By Theodore Friedmann; Jay C. Dunlap and Stephen F. Goodwin (Eds.)

ISBN-10: 0123748313

ISBN-13: 9780123748317

RNA interference (RNAi) is a mechanism that inhibits gene expression on the level of translation or through hindering the transcription of particular genes. RNAi objectives contain RNA from viruses and transposons (probably as a kind of innate immune response), and in addition performs a task in regulating improvement and genome upkeep. comprises vital reports of the broadest curiosity to geneticists and their colleagues in affiliated disciplines, delivering researchers an summary and synthesis of the most recent findings within the zone offers updated learn from leaders within the box compliment for Advances in Genetics: "Outstanding either in type and within the caliber of its contributions."--NATURE "Can be hugely urged to geneticists, and biologists in general...will turn out to be of excessive value for the advance of the technological know-how of genetics."--SCIENCE

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Multiple roles of TDP-43 in gene expression, splicing regulation, and human disease. Front Biosci. 13, 867–878. , and Baralle, F. E. (2001). Nuclear factor TDP-43 and SR proteins promote in vitro and in vivo CFTR exon 9 skipping. EMBO J. 20, 1774–1784. , Ayala, Y. , and Baralle, F. E. (2005). TDP-43 Binds Heterogeneous Nuclear Ribonucleoprotein A/B through Its C-terminal Tail: an important region for the inhibition of cystic fibrosis transmembrane conductance regulator exon 9 splicing. J. Biol.

If we take one of the players in this complex pathology, the presenilin gene, we can see that there is no clear winner between gain and loss-of-function models. In fact the mutations detected in the presenilin (PSEN1/PSEN2) genes are found associated with production of the A 42 product and with familial Alzheimer Disease. As initial knockout studies of presenilins did not produce this phenotype the conclusion was that they acted through a gain-of-function mechanism. , 2000). Actually taken together, these data would rather suggest a loss-of-function role for presenilin genes in AD rather than the opposite.

Al-Lozi, M. , et al. (2008). TDP-43 A315T mutation in familial motor neuron disease. Ann. Neurol. 63, 535–538. 30 Buratti and Baralle Gitcho, M. , Forman, M. , Goate, A. , and Cairns, N. J. (2009). VCP mutations causing frontotemporal lobar degeneration disrupt localization of TDP-43 and induce cell death. J. Biol. Chem. 284, 12384–12398. , Bachorik, J. , and Dreyfuss, G. (2008). RNA-binding proteins and posttranscriptional gene regulation. FEBS Lett. 582, 1977–1986. Gregory, R. , Yan, K. , and Shiekhattar, R.

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Advances in Genetics by Theodore Friedmann; Jay C. Dunlap and Stephen F. Goodwin (Eds.)


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