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Expression of a dominant-active Rab11 mutant in primary HD mouse neurons rectified this deficit, highlighting Rab11 as a promising candidate for modulating HD pathologies.
Collectively, the I130T mutant reduced GJIC to a lesser extent than the G60S mutant in primary cells known to express only Cx43.
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Concurrently, primary motoneuron axons in twister mutants exhibit ectopic branches.
Our goal here is to test the efficacy of lumacaftor in other Class II mutants in primary human bronchial epithelial (HBE) cells derived from CF patients.
Alternatively, DNA-damage signaling or other signaling events activated by oncogenic Ras or FGFR2 mutants in primary cells may serve to more directly downregulate c-Myc.
Next, we expressed CHIP WT and deletion mutants in primary rat cortical neurons, and showed that EndoG was downregulated in primary rat cortical neurons overexpressing CHIP WT but not in cells expressing the CHIP mutants.
This was confirmed by expressing wild-type Cyt1 and Cyt2 tails and uncleavable mutant tails in primary T cells.
To shed some light on this mystery, we studied the effects of HSPB8 mutant proteins in primary neuronal culture.
To address this question, we compared the effect of mutant HSPB8 in primary neuronal and glial cell cultures.
In experimental models, this reversed the toxic effects of mutant huntingtin in primary striatal and cortical neurons and in a transgenic C. elegans model of HD.
By studying the role of the microtubules destabilizing protein stathmin in EOC, we showed that stathmin co-overexpressed with mutant p53 in primary EOC and that overexpression correlates with shorter patients' survival.
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