Abstract:
:Huntington's disease (HD) is caused due to expansion of CAG repeats in the gene huntingtin (Htt). Adaptor protein Grb2, involved in Ras-MAP kinase pathway, is a known interactor of Htt. Mutant Htt-Grb2 interaction reduces Ras-MAPK signaling in HD models. In normal cells Grb2 forms Grb2-Sos1-Gab1 complex through its N-SH3 and C-SH3 domains respectively, essential for sustained activation of Ras. We found that C-SH3 of Grb2 mediates the interaction with mutant Htt and this interaction being stronger could replace Gab1, with mutant Htt becoming the preferred partner. This would have immense effect on downstream signaling events.
journal_name
Neurosci Resjournal_title
Neuroscience researchauthors
Baksi S,Basu S,Mukhopadhyay Ddoi
10.1016/j.neures.2014.06.009subject
Has Abstractpub_date
2014-10-01 00:00:00pages
77-83eissn
0168-0102issn
1872-8111pii
S0168-0102(14)00120-5journal_volume
87pub_type
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