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Publication : Stabilization of the survival motor neuron protein by ASK1.

First Author  Kwon JE Year  2011
Journal  FEBS Lett Volume  585
Issue  9 Pages  1287-92
PubMed ID  21496457 Mgi Jnum  J:172060
Mgi Id  MGI:5003381 Doi  10.1016/j.febslet.2011.04.011
Citation  Kwon JE, et al. (2011) Stabilization of the survival motor neuron protein by ASK1. FEBS Lett 585(9):1287-92
abstractText  The survival motor neuron (SMN) is a spliceosomal snRNP-interacting protein that was initially identified as a defective molecule in spinal muscular atrophy (SMA). The disease severity of SMA is determined by SMN protein level. Here, we show that apoptosis signal-regulating kinase 1 (ASK1) stabilizes SMN protein by inhibiting SMN poly-ubiquitination, and that the kinase activity of ASK1 is less important than its ability to bind to SMN. Furthermore, depletion of ASK1 by RNA interference revealed that ASK1 modulates neurite outgrowth by regulating SMN protein level in NSC34 motor neuron-like cells. Collectively, our results suggest that ASK1 acts as a novel binding partner of SMN and controls the steady-state level of SMN through complex formation with SMN in neurite outgrowth. STRUCTURED SUMMARY OF PROTEIN INTERACTIONS: ASK1physically interacts with SMN1 by anti tag coimmunoprecipitation(View interaction) SMN1physically interacts with ASK1 by anti tag coimmunoprecipitation(View interaction) ASK1physically interacts with SMN1 by anti bait coimmunoprecipitation(View interaction) ASK1physically interacts with SMNdelta7 by two hybrid(View interaction).
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