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Primary and secondary transcriptional effects in the developing human Down syndrome brain and heart.
Mao R, Wang X, Spitznagel EL, Frelin LP, Ting JC, Ding H, Kim JW, Ruczinski I, Downey TJ, Pevsner J
Genome Biol
2005,
6
:R107
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PubMed Central articles that cite the above article:
1.
Natural gene-expression variation in Down syndrome modulates the outcome of gene-dosage imbalance.
Prandini P, Deutsch S, Lyle R, Gagnebin M, Delucinge Vivier C, Delorenzi M, Gehrig C, Descombes P, Sherman S, Dagna Bricarelli F, Baldo C, Novelli A, Dallapiccola B, Antonarakis SE
Am J Hum Genet
2007 Aug,
81
:252-63
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Classification of human chromosome 21 gene-expression variations in Down syndrome: impact on disease phenotypes.
Aït Yahya-Graison E, Aubert J, Dauphinot L, Rivals I, Prieur M, Golfier G, Rossier J, Personnaz L, Creau N, Bléhaut H, Robin S, Delabar JM, Potier MC
Am J Hum Genet
2007 Sep,
81
:475-91
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The power of comparative and developmental studies for mouse models of Down syndrome.
Moore CS, Roper RJ
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2007 Jul,
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Validation of computational methods in genomics.
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Inducing segmental aneuploid mosaicism in the mouse through targeted asymmetric sister chromatid event of recombination.
Duchon A, Besson V, Pereira PL, Magnol L, Hérault Y
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Effects of aneuploidy on genome structure, expression, and interphase organization in Arabidopsis thaliana.
Huettel B, Kreil DP, Matzke M, Matzke AJ
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Functional genomic analysis of amniotic fluid cell-free mRNA suggests that oxidative stress is significant in Down syndrome fetuses.
Slonim DK, Koide K, Johnson KL, Tantravahi U, Cowan JM, Jarrah Z, Bianchi DW
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