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Spinocerebellar ataxia type 1 (SCA1) is a rare autosomal dominant disorder, which, like other spinocerebellar ataxias, is characterized by neurological symptoms including dysarthria, hypermetric saccades, and ataxia of gait and stance.
Muscles are often paired as agonistic and antagonistic muscles. [20] This can be a bit misleading as, in general, it is groups of muscles working together to either make or cancel a movement. [ 21 ] The present table lists some well-known relationships but is not at all complete.
McLeod syndrome (/ m ə ˈ k l aʊ d / mə-KLOWD) is an X-linked recessive genetic disorder that may affect the blood, brain, peripheral nerves, muscle, and heart.It is caused by a variety of recessively inherited mutations in the XK gene on the X chromosome.
Ataxia (from Greek α- [a negative prefix] + -τάξις [order] = "lack of order") is a neurological sign consisting of lack of voluntary coordination of muscle movements that can include gait abnormality, speech changes, and abnormalities in eye movements, that indicates dysfunction of parts of the nervous system that coordinate movement, such as the cerebellum.
Muscle strength is a result of three overlapping factors: physiological strength (muscle size, cross sectional area, available crossbridging, responses to training), neurological strength (how strong or weak is the signal that tells the muscle to contract), and mechanical strength (muscle's force angle on the lever, moment arm length, joint ...
Akt1 is also able to induce protein synthesis pathways, and is therefore a key signaling protein in the cellular pathways that lead to skeletal muscle hypertrophy and general tissue growth. A mouse model with complete deletion of the Akt1 gene manifests growth retardation and increased spontaneous apoptosis in tissues such as testes and thymus ...
In genetics, a maternal effect occurs when the phenotype of an organism is determined by the genotype of its mother. [1] For example, if a mutation is maternal effect recessive, then a female homozygous for the mutation may appear phenotypically normal, however her offspring will show the mutant phenotype, even if they are heterozygous for the mutation.
That imprinting might be a feature of mammalian development was suggested in breeding experiments in mice carrying reciprocal chromosomal translocations. [19] Nucleus transplantation experiments in mouse zygotes in the early 1980s confirmed that normal development requires the contribution of both the maternal and paternal genomes.