mitral valve prolapse/phosphatase

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Three patients with glucose-6 phosphatase catalytic subunit 3 deficiency

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Objectives Severe congenital neutropenia (SCN) is a primary immunodeficiency (PID) characterized by persistent severe neutropenia, recurrent infections, and oral aphthous lesions. Severe congenital neutropenia is caused by various genetic defects such as ELANE, GFI, HAX-1, JAGN1, SRP54, and

Extremely elevated serum alkaline phosphatase level upon treatment with teriparatide: a case report

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Background: Teriparatide is a homolog of human parathyroid hormone (1-34), which is approved for the treatment of postmenopausal and glucocorticoid-induced osteoporosis. Several minor and transient side effects have been reported for

MVP-Associated Filamin A Mutations Affect FlnA-PTPN12 (PTP-PEST) Interactions.

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Although the genetic basis of mitral valve prolapse (MVP) has now been clearly established, the molecular and cellular mechanisms involved in the pathological processes associated to a specific mutation often remain to be determined. The FLNA gene (encoding Filamin A; FlnA) was the first gene

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