anti β catenin  (Servicebio Inc)

Journal: Bioactive Materials

Article Title: Dynamic hydrogels orchestrate the differentiation fate of mesenchymal stem cells through epigenetic regulation of SETD7 to accelerate bone defect repair

doi: 10.1016/j.bioactmat.2026.01.019

Figure Lengend Snippet: SETD7-mediated β-catenin methylation enhances its nuclear accumulation and requires binding to nuclear YAP for osteogenic activity. (a) GO analysis of predicted miRNA targets (top 20 terms). (b) Co-IP of cytoplasmic β-catenin complexes from hMSCs in HA-CA and HA-ADA hydrogels, immunoblotted for SETD7 and methyl-lysine. (c) Nuclear β-catenin and H3 levels. (d, e) Quantification of (b) and (c). (f) Co-IP analysis following SETD7 overexpression (MOI = 20, 12 h transduction, 48 h culture). (g) Nuclear β-catenin levels after SETD7 overexpression. (h, i) Quantification of (f) and (g). (j) Co-IP analysis following SETD7 knockdown (MOI = 10, 24 h transduction, 48 h culture). (k) Nuclear β-catenin levels after SETD7 silencing. (l, m) Quantification of (j) and (k). (n, o) Nuclear YAP and H3 expression with quantification. (p, q) Co-IP analysis of nuclear YAP-β-catenin interaction in hMSCs cultured in HA-CA and HA-ADA hydrogels. (r) β-catenin/YAP co-localization by immunofluorescence. (s) β-catenin and YAP staining after gene silencing. (t, u) ARS staining and quantification of osteogenic differentiation following knockdown. n = 3. Data are presented as mean ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: After blocking with 5 % non-fat milk for 1 h at room temperature, membranes were incubated with primary antibodies including β-catenin (1:800, Santa Cruz Biotechnology, #sc-7963), YAP (1:1000, ABclonal, #A19134), SETD7 (1:1000, Proteintech, #24840-1-AP), methylated lysine (1:1200, Abcam, #ab23366), Runx2 (1:1000, ABclonal, #A2851), OCN (1:1000, ABclonal, #A20800), and PPARγ (1:1000, ABclonal, #A11183) overnight at 4 °C, followed by HRP-conjugated secondary antibodies for 1 h at room temperature.

Techniques: Methylation, Binding Assay, Activity Assay, Co-Immunoprecipitation Assay, Over Expression, Transduction, Knockdown, Expressing, Cell Culture, Immunofluorescence, Staining

Journal: Bioactive Materials

Article Title: Dynamic hydrogels orchestrate the differentiation fate of mesenchymal stem cells through epigenetic regulation of SETD7 to accelerate bone defect repair

doi: 10.1016/j.bioactmat.2026.01.019

Figure Lengend Snippet: Schematic illustration of the HA-ADA hydrogel system for enhanced bone regeneration through dynamic matrix-mediated mechanotransduction. (a) Experimental workflow. (b) Chemical composition of hydrogels showing HA-ADA or HA-CA polymers decorated with RGD motifs, which crosslink with Ac-β-CD under blue light to form distinct network architectures. (c) Comparative illustration of hydrogel performance in bone regeneration. HA-ADA hydrogels exhibit high network adaptability that enables cell spreading through dynamic “gate opening” mechanisms involving actin polymerization and F-actin bundle formation, leading to enhanced bone regeneration. In contrast, HA-CA hydrogels display low network adaptability with restricted “gate closed” states that limit cell spreading and result in reduced bone regeneration capacity. (d) Molecular mechanism underlying HA-ADA hydrogel-promoted osteogenesis. The dynamic matrix downregulates miR-376a-3p and miR-127-5p expression, thereby relieving their repression of SETD7. Elevated SETD7 subsequently methylates β-catenin, facilitating YAP/β-catenin signaling cascade activation to drive osteogenic differentiation.

Article Snippet: After blocking with 5 % non-fat milk for 1 h at room temperature, membranes were incubated with primary antibodies including β-catenin (1:800, Santa Cruz Biotechnology, #sc-7963), YAP (1:1000, ABclonal, #A19134), SETD7 (1:1000, Proteintech, #24840-1-AP), methylated lysine (1:1200, Abcam, #ab23366), Runx2 (1:1000, ABclonal, #A2851), OCN (1:1000, ABclonal, #A20800), and PPARγ (1:1000, ABclonal, #A11183) overnight at 4 °C, followed by HRP-conjugated secondary antibodies for 1 h at room temperature.

Techniques: Expressing, Activation Assay

Journal: Non-coding RNA Research

Article Title: Exosomal miRNA-218–5p derived from low-passage dermal papilla cells modulates hair follicle growth and development

doi: 10.1016/j.ncrna.2026.01.004

Figure Lengend Snippet: MiR-218-5p regulated HF growth- and development-related gene expression in HFSCs. (A) MiR-218–5p expression levels in HFSCs after transfection with miR-218–5p mimics or the inhibitor (unpaired two-tailed t -test, n = 3). (B) Expression of HF development-related genes in HFSCs is regulated by miR-218–5p. (C) β-Catenin and SFRP2 protein expression in HFSCs after treatment with miR-218–5p mimics or inhibitor (unpaired two-tailed t -test, n = 3). ∗ P < 0.05, ∗∗ P < 0.01.

Article Snippet: Anti-SFRP2 rabbit polyclonal antibody (Proteintech Biotech, Cat No. 12189-1-AP), anti-β-catenin polyclonal antibody (Proteintech, China, Cat No. 51067-2-AP), and anti-GAPDH mouse monoclonal antibody (Proteintech, China, Cat No. 60004-1-Ig) were the primary antibodies.

Techniques: Gene Expression, Expressing, Transfection, Two Tailed Test

Journal: Frontiers in Oncology

Article Title: Study of ß-catenin signaling pathway modulated by PTHrP in cell and animal colorectal cancer models

doi: 10.3389/fonc.2026.1773635

Figure Lengend Snippet: Molecular mechanisms triggered by PTHrP in CRC cells leading to nuclear β-catenin localization and its Wnt-independent activation. (A) Caco-2 cells were treated with PTHrP (10 -8 M) or its vehicle for 1 hour, and β-catenin phosphorylation at Ser552 was assessed by Western blot analysis. GAPDH was used as a loading control. (B) HCT116 cells were exposed to PTHrP (10 -8 M) for the indicated times, and β-catenin phosphorylation levels at Ser552 were analyzed by Western blot analysis, using GAPDH and actin as loading controls. (C) subcellular localization of β-catenin was assessed by immunocytochemistry technique in HCT116 cells treated with PTHrP for 90 minutes or 3 hours. The arrow indicates an increase in nuclear accumulation of β-catenin after 90 minutes of treatment. Scale bar = 30 µm. (D) Caco-2 and HCT116 cells were pretreated with the β-catenin-responsive transcription inhibitor iCRT14 or its vehicle (DMSO) and subsequently exposed to PTHrP (10 -8 M) for 5 days or 24 hours, respectively. Trypan blue dye was used to evaluate the number of viable cells. Data are expressed as mean ± SD. For western blot analysis, statistical significance was determined from two independent biological replicates (n=2). For immunocytochemistry analyses, CTCF was quantified from ten random microscopic fields. When using the trypan blue dye exclusion technique, statistical significance was determined from two independent biological replicates (n=2), three technical replicates each. *p< 0.05; **p< 0.01; ***p< 0.001. DMSO: dimethylsulfoxide. PTHrP: parathyroid hormone-related peptide.

Article Snippet: The samples were then incubated overnight at 4 °C in the presence or absence (negative control) of anti-β-catenin antibody (Fisher Scientific S.L., Spain).

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

Journal: Frontiers in Oncology

Article Title: Study of ß-catenin signaling pathway modulated by PTHrP in cell and animal colorectal cancer models

doi: 10.3389/fonc.2026.1773635

Figure Lengend Snippet: PTHrP attenuates oxaliplatin-induced cytotoxicity through β-catenin signaling. (A) HCT116 cells were pretreated with PTHrP (10 -8 M) or vehicle and subsequently exposed to oxaliplatin (10 µM), and cell viability was evaluated after 24 h. (B) HCT116 cells were pre-incubated with iCRT14 (50 μM) for 30 minutes and then treated with PTHrP 10– 8 M and finally, with oxaliplatin (10 μM) for 24 hours. The number of viable cells was counted by trypan blue staining [left panel (A, B) ] and neutral red uptake assay [right panel (A, B) ]. (C) HCT116 cells were treated with TCM or CCM, previously obtained from endothelial cells treated or not with PTHrP (10 –8 M) for 16 hours, respectively. Subsequently, the tumor cells were incubated with 10 µM oxaliplatin in 1% FBS for 24 hours (left and middle panel). HCT116 cells were preincubated with iCRT14, followed by the treatment with TCM or CCM and then oxaliplatin for 24 hours (right panel). DMSO was used as the vehicle of the inhibitor. The number of viable cells was determined by the trypan blue dye exclusion technique (left and right panel) and neutral red uptake assay (middle panel). Data are expressed as mean ± SD. When using the trypan blue dye exclusion technique, statistical significance was determined from two independent biological replicates (n=2), three technical replicates each. For neutral red uptake assay, statistical significance was determined from three independent biological replicates (n=3), five technical replicates each. *p<0.05; **p<0.01; ***p<0.001. CCM, conditioned medium from HMEC-1 without PTHrP collected at 16 hours; TCM, conditioned medium of HMEC-1 with 16 hours of PTHrP treatment; DMSO, dimethylsulfoxide; iCRT14, specific inhibitor of β-catenin transcriptional activity; FBS, fetal bovine serum; PTHrP, parathyroid hormone-related peptide.

Article Snippet: The samples were then incubated overnight at 4 °C in the presence or absence (negative control) of anti-β-catenin antibody (Fisher Scientific S.L., Spain).

Techniques: Incubation, Staining, Activity Assay

Journal: Frontiers in Oncology

Article Title: Study of ß-catenin signaling pathway modulated by PTHrP in cell and animal colorectal cancer models

doi: 10.3389/fonc.2026.1773635

Figure Lengend Snippet: The β-catenin protein levels analysis in vivo . (A) representative images (600x) and quantification of β-catenin immunohistochemical staining in tumor tissues derived from CT-26 cells in Balb/c mice. (B) representative images (400×) and quantification of β-catenin immunohistochemical staining in HCT116 xenografts generated in immunodeficient nude mice. The β-catenin subcellular localization is indicated by black arrows. Data are expressed as mean ± SD. Statistical significance was determined from the analysis of ten random fields per section, from three independent tumor sections per animal. *p< 0.05; **p< 0.01; ***p< 0.001. C, vehicle of PTHrP; C (-), negative control; PTHrP, parathyroid hormone-related peptide; Control, without oxaliplatin.

Article Snippet: The samples were then incubated overnight at 4 °C in the presence or absence (negative control) of anti-β-catenin antibody (Fisher Scientific S.L., Spain).

Techniques: In Vivo, Immunohistochemical staining, Staining, Derivative Assay, Generated, Negative Control, Control

Journal: Frontiers in Psychiatry

Article Title: Bioinformatics analysis of the mechanisms and efficacy of the Bushen Anzhi recipe in treating aging-related insomnia

doi: 10.3389/fpsyt.2026.1770410

Figure Lengend Snippet: Behavioral assessments and analysis of Wnt pathway-related protein expression. (A) Water maze trajectory; (B) Open-field trajectory; (C) Time to escape latency; (D) Time in quadrant 4; (E) Times of crossing the platform; (F) Average speed; (G) Times of climbing a wall; (H) GSK-3β content; (I) western blot bands of β-catenin and Wnt3a; (J) The level of β-catenin; (K) The level of Wnt3a. ARI, aging-related insomnia; BSAZ, Bushen Anzhi recipe; ### p < 0.001, Con vs. ARI. * p < 0.05, ** p < 0.01, *** p < 0.001, ARI vs. ARI-BSAZ.

Article Snippet: Samples were added to a pre-cast polyacrylamide gel, electrophoresed in a Running Buffer containing 10% SDS, transferred to PVDF membrane, and Anti-Wnt3a (1: 800, GB153750 , Servicebio, China), Anti-β-catenin(1:1000, GB150016 , Servicebio, China), Anti-β-tubulin(1:1000, GB15140, Servicebio, China) were incubated overnight, and the secondary antibody was added, and the automatic luminometer was used.

Techniques: Expressing, Western Blot

Journal: Cancer Medicine

Article Title: STEAP1 Suppresses Oral Squamous Cell Carcinoma by Targeting Wnt/β‐Catenin Signalling and EMT

doi: 10.1002/cam4.71862

Figure Lengend Snippet: STEAP1 Effect on the wnt/β‐catenin signalling pathway in OSCC cell lines. (A–J) The effect of STEAP1 on the wnt/β‐catenin signalling pathway in SAS and Tca‐8113 cells was assessed and quantitatively analysed by Western Blot. (* p < 0.05, ** p < 0.01, **** p < 0.0001).

Article Snippet: China); a mouse anti‐human β‐actin antibody (TA‐09, ZSBIO, China); a rabbit anti‐human P‐GSK‐3β antibody (BM4837, BOSTER, China); a rabbit anti‐human GSK‐3β antibody (A00791‐3, BOSTER, China); a rabbit anti‐human β‐catenin antibody (PA1212, BOSTER, China); primary rabbit anti‐human c‐Myc antibody ( T55150 , Abmart, China); primary rabbit anti‐human Axin2 antibody ( R23574 , ZENBIO, China); secondary goat anti‐mouse IgG antibody (ZB2305, ZSBIO, China); secondary goat anti‐rabbit IgG antibody (ZB2301, ZSBIO, China).

Techniques: Western Blot

Journal: bioRxiv

Article Title: Bacterial internalins exploit E-cadherin to promote head and neck tumor metastasis and drug resistance

doi: 10.64898/2026.04.20.719623

Figure Lengend Snippet: (A-B) β-catenin localization in TIGK cells treated with InlB (A) or InlA (B) for 2 h or overnight was assessed by immunofluorescence microscopy. Ctrl: PBS. Scale bars: 20 μm. (C) Immunoblot analysis of cytoplasmic and nuclear β-catenin levels in TIGK cells following overnight InlB treatment. Ctrl: PBS. (D) Immunoblot analysis of β-catenin phosphorylation in TIGK cells treated with InlB for 2 h or overnight. Ctrl: PBS.

Article Snippet: Primary antibodies used in this study include anti-His (Invitrogen, cat. no. MA1-21315); E-cadherin (R&D Systems, cat. no. AF648); β-catenin (R&D Systems, cat. no. MAB1329); AKT (Cell Signaling Technology, cat. no. 9272); phospho-AKT (Ser473; cat. no. 9271); p38 (cat. no. 9212); phospho-p38 (Thr180/Tyr182; cat. no. 9211); JNK (cat. no. 9252); phospho-JNK (Thr183/Tyr185; cat. no. 9251); NF-κB p65 (cat. no. 8242); phospho-NF-κB p65 (Ser536; cat. no. 3033); c-Jun (cat. no. 9165); phospho-c-Jun (Ser63; cat. no. 9164); ERK1/2 (cat. no. 9102); phospho-ERK1/2 (Thr202/Tyr204; cat. no. 4370); and β-actin (cat. no. 3700) (all from Cell Signaling Technology unless otherwise indicated).

Techniques: Immunofluorescence, Microscopy, Western Blot, Phospho-proteomics

Journal: bioRxiv

Article Title: Bacterial internalins exploit E-cadherin to promote head and neck tumor metastasis and drug resistance

doi: 10.64898/2026.04.20.719623

Figure Lengend Snippet: InlA and InlB bind E-cadherin, triggering β-catenin stabilization and nuclear translocation, which induces EMT transcription factors (Slug, Twist, ZEB1) and MMP9, promoting metastasis. Concurrently, internalin-E-cadherin engagement activates downstream ROCK, p38 and JNK MAPK signaling, attenuating cisplatin-induced apoptosis through upregulation of Bcl-2 and suppression of Bax, ultimately conferring chemoresistance. These coordinated pathways mechanistically link P. gingivalis infection to cancer progression and therapeutic resistance. Green arrows denote activation; red blocked arrows denote inhibition.

Article Snippet: Primary antibodies used in this study include anti-His (Invitrogen, cat. no. MA1-21315); E-cadherin (R&D Systems, cat. no. AF648); β-catenin (R&D Systems, cat. no. MAB1329); AKT (Cell Signaling Technology, cat. no. 9272); phospho-AKT (Ser473; cat. no. 9271); p38 (cat. no. 9212); phospho-p38 (Thr180/Tyr182; cat. no. 9211); JNK (cat. no. 9252); phospho-JNK (Thr183/Tyr185; cat. no. 9251); NF-κB p65 (cat. no. 8242); phospho-NF-κB p65 (Ser536; cat. no. 3033); c-Jun (cat. no. 9165); phospho-c-Jun (Ser63; cat. no. 9164); ERK1/2 (cat. no. 9102); phospho-ERK1/2 (Thr202/Tyr204; cat. no. 4370); and β-actin (cat. no. 3700) (all from Cell Signaling Technology unless otherwise indicated).

Techniques: Translocation Assay, Infection, Activation Assay, Inhibition