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. Author manuscript; available in PMC: 2020 Jun 25.
Published in final edited form as: Biochem Biophys Res Commun. 2019 May 3;514(2):530–537. doi: 10.1016/j.bbrc.2019.04.176

Figure 1: A-COP levels are unchanged in spinal cord from SMA mouse models.

Figure 1:

1a) Representative blot of spinal cord lysates from 5058 SMA pups and healthy siblings at postnatal day 6 probed for endogenous α-COP (H3 antibody), total SMN (Mansma2) and β–actin as a loading control. 1b) Representative blot of spinal cord lysates from Delta7 SMA pups and healthy siblings at postnatal day 6 probed for endogenous α-COP (H3 antibody), total SMN (Mansma2) and β–actin as a loading control. 1c,d) Quantification band intensity of SMN and α-COP protein levels from multiple spinal cord lysates (n=6 per genotype) from 5058 and Delta7 mouse models at postnatal day 6. Protein levels were normalized to heterozygous siblings using β–actin as a loading control. Error bars represent SEM.