Journal: iScience

Article Title: Sleeve gastrectomy improves cognition by enhancing central ERK/CREB/BDNF pathway through increased GIP secretion

doi: 10.1016/j.isci.2026.116292

Figure Lengend Snippet: Sleeve gastrectomy reduces neuronal loss and pTau pathology in the hippocampus of AD mice (A) Representative Nissl staining of the hippocampus (scale bars: 200 μm) with higher-magnification views of the CA3 region (scale bars: 20 μm). (B) Western blot analysis of hippocampal Tau, phosphorylated Tau (pTau), and β-actin protein levels. (C) Quantification of surviving neurons in the hippocampal CA3 region ( n = 3 per group). (D) Ratio of pTau to total Tau based on grayscale densitometry ( n = 3 per group). Data are presented as mean ± SD. ∗∗ p < 0.01, ∗∗∗∗ p < 0.0001 vs. WT sham group; ## p < 0.01, ### p < 0.001 vs. AD sham group.

Article Snippet: Anti-β-actin antibody , Servicebio , Cat# GB11001; RRID: AB_2801259.

Techniques: Staining, Western Blot

Journal: iScience

Article Title: Sleeve gastrectomy improves cognition by enhancing central ERK/CREB/BDNF pathway through increased GIP secretion

doi: 10.1016/j.isci.2026.116292

Figure Lengend Snippet: Sleeve gastrectomy activates the hippocampal ERK/CREB/BDNF signaling pathway in mice (A) Representative immunoblots of hippocampal pERK, ERK, pCREB, CREB, BDNF, and β-actin. (B) Quantitative ratio of BDNF to β-actin protein expression ( n = 3 per group). (C) pERK to total ERK ratio ( n = 3 per group). (D) pCREB to total CREB ratio ( n = 3 per group). Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01 vs. WT sham group; # p < 0.05, ## p < 0.01 vs. AD sham group.

Article Snippet: Anti-β-actin antibody , Servicebio , Cat# GB11001; RRID: AB_2801259.

Techniques: Western Blot, Expressing

Journal: iScience

Article Title: Sleeve gastrectomy improves cognition by enhancing central ERK/CREB/BDNF pathway through increased GIP secretion

doi: 10.1016/j.isci.2026.116292

Figure Lengend Snippet: GIP receptor silencing inhibits the ERK/CREB/BDNF pathway in hippocampal HT22 cells (A) Representative immunoblots of pTau, Tau, GIPR, pTrkB, TrkB, pERK, ERK, pCREB, CREB, BDNF, and β-actin (loading control) under four treatments: NC, Aβ, Aβ+GIP, and Aβ+GIP+siGIPR. (B) pTau to Tau ratio ( n = 3 per group). (C) pTrkB to TrkB ratio ( n = 3 per group). (D) pCREB to CREB ratio ( n = 3 per group). (E) pERK to ERK ratio ( n = 3 per group). (F) BDNF to β-actin ratio ( n = 3 per group). Data are presented as mean ± SD. ∗ p < 0.05, ∗∗∗ p < 0.001 vs. NC group; # p < 0.05, ## p < 0.01 vs. Aβ group; & p < 0.05, && p < 0.01 vs. Aβ+GIP group.

Article Snippet: Anti-β-actin antibody , Servicebio , Cat# GB11001; RRID: AB_2801259.

Techniques: Western Blot, Control

Journal: iScience

Article Title: Sleeve gastrectomy improves cognition by enhancing central ERK/CREB/BDNF pathway through increased GIP secretion

doi: 10.1016/j.isci.2026.116292

Figure Lengend Snippet: Combined GIP and GLP-1 treatment enhances ERK/CREB/BDNF pathway activation and reduces Tau phosphorylation in HT22 cells (A) Representative immunoblots of pTau, Tau, GIPR, GLP-1R, pTrkB, TrkB, pERK, ERK, pCREB, CREB, BDNF, and β-actin under five treatment conditions: NC (negative control), Aβ, Aβ + GLP-1, Aβ + GIP, and Aβ + GLP-1 + GIP. (B) pTau/Tau ratio ( n = 3 per group). (C) GLP-1R/β-actin ratio ( n = 3 per group). (D) GIPR/β-actin ratio ( n = 3 per group). (E) pERK/ERK ratio ( n = 3 per group). (F) pCREB/CREB ratio ( n = 3 per group). (G) pTrkB/TrkB ratio ( n = 3 per group). Data represent mean ± SD; ∗ p < 0.05, ∗∗∗∗ p < 0.0001 vs. NC; # p < 0.05, ### p < 0.001 vs. Aβ; & p < 0.05 vs. Aβ + GIP group.

Article Snippet: Anti-β-actin antibody , Servicebio , Cat# GB11001; RRID: AB_2801259.

Techniques: Activation Assay, Phospho-proteomics, Western Blot, Negative Control

Journal: Cancer Pathogenesis and Therapy

Article Title: Metabolic pathways and chemotherapy resistance in acute myeloid leukemia (AML): Insights into Enoyl-CoA hydratase domain-containing protein 3 ( ECHDC3 ) as a potential therapeutic target

doi: 10.1016/j.cpt.2025.08.002

Figure Lengend Snippet: Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.

Article Snippet: Western blotting was performed to determine the expression of mitochondrial proteins, using the Mitophagy Antibody Sampler Kit (Cat# 43110, Cell Signaling Technology [CST], MA, USA) and an anti-β-actin mouse monoclonal antibody (Cat# 3700, CST, MA, USA).

Techniques: Knockdown, Staining, Fluorescence, Membrane, Quantitative RT-PCR, Quantitation Assay, Activity Assay, Western Blot, Control, Reverse Transcription Polymerase Chain Reaction, Real-time Polymerase Chain Reaction