p70 ribosomal protein s6 kinase  (Cell Signaling Technology Inc)

Journal: Animal Nutrition

Article Title: Modulating starch digestion kinetics via feed processing: Implications for growth and metabolism in weaned pigs

doi: 10.1016/j.aninu.2025.08.011

Figure Lengend Snippet: Effect of corn processing on relative mRNA level for mTOR , 4E-BP1 , p70S6K and protein abundances of mTOR, phosphorylated mTOR (p-mTOR), eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), phosphorylated 4E-BP1 (p-4E-BP1), p70 ribosomal protein S6 kinase (p70S6K) and phosphorylated p70S6K (p-p70S6K) in the longissimus thoracis of piglets. Results are presented as means ± standard error of the mean (SEM), n = 4. Data columns with different letters were significantly different ( P ≤ 0.05).

Article Snippet: The membranes were blocked at room temperature, followed by incubation at 4 °C overnight with the following primary antibodies: mammalian target of rapamycin (mTOR, catalog No. 2983, Cell Signaling Technology, Danvers, MA, USA), phosphorylated mTOR (p-mTOR, catalog No. 5536, Cell Signaling Technology, Danvers, MA, USA), eukaryotic initiation factor 4E-binding protein 1 (4E-BP1, catalog No. 9644, Cell Signaling Technology, Danvers, MA, USA), phosphorylated 4E-BP1 (p-4E-BP1, catalog No. 2855, Cell Signaling Technology, Danvers, MA, USA), p70 ribosomal protein S6 kinase (p70S6K, catalog No. 2708, Cell Signaling Technology, Danvers, MA, USA), phosphorylated p70S6K (p-p70S6K, catalog No. 9234, Cell Signaling Technology, Danvers, MA, USA), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH, catalog No. 5174, Cell Signaling Technology, Danvers, MA, USA).

Techniques: Binding Assay

Journal: Redox Biology

Article Title: Aryl hydrocarbon receptor in club cells drives Th17-mediated lung injury following inhalation exposure to environmentally persistent free radicals

doi: 10.1016/j.redox.2026.104105

Figure Lengend Snippet: Generation and validation of club cell-specific AHR knockout mice ( Ahr ΔCC). (a) Schematic of breeding strategy to generate Ahr ΔCC mice by crossing Ahr fl/fl mice with Scgb1a1-CreER TM mice, followed by tamoxifen induction. (b) Immunofluorescence staining showing club cell marker CC10 (green), AHR (red) and DAPI (blue) in lung sections of Cre-negative Ahr fl/fl LM control (top panel) and Ahr ΔCC (bottom panel) mice. (c) Representative flow cytometry plots of lung epithelial cells gated as CD45 − CD31 − EpCAM + CC10 + cells isolated from lungs of LM (left) or Ahr ΔCC (center) mice and Fluorescence-minus-one (FMO) control for AHR staining (right). (d) Quantification of the percentage of AHR + CC10 + cells in the lungs of LM (white bar) and Ahr ΔCC (gray bar) mice. Data represent mean ± SEM, n = 3-4 mice per group. Statistical significance was determined using Student's t-test; ∗p < 0.05.

Article Snippet: Male Ahr tm3.1Bra /J mice carrying a floxed exon 2 allele of the Ahr gene (JAX stock #006203) and female B6N.129S6(Cg)- Scgb1a1 tm1(cre/ERT)Blh /J mice expressing tamoxifen-inducible Cre recombinase under the control of the club cell-specific Scgb1a1 promoter (JAX stock #016225) were obtained from Jackson Laboratory.

Techniques: Biomarker Discovery, Knock-Out, Immunofluorescence, Staining, Marker, Control, Flow Cytometry, Isolation, Fluorescence

Journal: JID Innovations

Article Title: The 4E-BP1 deletion modestly mitigates mTORC1-deficient epidermal barrier defects

doi: 10.1016/j.xjidi.2026.100453

Figure Lengend Snippet: The 4E-BP1 depletion slightly rescues the skin barrier function in Rap EKO mice. ( a ) Schematic representation of the floxed Rptor locus and complete Eif4ebp1 knockout, showing PCR fragment lengths before and after recombination. Genomic DNA PCR analysis from mouse tails confirms successful recombination of the floxed Rptor region in the presence of K14-driven Cre and complete Eif4ebp1 knockout. ( b ) Western blot analysis of 4E-BP1 protein expression in back skin from indicated genotypes. ( c ) Macroscopic appearance and body weight measurements of control, Rap EKO , and dKO newborn mice at P0. ( d ) Representative toluidine blue dye penetration assay with newborn mice and the quantification of the blue stained area (n = 5). ( e ) Representative H&E-stained sections of back skin and tongue from control, Rap EKO , and dKO newborns at P0. Dashed lines indicate the basement membrane. Bar = 100 μm. Right panels show quantification of epidermal thickness and HF density (n = 5). ( f ) Left: immunohistochemical staining for p-S6 and p-4E-BP1 in back skin sections at P0. Bar = 50 μm. Right: quantitative analysis of p-S6 and p-4E-BP1 immunoreactivity (n = 5). Dashed lines indicate the basement membrane. Data are presented as mean ± SEM; each dot represents an individual mouse. Statistical significance was determined by 2-way ANOVA with multiple comparisons. ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001, and ∗∗∗∗ P < .001. dKO denotes Rap EKO / Eif4ebp1 −/− , e denotes epidermis, and d denotes dermis. dKO, double-knockout; HF, hair follicle; K14, keratin 14; ns, not significant; p-4E-BP1, phosphorylated 4E-BP1; P0, postnatal day 0; P2, P0, postnatal day 2; p-S6, phosphorylated S6; WT, wild-type.

Article Snippet: Primary antibodies and dilutions included Ki-67 (1:200, Abcam, ab15580), K14 (1:500, Abcam, ab181595), loricrin (1:200, Invitrogen, PA5-30583), keratin 10 (1:200, Santa Cruz, SC-23877), FLG (1:250, BioLegend, #905804), phosphorylated S6 (1:200, Cell Signaling Technology, #5364s), and phosphorylated 4EBP1 (1:200, Cell Signaling Technology, #2855).

Techniques: Knock-Out, Western Blot, Expressing, Control, Staining, Membrane, Immunohistochemical staining, Double Knockout