Journal: Life science alliance

Article Title: STAT3 inhibition recovers regeneration of aged muscles by restoring autophagy in muscle stem cells.

doi: 10.26508/lsa.202302503

Figure Lengend Snippet: Figure 6. STAT3 inhibition induces autophagy by disrupting the STAT3/PKR complex and activating pro-autophagic gene transcription in vitro. C2C12 cell line was treated for 24 h with PBS (NT) or the STAT3i at the concentration of 50 μM, then harvested for analysis. (A) qRT–PCR for Myod and Socs3 normalized for Gapdh (n = 3 for MyoD and n = 4 for Socs3; values represent the mean ± s.d., **P < 0.01 and ***P < 0.001 by a t test). (B) qRT–PCR for Lc3, Atg9A, Ulk1, Atg7, Bnip3, Atg4, Becn1, and Bcl2 normalized for Gapdh (n = 3; values represent the mean ± s.d., *P < 0.05, **P < 0.01, and ***P < 0.001 by a t test). (C) Phospho-eIF2α levels in NT or STAT3i-treated

Article Snippet: The following antibodies were used: LC3B (#2775S; Cell Signaling), p62 (#P0067; Sigma-Aldrich), total STAT3 (#4904S; Cell Signaling), P-STAT3 (#4113S; Cell Signaling), MYOD (5.8; Novus Biologicals), phospho-eIF2α (#3398S; Cell Signaling), GAPDH (Santa Cruz), and vinculin (sc-73614; Santa Cruz).

Techniques: Inhibition, In Vitro, Concentration Assay, Quantitative RT-PCR

Journal: The Journal of Biological Chemistry

Article Title: Coordinated regulation of the ribosome and proteasome by PRMT1 in the maintenance of neural stemness in cancer cells and neural stem cells

doi: 10.1016/j.jbc.2021.101275

Figure Lengend Snippet: Effect of MYOD1-induced differentiation on the expression of ribosome and proteasome components and epigenetic factors. A , phenotypic change in A375 cells infected with virus containing MYOD1. Cells infected with virus containing the empty vector were used as a control. B , IB detection of expression change of a series of proteins, as indicated, in control A375 cells and cells with forced MYOD1 expression. C , phenotypic change in A549 cells in response to MYOD1 expression. D , detection of protein expression, as indicated, in control cells and cells with MYOD1 expression using IB. E , IF detection of expression and subcellular distribution of a muscle cell marker, ribosome and proteasome proteins, and the proteasome 20S subunit in control cells and cells with MYOD1 expression. F , expression alteration in a series of proteins, as indicated, in wild-type C2C12 (C2C12 WT ) cells and the cells with knockout of Myod1 gene (C2C12 Myod1 −/− ).

Article Snippet: Primary antibodies were EZH2 (Cell Signaling Technology, #5246), HDAC1 (Cell Signaling Technology, #5356), LSD1 (Cell Signaling Technology, #2139), MAP2 (Abcam, #ab183830), MEF2C (Cell Signaling Technology, #5030), MYOD1 (Novus Biologicals, #NB100-56511), NESTIN (R&D systems, #AF2736), NEUROD1 (Cell Signaling Technology, #4373), NF-L (Cell Signaling Technology, #2837), PAX6 (Abcam, #ab195045), PRMT1 (Cell Signaling Technology, #2449), PSMA2 (Abclonal, #A2504), PSMD2 (Abclonal, #A1999), RPL26 (Abclonal, #A16680), RPS3 (Abclonal, #A2533), SOX1 (Abcam, #ab109290), SOX2 (Cell Signaling Technology, #23064), TUBB3 (Cell Signaling Technology, #5568), 20S α + β (Abcam, #ab22673).

Techniques: Expressing, Infection, Virus, Plasmid Preparation, Control, Marker, Knock-Out