Identification of PTP1C mutation as the genetic defect in motheaten and viable motheaten mice: a step toward defining the roles of protein tyrosine phosphatases in the regulation of hemopoietic cell differentiation and function.

Abstract excerpt

Homozygosity for the motheaten (me) or viable motheaten (mev) mutations causes severe dysregulation of murine hematopoiesis with the consequent development of both immunodeficiency and systemic autoimmunity. Expression of this phenotype has now been linked to loss-of-function mutations in the gene encoding PTP1C, an intracellular tyrosine phosphatase predominantly expressed in cells of hemopoietic origin. As...

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