integrin α v β 3  (R&D Systems)

Journal: eBioMedicine

Article Title: Parvimonas micra exacerbates periodontitis by infiltrating host cells through TmpC and circumventing lysosomal elimination via AppA

doi: 10.1016/j.ebiom.2026.106187

Figure Lengend Snippet: P. micra interacts with PDLSCs through TmpC-integrin α v β 3 axis. ( A ) Schematic representation of His pull-down. ( B ) Co-IP assay showing the interaction between purified His-TmpC and integrin α v β 3 of PDLSCs. ( C ) Sensorgrams of integrin α v β 3 binding to immobilised TmpC and K D value. ( D ) The interaction between TmpC (blue), integrin α v (green) and integrin β 3 (red), as predicted by molecular docking. ( E–F ) Bacterial attachment assay revealing altered bacterial recovery rate in PDLSCs treated with siIntegrin α v+ β 3 ( E ) or Cyclo ( F ). ( G–H ) Flow cytometry showing the percentages of invaded PDLSCs treated with siIntegrin α v+ β 3 ( G ) or Cyclo ( H ). ( I ) Knockdown of integrin α v β 3 altered downstream pFAK and the activation of NF-κB and ERK1/2 signalling pathways triggered by P. micra . β-actin was set as control. ( J ) Western blot showing altered activation of NF-κB and ERK1/2 signalling pathways triggered by P. micra in PDLSCs pretreated with Cyclo. β-actin was set as control. ( K ) Representative image and quantification of ALP staining in Cyclo-pretreated PDLSCs infected with P. micra WT or P. micra ΔtmpC . ( L ) Representative image and quantification of ARS staining of PDLSCs with blocked TmpC-integrin α v β 3 interaction. ( M ) Western blot of Col1, ALPL, Runx2 in Cyclo-pretreated PDLSCs infected with P. micra WT or P. micra ΔtmpC . GAPDH was set as control. ( N ) Flow cytometric analysis of FDAA-labelled P. micra internalisation in Cyclo-pretreated PDLSCs. ( O ) Schematic diagram showing the experimental design and timeline of rat models infected with P. micra and/or treated with Cyclo. ( P ) Quantitative analyses of CEJ-ABC, BV/TV, BMD and Tb.Sp. of the alveolar bone. Data are represented as the mean ± SD of three independent experiments ( n = 3) in (E–N) and six independent experiments ( n = 6) in (P). P values were determined by two-tailed unpaired Student's t -test in (E–H) and one-way ANOVA test in (I–N, P). ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; ns, not significant.

Article Snippet: Commercially available integrin α v β 3 (R&D Systems, 3050-AV-050) was diluted in sodium acetate (pH 5.0) and passed over the sensor chip in various concentrations from 0 μM to 160 μM, with the 5 μM concentration as internal control.

Techniques: Co-Immunoprecipitation Assay, Purification, Binding Assay, Flow Cytometry, Knockdown, Activation Assay, Control, Western Blot, Staining, Infection, Two Tailed Test

Journal: bioRxiv

Article Title: IR-B deficiency and fatty acid dysregulation accelerate prostate cancer progression via PI3K/AKT signaling

doi: 10.64898/2026.01.30.702723

Figure Lengend Snippet: (A) Volcano plot showing differentially expressed genes between LL H (control) and pLL +H prostate DLP lobes. (B) Hierarchical clustering and heatmap of significantly differentially expressed genes; enriched gene ontology (GO) terms indicated. (C) Bubble plot of enriched KEGG pathways for upregulated genes. (D) Real-time PCR quantification of IRS-1, IRS-2, IRS-3, and IGF2 mRNA in LL H and pLL +H prostate DLP lobes. mean ± SEM. (E) Western blot analysis of p- IR, total IR, p- IRS, total IRS1, p- AKT, total AKT, and PI3K protein in LL, pLL + , LL H and pLL +H prostate DLP lobes. (F) Heatmap showing differential metabolites between pLL +H and LL H mice. (G) Classification of metabolite type in prostate DLP lobes of LL H and pLL +H mice. (H) Volcano plot of significantly differential metabolites; fatty acids highlighted.

Article Snippet: The following primary antibodies were used: IRS, phospho-IRS1(Tyr896), GSK3β and phospho-GSK3β(Ser9), GPR120, GLUT1, Bcl-2, BAX (Abbkine, USA); IR and phospho-IR, AR, AKT1 and phospho-AKT, PI3K p85 alpha, GAPDH (Proteintech, Wuhan, China); Ki-67 (Cell Signaling Technology, USA); GLUT12 (Boster Bioengineering Co., Ltd., Wuhan); GSK3α/β and phospho-GSK3β (Y216) and phosphor-GSK3α (Y279) (Abcam,USA).

Techniques: Control, Real-time Polymerase Chain Reaction, Western Blot

Journal: bioRxiv

Article Title: IR-B deficiency and fatty acid dysregulation accelerate prostate cancer progression via PI3K/AKT signaling

doi: 10.64898/2026.01.30.702723

Figure Lengend Snippet: (A & B) Western blot and quantification showing AR expression reduced by ω-3 and increased by ω-6. (C & D) Western blot and quantification of p -PI3K, PI3K, p -AKT, and AKT at 3 and 6 months; ω-3 decreases phosphorylation, ω-6 increases it. (E, F, G, & H) Western blot and quantification of BCL2 and BAX at 3 and 6 months. ω-3 increases pro-apoptotic BAX and decreases anti-apoptotic BCL2, ω-6 shows opposite pattern. (I & J) Western blot of cultured cells treated with EPA, DHA, or AA, corfirming protein expression treads. Data mean ± SEM. *p<0.05, **p<0.01, ***p<0.001.

Article Snippet: The following primary antibodies were used: IRS, phospho-IRS1(Tyr896), GSK3β and phospho-GSK3β(Ser9), GPR120, GLUT1, Bcl-2, BAX (Abbkine, USA); IR and phospho-IR, AR, AKT1 and phospho-AKT, PI3K p85 alpha, GAPDH (Proteintech, Wuhan, China); Ki-67 (Cell Signaling Technology, USA); GLUT12 (Boster Bioengineering Co., Ltd., Wuhan); GSK3α/β and phospho-GSK3β (Y216) and phosphor-GSK3α (Y279) (Abcam,USA).

Techniques: Western Blot, Expressing, Phospho-proteomics, Cell Culture

Journal: bioRxiv

Article Title: IR-B deficiency and fatty acid dysregulation accelerate prostate cancer progression via PI3K/AKT signaling

doi: 10.64898/2026.01.30.702723

Figure Lengend Snippet: Left: Dysregulation of IR isoforms mediates cell proliferation and glucose metabolism via PI3K/AKT signaling in Hi-Myc mice. Right: IR-B knockout leads to glucose metabolism disorder and compensatory increase of ω-3 polyunsaturated fatty acids, which upregulate GPR120 expression and enhance glucose uptake through GLUT1.

Article Snippet: The following primary antibodies were used: IRS, phospho-IRS1(Tyr896), GSK3β and phospho-GSK3β(Ser9), GPR120, GLUT1, Bcl-2, BAX (Abbkine, USA); IR and phospho-IR, AR, AKT1 and phospho-AKT, PI3K p85 alpha, GAPDH (Proteintech, Wuhan, China); Ki-67 (Cell Signaling Technology, USA); GLUT12 (Boster Bioengineering Co., Ltd., Wuhan); GSK3α/β and phospho-GSK3β (Y216) and phosphor-GSK3α (Y279) (Abcam,USA).

Techniques: Knock-Out, Expressing