis of a given affected boy solely based on the analysis of WASP expression.
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         Wiskott–Aldrich Syndrome
         X-linked thrombocytopenia
         X-linked neutropenia
          WASP gene
         Mutation analysis
         Genotype–phenotype correlation
         Immunology
         Allergology
         Medicine/Public Health
         general
         Internal Medicine
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