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Polyglutamine Genes Interact To Modulate The Severity And Progression Of Neurodegeneration In Drosophila
Six forms of spinal cerebellar ataxia (SCA1, 2, 3, 6, 7, and 17) are caused by dominant mutations in the respective genes. Patients suffering from
these different forms of SCA have similar symptoms of progressive adult-onset neurodegeneration, and the same causative mutation, a CAG repeat
expansion encoding an expanded run of polyglutamine. While the affected proteins are distinct and share no sequence similarity beyond the
polyglutamine domains, clinical and other observations hint at interactions between the genes that cause different forms of SCA.
This week in the
open-access journal PLoS Biology, Derek Lessing and Nancy Bonini show how using Drosophila as a model for human disease, they can now detail an
interaction between the genes associated with SCA3 and SCA2. They find that toxicity and neurodegeneration induced by pathogenic forms of SCA3 depends
on the normal activity of the fly counterpart of the gene associated with SCA2, ataxin-2. This interaction depends on a conserved protein-interaction
motif of Ataxin-2, and a protein that binds this motif, cytoplasmic poly(A)-binding protein (PABP), also modulates SCA3 degeneration.
These results
suggest that the normal roles of Ataxin-2 and PABP, potentially to regulate the translation of select target mRNAs, are critical to SCA3 disease.
These studies also highlight how a fly model can serve to enhance and extend intriguing clinical findings of the human disease.
Polyglutamine genes interact to modulate the severity and progression of neurodegeneration in Drosophila
Lessing D, Bonini NM
PLoS
Biol 6(2): e29. doi:10.1371/journal.pbio.0060029
Please click here to view article online
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Polyglutamine gene care interacþioneazã pentru a modula de severitatea ºi progresia de Neurodegeneration în Drosophila - Polyglutamine Genes Interact To Modulate The Severity And Progression Of Neurodegeneration In Drosophila - articole medicale engleza - startsanatate