catalytic subunit alpha  (Proteintech)

Journal: Molecular Biomedicine

Article Title: Obestatin treatment links mitochondrial homeostasis and skeletal muscle repair in Duchenne muscle dystrophy

doi: 10.1186/s43556-025-00370-8

Figure Lengend Snippet: Obestatin promotes activation of NFTAc1. a Comparation of the effect of obestatin (10 nM) and insulin (1.72 µM) on utrophin, ß-dystroglycan, and α7-integrin protein expression on differentiating human DMD cells. b Analysis of pNFATc1(S172) and NFATc1 after obestatin (10 nM) or insulin (1.72 µM) administration on differentiating human DMD cells. c Representative immunofluorescence images of obestatin- or control-treated human DMD myotubes showing NFATc1 cellular location. Right panel , measurement of the number of nuclei showing NFATc1 location. Data are shown as mean ± SEM (* P < 0.05). d Representative images of vehicle- and obestatin-treated TAs showing NFATc1 expression. Right panel , measurement of the number of nuclei showing NFATc1 location. Data are shown as mean ± SEM (* P < 0.05). e Immunoblot analysis of PPP3 catalytic subunit (PPP3CA), pNFATc1(S172), NFATc1, utrophin, slow-MHC, fast-MHC, β-dystroglycan, α-syntrophin, NOS1, β1D-integrin, and α7-integrin in extracts of DMD cells transfected with control or PPP3CA siRNAs after obestatin treatment (10 nM). The inset shows Proposed model by which obestatin signalling triggers PPP3 to regulate the transcriptional activity of NFATc1. Data were expressed as mean ± SEM ( n = 3 per group; *, # P < 0.05)

Article Snippet: To knockdown PPP3 expression in human DMD cells, siRNA specifically targeting human PPP3 catalytic subunit alpha (sc-36303, Santa Cruz Biotechnology, CA, US) was used.

Techniques: Activation Assay, Expressing, Immunofluorescence, Control, Western Blot, Transfection, Activity Assay

Journal: Molecular Biomedicine

Article Title: Obestatin treatment links mitochondrial homeostasis and skeletal muscle repair in Duchenne muscle dystrophy

doi: 10.1186/s43556-025-00370-8

Figure Lengend Snippet: Obestatin promotes activation of mitochondrial homeostasis via calcineurin and TFEB activity. a Immunoblot analysis of PPP3CA, PINK1, DRP1, FIS1, TFAM, PGC1a, OPA1, and MFN2 in extracts of DMD cells transfected with control or PPP3CA siRNAs after obestatin treatment (10 nM). b Immunoblot analysis of PPP3CA, pTFEB(S211), and TFEB in extracts of DMD cells transfected with control or PPP3CA siRNAs after obestatin treatment (10 nM). The inset shows the proposed model by which obestatin signalling triggers PPP3 to regulate the transcriptional activity of TFEB. c Analysis of nuclear translocation of TFEB after obestatin treatment (10 nM) in human DMD myotubes. In A-C, data were expressed as mean ± SEM ( n = 3 per group; *, # P < 0.05). d Proposed model by which obestatin signalling triggers PPP3, NFATc1 and TFEB activity to regulate mitochondrial homeostasis, autophagy, muscle fibber type specification and sarcolemma repair obestatin signalling under dystrophic conditions

Article Snippet: To knockdown PPP3 expression in human DMD cells, siRNA specifically targeting human PPP3 catalytic subunit alpha (sc-36303, Santa Cruz Biotechnology, CA, US) was used.

Techniques: Activation Assay, Activity Assay, Western Blot, Transfection, Control, Translocation Assay