Genetic variation of the extra-large stimulatory G protein alpha-subunit leads to Gs hyperfunction in platelets and is a risk factor for bleeding. [electronic resource]
Producer: 20020408Description: 733-8 p. digitalISSN:- 0340-6245
- Abnormalities, Multiple -- genetics
- Adenosine -- pharmacology
- Adenylyl Cyclases -- metabolism
- Adolescent
- Alprostadil -- pharmacology
- Alternative Splicing
- Amino Acid Sequence
- Amino Acid Substitution
- Bleeding Time
- Blood Platelets -- physiology
- Child
- Chromogranins
- Cyclic AMP -- biosynthesis
- Female
- Fingers -- abnormalities
- GTP-Binding Protein alpha Subunits, Gs -- genetics
- Gene Frequency
- Genomic Imprinting
- Hemorrhagic Disorders -- epidemiology
- Heterotrimeric GTP-Binding Proteins
- Humans
- Hyperkinesis -- genetics
- Hypoparathyroidism -- genetics
- Iloprost -- pharmacology
- Intellectual Disability -- genetics
- Male
- Molecular Sequence Data
- Muscle Hypotonia -- genetics
- Mutagenesis, Insertional
- Nerve Tissue Proteins
- Phenotype
- Platelet Aggregation -- drug effects
- Platelet Function Tests
- Polymorphism, Genetic
- Protein Subunits
- Repetitive Sequences, Amino Acid
- Risk Factors
- Second Messenger Systems
- Structure-Activity Relationship
- Wounds and Injuries -- complications
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Publication Type: Case Reports; Journal Article; Research Support, Non-U.S. Gov't
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