The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
Female with autistic disorder and monosomy X (Turner syndrome): Parent-of-origin effect of the X chromosome
Abstract
Genetic analysis in both mouse and Drosophila has indicated that the product of the CLOCK gene is an essential component of a circadian rhythm timing system. A single nucleotide polymorphism (SNP), T3111C, in the 3' flanking region of the human CLOCK gene has been identified. Homozygotes or heterozygotes for the 3111C allele have been reported to have higher mean scores on a measure of evening preference for activity (vs. morning preference) than subjects homozygous for the 3111T allele. Since major depression is hypothesized to be closely linked to circadian rhythms, we explored whether this polymorphism might be related to susceptibility to major depression. We also ascertained allele frequency in an African-American control population, to begin to evaluate population variation at this locus. CLOCK T3111C allele frequencies were determined in 280 European American (EA) subjects, 143 with a history of major depression and 137 screened controls, and in 58 African American (AA) screened control subjects, using a polymerase chain reaction (PCR) - restriction fragment length polymorphism (RFLP) method. There was no significant difference between EA depressed and control subjects in allele frequency. There was a significant difference in allele frequency between EA and AA subjects, demonstrating a potential for population stratification. In none of these groups were significant deviations from Hardy-Weinberg equilibrium found. The present data do not support an association between CLOCK gene alleles at the T3111C locus and major depression.
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“with an increased rate of ASD diagnosis in Turner syndrome (TS, XO, ~3% ASD) [52,53,54], Klinefelter syndrome (KS, XXY, ~10% ASD) [55,56*], and 47,XYY syndrome (~20% ASD), but no increased rate in X chromosome trisomy [57,58**].”
From Sex differences in autism spectrum disorders (2013) · cites this paper as [52]
In the citing paper
“in patients with MDD, there appears to be no general association between the disease and this SNP (Desan et al., 2000).”
From Circadian genes, rhythms and the biology of mood disorders (2007) · cites this paper as Desan et al., 2000
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Cites
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Cited by
Molecular genetics of attention-deficit/hyperactivity disorder
Faraone, S. V., Perlis, R. H., Doyle, A. E., Smoller, J. W., Goralnick, J. J., Holmgren, M. A., & Sklar, P. (2005) · Biological Psychiatry · doi:10.1016/j.biopsych.2004.11.024 · Cited by 2,357
Neurocognitive consequences of sleep deprivation
Goel, N., Rao, H., Durmer, J., & Dinges, D. (2009) · Seminars in Neurology · doi:10.1055/s-0029-1237117 · Cited by 2,154
Identification and Evaluation of Children With Autism Spectrum Disorders
Johnson, C. P., Myers, S. M., & and the Council on Children With Disabilities (2007) · Pediatrics · doi:10.1542/peds.2007-2361 · Cited by 2,011
Neuroscience of attention-deficit/hyperactivity disorder: the search for endophenotypes
Castellanos, F. X., & Tannock, R. (2002) · Nature Reviews Neuroscience · doi:10.1038/nrn896 · Cited by 1,827
The genetics of mammalian circadian order and disorder: implications for physiology and disease
Takahashi, J. S., Hong, H.-K., Ko, C. H., & McDearmon, E. L. (2008) · Nature Reviews Genetics · doi:10.1038/nrg2430 · Cited by 1,611
Metadata
- Authors
- Donnelly, S. L., Wolpert, C. M., Menold, M. M., Bass, M. P., Gilbert, J. R., Cuccaro, M. L., Delong, G. R., & Pericak-Vance, M. A.
- Venue
- American Journal of Medical Genetics
- Published
- 2000
- References
- 58
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- Donnelly, S. L., Wolpert, C. M., Menold, M. M., Bass, M. P., Gilbert, J. R., Cuccaro, M. L., Delong, G. R., & Pericak-Vance, M. A. (2000). Female with autistic disorder and monosomy X (Turner syndrome): Parent-of-origin effect of the X chromosome. American Journal of Medical Genetics. https://doi.org/10.1002/1096-8628(20000612)96%3A3
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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