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We began analyzing https://link.springer.com/article/10.1007/s12026-008-8084-3, but it redirected us to https://link.springer.com/article/10.1007/s12026-008-8084-3. The analysis below is for the second page.

Title[redir]:
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 {✒️}

strong phenotype–genotype correlation intermittent x-linked thrombocytopenia phenotype/genotype correlation x-linked thrombocytopenia x-linked neutropenia wiskott-aldrich syndrome gene wiskott–aldrich syndrome protein month download article/chapter classic wiskott–aldrich syndrome reduced b-cell adhesion formyl-methionyl-leucyl-phenylalanine wiskott–aldrich syndrome related subjects constitutively activating mutation impaired dendritic-cell homing full article pdf wasp gene mutations nk cell cytotoxicity privacy choices/manage cookies monocyte chemoattractant protein–1 congenital neutropenia check access instant access defined functional domains cd3-mediated stimulation wiskott–aldrich wasp gene wasp expression european economic area cdc42-binding site long-term prognosis angeborener morbus werihofii humblet-baron single-center cohort puck jm primary immunodeficiency diseases conditions privacy policy article ochs site mutation i294t mutation defective actin reorganization actin cytoskeletal rearrangement article log impaired peripheral homeostasis missense mutations occur immune synapse formation gene mutated accepting optional cookies blaese rm oxford university press

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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.
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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
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