anti src  (Cell Signaling Technology Inc)

Journal: bioRxiv

Article Title: In vivo human embryonic spinal cord atlas validates stem cell–derived human dorsal interneurons and reveals ASD spinal signatures

doi: 10.64898/2025.12.22.696129

Figure Lengend Snippet: (A, B) EBs were generated at day 0 after either d4 (A) or d10 (B) NMP formation and then treated with RA for 10 days (control). In the experimental samples, BMPs were added at day 1 (BMP4+1), day 2 (BMP4+2) or day 4 (BMP4+4) after EB formation, until day 10. Samples were further differentiated for 6 days and then processed for immunohistochemistry (IHC). (C) EBs were labeled with antibodies against LHX2 (dI1, green), FOXD3 (dI2, white), ISL1 (dI3, red) and DAPI (all nuclei, blue). (D, E) Quantification of EBs formed from either d4 (D) or d10 (E) NMPs, suggests that dI1s form robustly from the BMP4+1 condition for both d4 and d10 NMPs. In contrast, dI3s form most robustly from BMP4+4 condition for d4 NMPs and the BMP4+1 condition for d10 NMPs. Probability of similarity between control and experimental groups: * p<0.05, ** p<0.005, *** p<0.0005; two-way ANOVA.

Article Snippet: The following antibodies were used: LHX2 (mouse; DSHB, PCRP-LHX2-1C11; 1:50), FOXD3 (guinea pig, a gift from Thomas Mueller, Germany, 1:10,000), ISL1 (goat; R&D systems, AF1837; 1:500), PAX2 (rabbit; Invitrogen, 71-6000; 1:500), LMX1B (guinea pig; Thomas Muller Lab), LHX1/5 (mouse; DSHB, 4F2; 1:50) for 12–14 hours (overnight) at 2–8°C in a humidified chamber.

Techniques: Generated, Control, Immunohistochemistry, Labeling

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Calotropin attenuates ischemic heart failure after myocardial infarction by modulating SIRT1/FOXD3/SERCA2a pathway.

doi: 10.1016/j.biopha.2024.117384

Figure Lengend Snippet: Fig. 6. FOXD3 activated the transcription of SERCA2a. (A) Western blot analysis of FOXD3 in H9c2 cells transfected with FOXD3 overexpression plasmid or control vector. (B) The effect of SERCA2a mRNA expression in H9c2 cells transfected with FOXD3 overexpressing plasmid or control vector. n = 3; The data were expressed as mean ± SD and analyzed using One-way ANOVA follow by Tukey post-hoc tests; ** P<0.01, vs vector group. (C and D) The effect of SERCA2a protein expression in H9c2 cells transfected with FOXD3 overexpressing plasmid or control vector. n = 3; The data were expressed as mean ± SD and analyzed using One-way ANOVA follow by Tukey post-hoc tests; * P<0.05, vs vector group. (E) The effects of FOXD3 overexpression on SERCA2a promoter relative activity in the 293 t cells. n = 3; The data were expressed as mean ± SEM and analyzed using One-way ANOVA follow by Tukey post-hoc tests; *** P<0.001, vs vector group. (F) Western blot analysis of FOXD3 in H9c2 cells transfected with FOXD3 siRNA. (G) The effect of CAL on SERCA2a mRNA level after FOXD3 silence. n = 3; The data were expressed as mean ± SD and analyzed using One-way ANOVA follow by Tukey post-hoc tests; * P<0.05, CAL vs CAL+FOXD3 siRNA.

Article Snippet: Then they were incubated with primary antibodies against SERCA2a (1:1000, A11692, ABclonal), SIRT1 (1:1000, A0230, ABclonal), forkhead Box D3 (FOXD3) (1:1000, 5G9B10, Santa Cruz), GAPDH (1:10000, AC010, ABclonal), and β-Actin (1:100000, A026, ABclonal).

Techniques: Western Blot, Transfection, Over Expression, Plasmid Preparation, Control, Expressing, Activity Assay

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Calotropin attenuates ischemic heart failure after myocardial infarction by modulating SIRT1/FOXD3/SERCA2a pathway.

doi: 10.1016/j.biopha.2024.117384

Figure Lengend Snippet: Fig. 7. CAL promoted SERCA2a transcription via SIRT1-dependent deacetylation of FOXD3 in HF post-MI. (A) The effect of CAL on FOXD3 expression in the presence of EX527 in LAD-induced HF rat heart tissue. (B) The effect of CAL on FOXD3 expression in the presence of EX527 in OGD/R-induced H9c2 cells. (C-F) The effect of CAL on the FOXD3 location. ##P<0.01, ### P<0.001, vs control group; ** P<0.01, vs OGD/R group. (G) Immunofluorescence images for FOXD3. (H)The effect of CAL on FOXD3 acetylation in the presence of EX527 in LAD-induced HF rat heart tissue. (I) The effect of CAL on FOXD3 acetylation in the presence of EX527 in OGD/ R-induced H9c2 cells.

Article Snippet: Then they were incubated with primary antibodies against SERCA2a (1:1000, A11692, ABclonal), SIRT1 (1:1000, A0230, ABclonal), forkhead Box D3 (FOXD3) (1:1000, 5G9B10, Santa Cruz), GAPDH (1:10000, AC010, ABclonal), and β-Actin (1:100000, A026, ABclonal).

Techniques: Expressing, Control, Immunofluorescence

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Calotropin attenuates ischemic heart failure after myocardial infarction by modulating SIRT1/FOXD3/SERCA2a pathway.

doi: 10.1016/j.biopha.2024.117384

Figure Lengend Snippet: Fig. 8. Calotropin improved cardiac function and prevented adverse ventric ular remodeling in ischemic heart failure after MI via the SIRT1/FOXD3/SER CA2a pathway.

Article Snippet: Then they were incubated with primary antibodies against SERCA2a (1:1000, A11692, ABclonal), SIRT1 (1:1000, A0230, ABclonal), forkhead Box D3 (FOXD3) (1:1000, 5G9B10, Santa Cruz), GAPDH (1:10000, AC010, ABclonal), and β-Actin (1:100000, A026, ABclonal).

Techniques: