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Proteintech anti β actin
Anti β Actin, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+%CE%B2+actin/HNRNPA3+Antibody/pmc13019968-266-8-13
Average 93 stars, based on 24 article reviews

anti β actin - by Bioz Stars, 2026-10

93/100 stars

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Article Title: YY1/Asprosin/PFKP axis regulates glycolytic metabolic and exacerbates pathological cardiac hypertrophy.
Article Snippet: Primary antibodies as follows: anti-Asprosin (FNab09797, Finetest, AR TI CL E IN P RE SS Wuhan, China, 1:500), anti-β-MHC (22280-1-AP, Proteintech, Wuhan, China, 1:500), anti-ANP (DF6497, Affinity, Changzhou, 1:500), anti-PFKP (13389-1-AP, Proteintech, Wuhan, China,1:500), anti-PFKP (68129-1-Ig, Proteintech, Wuhan, China,1:500), anti-DTX3L (A18551, Abclonal, Wuhan, China, 1:500), anti-HA (81290-1-RR, Proteintech, Wuhan, China, 1:500), anti-Flag (66008-4-Ig, Proteintech, Wuhan, China, 1:500), anti-Myc (16286-1-AP, Proteintech, Wuhan, China, 1:500), PDK4 (12949-1-AP, Proteintech, China, 1:500), p-PDH (ab177461, Abcam, USA, 1:500), PDH (18068-1-AP, Proteintech, China, 1:500), PFKL (GTX105697, Genetex, USA, 1:500), PFKM (55028-1-AP, Proteintech, China, 1:500), Anti-β-actin (66009-1- Ig, Proteintech, China, 1:500), Anti-α-Tubulin (FNab0033, Finetest, China, 1:500), Anti-His (66005-1-Ig, Proteintech, China, 1:500), Anti-FBN1(YT1684, Immunoway, China, 1:500), and anti-Ubiquitin (Ab134953, Abcam, Cambridge, UK, 1:500).

Article Title: The GOLM1-ACLY pathway regulates macrophage-secreted EFEMP1 via H3K27ac modifications to drive tumor progression
Article Snippet: The following antibodies were used in this experiment: anti-OCT4 (11263-1-AP, Proteintech, USA), anti-SOX2 (11064-1-AP, Proteintech, USA), anti-NANOG (sc-374001, Santa Cruz, USA), anti-MYC (sc-42, Santa Cruz, USA), anti-GOLM1 (15126-1-AP, Proteintech, USA), anti-EFEMP1 (ab228797, Abcam, UK), anti-GAPDH (60004-1-Ig, Proteintech, USA), anti-IgG (30000-0-AP, Proteintech, USA), anti-β-actin (66009-1-Ig, Proteintech, USA), anti-Tubulin (10094-1-AP, Proteintech, USA) anti-acetyl-histone H3 (9927 T, CST, USA), anti-HA (AE025, ABclonal, China), anti-ACLY (15421-1-AP, Proteintech, USA), anti-P-ATP-citrate synthase (sc-374647, Santa Cruz, USA), anti-EGFR (ab52894, Abcam, UK), anti-P38 MAPK (14064-1-AP, Proteintech, USA), anti-P-p38 MAPK (28796–1-AP, Proteintech, USA), anti-AKT (60203-2-Ig, Proteintech, USA), anti-P-AKT, (80455-1-RR, Proteintech, USA) and anti-His (AE086, ABclonal, China) antibodies.

Article Title: Peroxiredoxin 4 suppresses ferroptosis in esophageal squamous cell carcinoma by activating the phosphoinositide 3-kinase signaling pathway
Article Snippet: The primary antibodies were as follows: Anti-PRDX4 (1:2,000 dilution; cat. no. 10703-1-AP), anti-E-cadherin (1:20,000 dilution; cat. no. 20874-1-AP), anti-N-cadherin (1:2,000 dilution; cat. no. 22018-1-AP), anti-Vimentin (1:20,000 dilution; cat. no. 10366-1-AP), and anti-GPX4 (1:1,000 dilution; cat. no. 30388-1-AP; all from Proteintech Group, Inc.), anti-solute carrier family 7 member 11 (SLC7A11; 1:1,000 dilution; cat. no. DF12509; Affinity Biosciences, Ltd.), anti-prostaglandin-endoperoxide synthase 2 (PTGS2; 1:1,000 dilution; cat. no. 27308-1-AP; Proteintech Group, Inc.), anti-p-PI3K (1:1,000 dilution; cat. no. AP0427; ABclonal Biotech Co., Ltd.), anti-PI3K (1:1,000 dilution; cat. no. A19742; ABclonal Biotech Co., Ltd.), anti-p-AKT (1:2,000 dilution; cat. no. 28731-1-AP; Proteintech Group, Inc.), anti-AKT (1:2,000 dilution; cat. no. 10176-2-AP; Proteintech Group, Inc.) and anti-β-actin (1:2,000 dilution; cat. no. 20536-1-AP; Proteintech Group, Inc.).

Incubation:

Article Title: Bioengineered extracellular vesicles escape lysosomal degradation and deliver Tet-PKM2 for macrophage immunometabolic reprogramming and periodontitis treatment
Article Snippet: .. After being washed, the membranes were incubated with the following primary antibodies overnight at 4 °C: anti-PKM2 (1:1000; Cell Signaling Technology, 4053S), anti-HSP70 (1:1000; Cell Signaling Technology, 4872T), anti-TSG101 (1:1000; Abcam, ab125011), anti-CD63 (1:1000; Cell Signaling Technology, SC55275), anti-calnexin (1:1000; Cell Signaling Technology, 2433T), anti-GM130 (1:1000; Cell Signaling Technology, 12480T), anti-Hif-1α (1:1000; Cell Signaling Technology, 36169T), and anti-β-actin (1:5000; Proteintech, 66009-1-Ig). .. The membranes were subsequently washed and probed with appropriate (anti-rabbit or anti-mouse) HRP-conjugated secondary antibodies (1:5000; Proteintech).

Article Title: Histone H3K9 lactylation activates the TXNIP/NLRP3 pathway to drive macrophage inflammation after spinal cord injury
Article Snippet: .. Membranes were blocked in 5% nonfat milk/TBST for 1.5 h, washed, and incubated overnight at 4 °C with primary antibodies in TBST: anti- Pankla (PTM-1401, PTM Bio, 1:1000), anti- Histone H3(HL102-01, Transgen, 1:1000), anti-β-actin (66009-1-Ig, Proteintech, 1:5000), anti-H3K9la (PTM-1421RM, PTM Bio, 1:1000), anti-H3K14la (PTM-1414, PTM Bio, 1:1000), anti-H3K18la (PTM-1406RM, PTM Bio, 1:1000), anti-H3K9ac (PTM-112RM, PTM Bio, 1:5000), anti- H3K9me (PTM-643, PTM Bio, 1:1000), anti-H3K27ac (PTM-116 RM, PTM Bio, 1:1000), anti- Caspase 1(81482-1-RR, Proteintech, 1:10000), anti- NLRP3(MA5-32255, Invitrogen, 1:1000), anti-TXNIP (14715, CST, 1:1000), anti-IL-1β(26048-1-AP, Proteintech, 1:3000), anti-TNF-α(17590-1-AP, Proteintech, 1:5000), anti-iNOS(22226-1-AP, Proteintech, 1:500). ..

Generated:

Article Title: Lactylome Reprogramming Mediates Therapeutic Response and Adaptation to Neoadjuvant Chemotherapy in Esophageal Squamous Cell Carcinoma.
Article Snippet: Anti-GAPDH (PTM-5150), anti-Flag mouse (PTM-6075), anti-pan Kla (PTM-1401RM), Jo urn al Pr -pr oo f Lactylome Profiling Reveals Mechanisms Underlying ESCC Survival Adaptation to Chemotherapy anti-PARP1 (PTM-5171), anti-β-tubulin (PTM-6414), and anti-γ-H2AX (PTM-753) antibodies were purchased from PTM BIO (Hangzhou, China). .. Anti-β-actin (66009-1- Ig), anti-Flag-rabbit (20543-1-AP), anti-HA (51064-2-AP), and anti-SIRT2 (19655-1-AP) antibodies were generated by Proteintech Group (Wuhan, China). .. Anti-pADPr (sc56198) antibody was obtained from Santa Cruz Biotechnology (Dallas, USA).

Western Blot:

Article Title: A conserved mammalian mecciRNA, mecciATP6, regulates mitochondrial homeostasis through interaction with HNRNPA3
Article Snippet: Gray-scale intensities were quantified using ImageJ software. .. The following antibodies were used in Western blotting: anti-β-actin (Transgene, HC201) and anti-HNRNPA3 (Proteintech, 25142-1-AP). ..

Article Title: Tannic acid inhibits viral replication by disrupting nucleocapsid condensation
Article Snippet: Background: Viruses continue to threaten global health, highlighting the urgent need for antiviral strategies with broad-spectrum activity.. The nucleocapsid (N) protein undergoes liquid–liquid phase separation (LLPS), a conserved process essential for viral assembly.. However, pharmacological targeting of this process remains largely unexplored.

Image Search Results

TAPC interacts with VEGFR2 and modulates downstream signaling. (a) Cell viability assay of MC38 cells treated with increasing concentrations of TAPC. (b) Immunoblot analysis of VEGFR2 and key regulators of the PI3K–AKT signaling pathway (PI3K, AKT, and STAT3) in MC38 cells treated with PEG-PO or TAPC (5 and 10 μM). β-Actin was used as a loading control. (c) Pull-down assay of VEGFR2 from MC38 cell lysates using biotinylated TAPC, beads-only sample served as control. (d) Confocal IF imaging of MC38 cells incubated with Cy5.5-labeled TAPC and stained for VEGFR2, nuclei counterstained with DAPI. Scale bars: 20 μm. (e) BLI analysis of TAPC binding to recombinant VEGFR2 using serial concentrations (100, 66.7, 44.4, 29.6, 19.8, 13.2, and 8.8 μM). (f) Molecular dynamics simulations showing predicted protein–ligand complexes (top) and binding pocket visualizations (bottom) of VEGFR2 with TAPC, NDMPFI, MBAMF, and TPFE. (g) Binding free energy calculations of these complexes, including van der Waals, electrostatic, solvation, and total energy components. (h) Extracellular acidification rate (ECAR) of MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM), with sequential addition of glucose, oligomycin, and 2-deoxyglucose (2-DG). (i) Quantification of glycolysis and glycolytic capacity in MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM) (n = 8). Data are presented as mean ± SEM. Statistical significance was assessed using one-way ANOVA with Tukey's multiple comparisons test; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Journal: Bioactive Materials

Article Title: Aminated fullerene-based nanoplatform enables synergistic VEGFR2-targeted anti-angiogenesis and tumor immunotherapy

doi: 10.1016/j.bioactmat.2026.03.016

Figure Lengend Snippet: TAPC interacts with VEGFR2 and modulates downstream signaling. (a) Cell viability assay of MC38 cells treated with increasing concentrations of TAPC. (b) Immunoblot analysis of VEGFR2 and key regulators of the PI3K–AKT signaling pathway (PI3K, AKT, and STAT3) in MC38 cells treated with PEG-PO or TAPC (5 and 10 μM). β-Actin was used as a loading control. (c) Pull-down assay of VEGFR2 from MC38 cell lysates using biotinylated TAPC, beads-only sample served as control. (d) Confocal IF imaging of MC38 cells incubated with Cy5.5-labeled TAPC and stained for VEGFR2, nuclei counterstained with DAPI. Scale bars: 20 μm. (e) BLI analysis of TAPC binding to recombinant VEGFR2 using serial concentrations (100, 66.7, 44.4, 29.6, 19.8, 13.2, and 8.8 μM). (f) Molecular dynamics simulations showing predicted protein–ligand complexes (top) and binding pocket visualizations (bottom) of VEGFR2 with TAPC, NDMPFI, MBAMF, and TPFE. (g) Binding free energy calculations of these complexes, including van der Waals, electrostatic, solvation, and total energy components. (h) Extracellular acidification rate (ECAR) of MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM), with sequential addition of glucose, oligomycin, and 2-deoxyglucose (2-DG). (i) Quantification of glycolysis and glycolytic capacity in MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM) (n = 8). Data are presented as mean ± SEM. Statistical significance was assessed using one-way ANOVA with Tukey's multiple comparisons test; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: Antibodies were listed as follows: Anti-VEGF Receptor 2 antibody [EPRER16Y] (Abcam, Cat: ab134191), Anti-PI 3 Kinase catalytic subunit gamma (Abcam, Cat: ab302958), Anti-AKT (phosphor T308) antibody (Abcam, Cat: ab38449), Anti-STAT3 antibody [EPR787Y] (Abcam, Cat: ab68153), β-Actin (13E5) rabbit mAb (CST, Cat: #4970), Anti-CD31 antibody [EPR17260-263] (Abcam, Cat: ab222783), FITC anti-mouse CD45 (Biolegend, Cat: 103108), PerCP/Cyanine5.5 anti-mouse CD4 (Biolegend, Cat: 100434), FOXP3 Monoclonal Antibody (NRRF-30), PE, eBioscience (Thermo, Cat: 12-4771-82), CD3 (Abcam, Cat: ab16669), CD4 (Servicebio, Cat: GB15064).

Techniques: Viability Assay, Western Blot, Control, Pull Down Assay, Imaging, Incubation, Labeling, Staining, Binding Assay, Recombinant

In vivo anti-tumor and anti-angiogenic effects of TAPC@CNPs. (a) Schematic illustration of the therapeutic study in Balb/c mice bearing subcutaneous MC38 tumors (n = 7). (b) Body weights of mice during treatment. (c) Photographs of excised tumors collected at endpoint. (d) Tumor growth curves during treatment. Tumor volume was calculated using the formula (length × width 2 )/2. (e) Tumor weights measured at endpoint. (f) Immunoblot analysis of VEGFR2 expression in tumor lysates from different treatment groups, β-actin was used as a reference protein. (g) IHC staining of CD31 in tumor sections from different treatment groups. Scale bar, 100 μm. (h) H&E staining of major organs (heart, liver, spleen, lung, kidney) and tumor tissues. (i) Serum ALT and AST levels measured at endpoint. Data are presented as mean ± SEM. Statistical analysis was performed by one-way ANOVA with Tukey's multiple comparisons test, ns indicates not significant, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗∗p < 0.0001.

Journal: Bioactive Materials

Article Title: Aminated fullerene-based nanoplatform enables synergistic VEGFR2-targeted anti-angiogenesis and tumor immunotherapy

doi: 10.1016/j.bioactmat.2026.03.016

Figure Lengend Snippet: In vivo anti-tumor and anti-angiogenic effects of TAPC@CNPs. (a) Schematic illustration of the therapeutic study in Balb/c mice bearing subcutaneous MC38 tumors (n = 7). (b) Body weights of mice during treatment. (c) Photographs of excised tumors collected at endpoint. (d) Tumor growth curves during treatment. Tumor volume was calculated using the formula (length × width 2 )/2. (e) Tumor weights measured at endpoint. (f) Immunoblot analysis of VEGFR2 expression in tumor lysates from different treatment groups, β-actin was used as a reference protein. (g) IHC staining of CD31 in tumor sections from different treatment groups. Scale bar, 100 μm. (h) H&E staining of major organs (heart, liver, spleen, lung, kidney) and tumor tissues. (i) Serum ALT and AST levels measured at endpoint. Data are presented as mean ± SEM. Statistical analysis was performed by one-way ANOVA with Tukey's multiple comparisons test, ns indicates not significant, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗∗p < 0.0001.

Techniques: In Vivo, Western Blot, Expressing, Immunohistochemistry, Staining

AE regulates hTERT expression and its upstream transcription factors c-Myc and E2F1 in NPC cells in a dose-dependent manner. 5–8F and C666-1 cells were treated with AE at concentrations of 0, 10, 20, and 30 μM for 48 h. (A) Protein expression levels of hTERT, c-Myc, and E2F1 were detected by Western blotting. β-actin served as the loading control. Representative blots are shown, with densitometric quantification presented as fold change relative to the control group. (B) Relative mRNA expression levels of hTERT, c-Myc, and E2F1 were detected by qRT-PCR, normalized to β-actin. All data are presented as mean ± SD, n = 3. ns P > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001 compared to the control group (0 μM).

Journal: Frontiers in Pharmacology

Article Title: Aloe-emodin inhibits nasopharyngeal carcinoma by modulating telomerase activity involving the c-Myc/E2F1 axis

doi: 10.3389/fphar.2026.1850685

Figure Lengend Snippet: AE regulates hTERT expression and its upstream transcription factors c-Myc and E2F1 in NPC cells in a dose-dependent manner. 5–8F and C666-1 cells were treated with AE at concentrations of 0, 10, 20, and 30 μM for 48 h. (A) Protein expression levels of hTERT, c-Myc, and E2F1 were detected by Western blotting. β-actin served as the loading control. Representative blots are shown, with densitometric quantification presented as fold change relative to the control group. (B) Relative mRNA expression levels of hTERT, c-Myc, and E2F1 were detected by qRT-PCR, normalized to β-actin. All data are presented as mean ± SD, n = 3. ns P > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001 compared to the control group (0 μM).

Article Snippet: Primary antibodies against hTERT (Cat# HY- P81110 ), c-Myc (Cat# 67447-1-Ig), E2F1 (Cat# GB11571-100), Ki67 (Cat# GB111499-100), Cleaved Caspase-3 (Cat# GB11532-100), and β-actin (Cat# 66009-1-Ig) were purchased from MedChemExpress, Proteintech, and Servicebio.

Techniques: Expressing, Western Blot, Control, Quantitative RT-PCR

AE suppresses NPC cell viability via the c-Myc/hTERT axis. C666-1 cells were transfected with empty vector or c-Myc overexpression plasmid (c-Myc OE), followed by 48 h treatment with 20 μM AE or DMSO. (A) qPCR verification of c-Myc overexpression efficiency. c-Myc mRNA normalized to vector group; ***P < 0.001 vs. vector. (B) Western blot demonstrating AE triggers proteasome-dependent c-Myc degradation. Cells were incubated with 20 μM AE for 48 h, with 10 μM MG132 supplemented in the final 6 h β-actin served as internal reference; **P < 0.01 vs. vector, *P < 0.05 vs. AE. (C) CCK-8 cell viability rescue assay. AE significantly reduced cell viability (***P < 0.001 vs. vector). Single c-Myc OE exerted no significant impact (ns vs. vector), whereas c-Myc overexpression partially rescued AE-mediated growth suppression ( # P < 0.05 vs. AE). (D) qPCR detection of hTERT mRNA levels. AE downregulated hTERT transcription (*P < 0.05 vs. vector). c-Myc OE significantly elevated hTERT (*P < 0.05 vs. vector), and co-transfection restored hTERT expression ( # P < 0.05 vs. AE). (E) qPCR detection of endogenous c-Myc mRNA. AE decreased basal c-Myc mRNA (*P < 0.05 vs. vector); c-Myc OE markedly upregulated c-Myc transcripts (**P < 0.01 vs. vector), and ectopic c-Myc expression partially reversed AE-induced c-Myc repression ( # P < 0.05 vs. AE). All data are presented as mean ± SD, n = 3. ns, P > 0.05; *P < 0.05, **P < 0.01, ***P < 0.001 versus vector group; # P < 0.05 versus AE single treatment group.

Journal: Frontiers in Pharmacology

Article Title: Aloe-emodin inhibits nasopharyngeal carcinoma by modulating telomerase activity involving the c-Myc/E2F1 axis

doi: 10.3389/fphar.2026.1850685

Figure Lengend Snippet: AE suppresses NPC cell viability via the c-Myc/hTERT axis. C666-1 cells were transfected with empty vector or c-Myc overexpression plasmid (c-Myc OE), followed by 48 h treatment with 20 μM AE or DMSO. (A) qPCR verification of c-Myc overexpression efficiency. c-Myc mRNA normalized to vector group; ***P < 0.001 vs. vector. (B) Western blot demonstrating AE triggers proteasome-dependent c-Myc degradation. Cells were incubated with 20 μM AE for 48 h, with 10 μM MG132 supplemented in the final 6 h β-actin served as internal reference; **P < 0.01 vs. vector, *P < 0.05 vs. AE. (C) CCK-8 cell viability rescue assay. AE significantly reduced cell viability (***P < 0.001 vs. vector). Single c-Myc OE exerted no significant impact (ns vs. vector), whereas c-Myc overexpression partially rescued AE-mediated growth suppression ( # P < 0.05 vs. AE). (D) qPCR detection of hTERT mRNA levels. AE downregulated hTERT transcription (*P < 0.05 vs. vector). c-Myc OE significantly elevated hTERT (*P < 0.05 vs. vector), and co-transfection restored hTERT expression ( # P < 0.05 vs. AE). (E) qPCR detection of endogenous c-Myc mRNA. AE decreased basal c-Myc mRNA (*P < 0.05 vs. vector); c-Myc OE markedly upregulated c-Myc transcripts (**P < 0.01 vs. vector), and ectopic c-Myc expression partially reversed AE-induced c-Myc repression ( # P < 0.05 vs. AE). All data are presented as mean ± SD, n = 3. ns, P > 0.05; *P < 0.05, **P < 0.01, ***P < 0.001 versus vector group; # P < 0.05 versus AE single treatment group.

Techniques: Transfection, Plasmid Preparation, Over Expression, Western Blot, Incubation, CCK-8 Assay, Rescue Assay, Cotransfection, Expressing

Knockdown of hTERT enhances the regulatory effects of AE on hTERT, c-Myc, and E2F1 protein expression. 5–8F and C666-1 cells were treated with Control, NC (negative control siRNA), si-hTERT (hTERT knockdown), AE (20 μM), or si-hTERT + AE for 48 h. Protein expression levels of hTERT, c-Myc, and E2F1 were analyzed by Western blotting. β-actin served as the loading control. Representative blots are shown, with densitometric quantification presented as fold change relative to the control group. Data are presented as mean ± SD, n = 3. ns P > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001 vs. control group; # P < 0.05, ## P < 0.01 vs. AE group.

Journal: Frontiers in Pharmacology

Article Title: Aloe-emodin inhibits nasopharyngeal carcinoma by modulating telomerase activity involving the c-Myc/E2F1 axis

doi: 10.3389/fphar.2026.1850685

Figure Lengend Snippet: Knockdown of hTERT enhances the regulatory effects of AE on hTERT, c-Myc, and E2F1 protein expression. 5–8F and C666-1 cells were treated with Control, NC (negative control siRNA), si-hTERT (hTERT knockdown), AE (20 μM), or si-hTERT + AE for 48 h. Protein expression levels of hTERT, c-Myc, and E2F1 were analyzed by Western blotting. β-actin served as the loading control. Representative blots are shown, with densitometric quantification presented as fold change relative to the control group. Data are presented as mean ± SD, n = 3. ns P > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001 vs. control group; # P < 0.05, ## P < 0.01 vs. AE group.

Techniques: Knockdown, Expressing, Control, Negative Control, Western Blot

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.

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

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.

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

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.

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

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.

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

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