Journal: Journal of Animal Science and Biotechnology

Article Title: ZBED6 deletion activates FNDC1 -mediated PI3K/AKT and MAPK/ERK1/2 signaling pathways to promote myogenesis in pigs

doi: 10.1186/s40104-026-01504-w

Figure Lengend Snippet: ZBED6 deletion activates FNDC1 -mediated PI3K/AKT and MAPK/ERK1/2 signaling pathways. A RNA-seq data from ZBED6-deficient pigs, ZBED6 knockout myoblasts and myotubes, and FNDC1 knockdown C2C12 cells were comprehensively analyzed to screen downstream signaling pathways. B Protein expression levels and statistical analysis of p-AKT, AKT, p-mTOR and mTOR in WT and ZBED6 −/− pigs, n = 3 pigs/genotype. C and D Protein expression levels and statistical analysis, n = 3 pigs/genotype. E and F Protein expression levels and statistical analysis of p-mTOR, mTOR, p-AKT, AKT, p-ERK1/2 and ERK1/2, n = 3 independent cell-culture experiments. Data are expressed as mean ± SEM. In (B), and (D), the P values were determined by two-tailed Student's t -tests. In (F), the P values were determined by two-way ANOVA followed by Sidak's multiple comparisons test, different letters (a, b and c) between bars indicate P < 0.05

Article Snippet: Primary porcine skeletal muscle satellite cells were treated with 10 μmol/L LY294002, a PI3K inhibitor (MCE, HY-10108), or 1 μmol/L SCH772984, an ERK1/2 inhibitor (MCE, HY-50846).

Techniques: Protein-Protein interactions, RNA Sequencing, Knock-Out, Knockdown, Expressing, Analysis, Cell Culture, Two Tailed Test

Journal: Journal of Animal Science and Biotechnology

Article Title: ZBED6 deletion activates FNDC1 -mediated PI3K/AKT and MAPK/ERK1/2 signaling pathways to promote myogenesis in pigs

doi: 10.1186/s40104-026-01504-w

Figure Lengend Snippet: Inhibition of PI3K/AKT and MAPK/ERK1/2 pathways reduces the effects of the ZBED6-FNDC1 axis on myogenesis. A and B representative immunofluorescence staining for EdU ( A ) and percentage of EdU positive cells ( B ) in ZBED6 knockdown primary porcine skeletal muscle satellite cells treated with SCH772984, n = 3 independent cell-culture experiments. C and D . representative immunofluorescence staining for EdU ( C ) and percentage of EdU positive cells ( D ) in ZBED6 knockdown primary porcine skeletal muscle satellite cells treated with LY294002, n = 3 independent cell-culture experiments. E and F representative immunofluorescence staining for MYHC ( E ) and fusion index ( F ) in ZBED6 knockdown primary porcine skeletal muscle satellite cells treated with SCH772984, n = 3 independent cell-culture experiments. G and H representative immunofluorescence staining for MYHC ( G ) and fusion index ( H ) in ZBED6 knockdown primary porcine skeletal muscle satellite cells treated with LY294002, n = 3 independent cell-culture experiments. Data are represented as mean ± SEM. In (B), (D), (F), and (H), the P values were determined by two-way ANOVA followed by Sidak's multiple comparisons test, different letters (a and b) between bars indicate P < 0.05

Article Snippet: Primary porcine skeletal muscle satellite cells were treated with 10 μmol/L LY294002, a PI3K inhibitor (MCE, HY-10108), or 1 μmol/L SCH772984, an ERK1/2 inhibitor (MCE, HY-50846).

Techniques: Inhibition, Immunofluorescence, Staining, Knockdown, Cell Culture

Journal: Pigment Cell & Melanoma Research

Article Title: Allele‐Specific GNAQ Q209 Mutations Reveal Context‐Dependent Oncogenic Programs in Uveal Melanoma

doi: 10.1111/pcmr.70121

Figure Lengend Snippet: Q209R preferentially engages FAK‐YAP signaling. (A) Western blot analysis of GNAQ, BAP1, Melan‐A, p‐ERK1/2 (Thr202/Tyr204), ERK1/2, FRA1, p‐AKT (Ser473), AKT, p‐4EBP1 (Ser65), and 4EBP1 expression in mouse UM cell lines harboring GNAQ Q209R or GNAQ Q209L . HSP90 was used as an internal loading control. (B) Quantification of the relative ratio between p‐AKT (Ser473) and AKT in Q209R and Q209L UM cell lines from (A). (C) Quantification of the relative ratio between p‐4EBP1 (Ser65) and 4EBP1 in Q209R and Q209L UM cell lines from (A). (D) Western blot analysis of p‐FAK (Tyr397), FAK, p‐YAP (Ser127), and YAP in mouse UM cell lines harboring GNAQ Q209R or GNAQ Q209L . HSP90 was used as an internal loading control. (E) Quantification of the relative ratio between p‐FAK (Tyr397) and FAK in Q209R and Q209L UM cell lines from (D). (F) Quantification of the relative ratio between p‐YAP (Ser127) and YAP in Q209R and Q209L UM cell lines from (D). Orthotopic tumor‐derived cell lines (QBM12.1 [Q209R], QBM12.3 [Q209R], QBM24 [Q209R], QBM45 [Q209L], QBM47 [Q209L]) and liver metastatic lines (QBM12L [Q209R], QBM12L2 [Q209R], QBM51L [Q209L], QBM53L [Q209L]) were used in A–F. (G) Representative IHC images showing YAP expression in primary tumors from Gnaq CA ; Bap1 CKO ; Myc CKI mice harboring either GNAQ Q209R or GNAQ Q209L . (H) Quantification of the nuclear‐to‐cytoplasmic YAP intensity ratio (H‐score) among primary tumors from Gnaq CA ; Bap1 CKO ; Myc CKI mice harboring either GNAQ Q209R or GNAQ Q209L . (I) Representative IHC images showing YAP expression in liver metastasis derived from intrasplenic transplantation of mouse UM cell lines harboring GNAQ Q209R or GNAQ Q209L . (J) Quantification of nuclear YAP intensity (H‐score) among liver metastasis derived from intrasplenic transplantation of mouse UM cell lines harboring GNAQ Q209R or GNAQ Q209L .

Article Snippet: Antibodies against GNAQ (CST, #14373, RRID:AB_2665457), BAP1 (Abcam, ab255611), Melan‐A (Abcam, ab210546, RRID:AB_2889292), ERK1/2 (CST, #4695, RRID:AB_390779), p‐ERK1/2 (Thr202/Tyr204) (CST, #4370, RRID:AB_2315112), FRA1 (Abcam, ab252421, RRID:AB_2904513), AKT (CST, #4691, RRID:AB_915783), p‐AKT (Ser473) (CST, #4060, RRID:AB_2315049), p‐FAK (Tyr397) (CST, #8556, RRID:AB_10891442), FAK (CST, #3285, RRID:AB_2269034), 4E‐BP1 (CST, #9452, RRID:AB_331692), p‐4E‐BP1 (Ser65; CST, #9451, RRID:AB_330947), YAP (CST, #4912, RRID:AB_2218911), and p‐YAP (Ser127) (CST, #4911, RRID:AB_2218913) were used at 1:1000 as indicated.

Techniques: Western Blot, Analysis, Expressing, Control, Derivative Assay, Transplantation Assay