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[1][6] More than 95% of affected individuals demonstrate a homozygous deletion/mutation involving exon 7 in SMN1 (survival motor neuron 1), resulting in the biochemical deficiency of the SMN protein, part of a complex that functions in the assembly of small nuclear ribonucleoprotein particles (snRNP)

doi: 10.1017/S000711451900148X 90

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