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| Untersuchte Arbeit: Seite: 18, Zeilen: 20-25 |
Quelle: Philip Bassett 2011 Seite(n): 8, Zeilen: 9 ff. |
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| As clinical variability is not explained by differences in gene content within the deletion, allelic variation(s) in the non-deleted homologous region is considered a possible contributor to phenotypic variability. Most of the genes from the 22q11.2 deletion region are expressed in fetal and adult brain, thus are candidates for both the psychiatric phenotype of patients with 22q11.2 deletions and susceptibility to psychiatric disorders in the general population (Meechan et al. 2010).
19. Meechan DW, Maynard TM, Tucker ES, Lamantia AS. Three phases of DiGeorge/22q11 deletion syndrome pathogenesis during brain development: patterning, proliferation, and mitochondrial functions of 22q11 genes. Int J Dev Neurosci. 2011 May;29(3):283-94. |
As clinical variability is not explained by differences in gene content within the deletion, allelic variation(s) in the non-deleted homologous region is considered a possible contributor to phenotypic variability. [...]
[...] Most of the genes from the 22q11.2 deletion region are expressed in fetal and adult brain, thus are candidates for both the psychiatric phenotype of patients with 22q11.2 deletions and susceptibility to psychiatric disorders in the general population (Meechan et al. 2010). Meechan DW, Maynard TM, Tucker ES, Lamantia AS. Three phases of DiGeorge/22q11 deletion syndrome pathogenesis during brain development: patterning, proliferation, and mitochondrial functions of 22q11 genes. Int J Dev Neurosci. 2010 in press. |
The source is not given. Meechan et al. (2011) does not contain the text. |
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