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Involved in nonsense-mediated decay (NMD) of mRNAs containing premature stop codons. Additionally we are shipping and many more products for this protein.
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knockdown of SMG-8 produced the best effect for restoring defective mRNA and protein levels without affecting cell growth, cell-cycle progression, or endoplasmic reticulum stress in Ullrich congenital muscular dystrophy fibroblasts
large-scale conformational changes induced by SMG-8 after SMG-9 (show SMG9 Antibodies)-mediated recruitment tune SMG-1 (show SMG1 Antibodies) kinase activity to modulate nonsense-mediated mRNA decay
Results found that SMG8-SMG9 (show SMG9 Antibodies) is a G-domain heterodimer with architectural similarities to the dynamin-like family of GTPases. The SMG8-SMG9 (show SMG9 Antibodies) heterodimer forms in the absence of nucleotides. Nucleotide binding occurs at the G domain of SMG9 (show SMG9 Antibodies) but not of SMG8.
Genetic characterization of smg-8 mutants reveals no role in C. elegans nonsense mediated decay.
Involved in nonsense-mediated decay (NMD) of mRNAs containing premature stop codons. Is recruited by release factors to stalled ribosomes together with SMG1 and SMG9 (forming the SMG1C protein kinase complex) and, in the SMG1C complex, is required to mediate the recruitment of SMG1 to the ribosome:SURF complex and to suppress SMG1 kinase activity until the ribosome:SURF complex locates the exon junction complex (EJC). Acts as a regulator of kinase activity (By similarity).
amplified in breast cancer gene 2 protein
, protein SMG8
, protein smg-8 homolog
, smg-8 homolog, nonsense mediated mRNA decay factor
, CG6729 gene product