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primary antibodies against actb (actin beta)  (ABclonal Biotechnology)


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    ABclonal Biotechnology primary antibodies against actb (actin beta)
    Primary Antibodies Against Actb (Actin Beta), supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+against+actb+(actin+beta)/primary+antibodies+against+actb++actin+beta+/pm35255774-224-6-9
    Average 90 stars, based on 1 article reviews
    primary antibodies against actb (actin beta) - by Bioz Stars, 2026-09
    90/100 stars

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    other:

    Article Title: CDK9 inhibition blocks the initiation of PINK1-PRKN-mediated mitophagy by regulating the SIRT1-FOXO3-BNIP3 axis and enhances the therapeutic effects involving mitochondrial dysfunction in hepatocellular carcinoma
    Article Snippet: Primary antibodies included those against ACTB/β-actin (ABclonal Technology, AC026; 1:200000), POLR2A (ABclonal, A11181; 1:2000), p-POLR2A-S2(ABclonal, AP0749; 1:2000), CDK9 (Cell Signaling Technology, 2316; 1:2000), SIRT1 (Cell Signaling Technology, 2493; 1:2000), p-SIRT1 (Abcam, ab76039; 1:2000), FOXO3 (Proteintech, 66428-1-lg; 1:2000), BNIP3 (ABclonal, A5683; 1:2000), PINK1 (Cell Signaling Technology, 6946; 1:2000), PRKN/parkin (Cell Signaling Technology, 4211; 1:2000), TOMM20 (Proteintech, 11802-1-AP; 1:2000), COX4I1 (ABclonal, A6564; 1:2000), pan acetyl-lysine polyclonal antibody (ABclonal, A2391; 1:2000), and MAP1LC3A (Cell Signaling Technology, 4108; 1:2000).

    Article Title: Inhibition of mitochondrial fusion via SIRT1/PDK2/PARL axis breaks mitochondrial metabolic plasticity and sensitizes cancer cells to glucose restriction therapy.
    Article Snippet: Primary antibodies included those against ACTB/ β-actin (ABclonal, AC026; 1:200000), SIRT1 (CST, D739, 1:2000), pan acetyl-lysine polyclonal antibody (ABclonal, A2391; 1:2000), GLUT1 (Proteintech, 21829–1-AP; 1:2000), PGC1-α (Proteintech, 66369–1-Ig; 1:2000), PDK2 (Proteintech, 15647–1-AP; 1:2000), GAPDH (ABclonal, AC002; 1:200000), Caspase-3 (ABclonal, A2156; 1:1000), Activecaspase-3 (ABclonal, A11021; 1:1000), OPA1 (ABclonal, A9833; 1:2000), OMA1 (ABclonal, A14437; 1:1000), YME1L1 (ABclonal, A10402; 1:2000), MFN1 (ABclonal, A9880; 1:2000), MFN2 (ABclonal, A12771; 1:2000), DRP1 (ABclonal, A2586; 1:2000), p-DRP1-S637 (ABclonal, AP0812; 1:1000), p-DRP1-S616 (ABclonal, AP1353; 1:1000), FIS1 (Proteintech, 66635–1-Ig; 1:2000), PARL (ABclonal, A8232; 1:2000), Caspase-9 (Abcam, ab202068; 1:2000).

    Article Title: Ailanthone blocks mitophagy to promote mtDNA leakage through BAX-BAK1 pores and suppress hepatocellular carcinoma cell proliferation
    Article Snippet: Primary antibodies included those against ACTB/β-Actin (ABclonal Technology, AC026; 1:200000), LC3-I/II (CST, 12741 1:1000), COX4I1 (Proteintech, 66110-1-Ig, 1:8000), PINK1 (CST, 6946, 1:1000), PRKN (CST, 4211, 1:1000), BAK1 (Proteintech, 29552-1-AP, 1:10000), BAX (Proteintech, 50599-2-lg, 1:10000), Ub (CST, 3,936, 1:1000), TNF-α (Proteintech, 60291-1-Ig, 1:8000), IL-1β (Proteintech, 16806-1-AP, 1:1000), IL-6 (Proteintech, 21865-1-AP, 1:1000).



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    Fig. 7. SP1 regulates SLC7A3 expression. A-B. mRNA expression (A) and protein level (B) of SLC7A3 in OS cells with SP1 knockdown or overexpression (n = 3). C. Arginine uptake ratio in OS cells with/without SP1 knockdown upon SLC7A3 overexpression (n = 3). D. Schematic diagram showing possible regulatory sites for SP1 in the SLC7A3 promoter predicted by the JASPAR database (top). Construction of the SLC7A3 luciferase plasmids: wild-type SLC7A3 promoter (WT) and deletion mutants lacking region 1 (ΔRegion 1), region 2 (ΔRegion 2), or both (ΔRegion 1 + 2) (bottom). E. Homology analysis of region 1 and region 2 in the SLC7A3 promoter. F. 143B cells with/without SIRPA knockdown were transfected with plasmids encoding SP1(-500/0)-Luc WT, ΔRegion1, ΔRegion2, and ΔRegion1+2. Then, luciferase levels were measured in extracts after 48 h. G-H. ChIP assay of DNA fragments containing putative region 1 and region 2 within the SLC7A3 promoter region followed by PCR. The SLC7A3 promotor region beyond SP1 regulation (CTR) and the β-actin region <t>(ACTB)</t> were used as negative controls; an anti- histone antibody and rabbit IgG were used as assay controls (G). The histogram shows the relative amount of each DNA fragment binding to SP1 (H). The data are presented as the means±SDs. *P < 0.05, **P < 0.01 by one-way ANOVA.
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    Fig. 7. SP1 regulates SLC7A3 expression. A-B. mRNA expression (A) and protein level (B) of SLC7A3 in OS cells with SP1 knockdown or overexpression (n = 3). C. Arginine uptake ratio in OS cells with/without SP1 knockdown upon SLC7A3 overexpression (n = 3). D. Schematic diagram showing possible regulatory sites for SP1 in the SLC7A3 promoter predicted by the JASPAR database (top). Construction of the SLC7A3 luciferase plasmids: wild-type SLC7A3 promoter (WT) and deletion mutants lacking region 1 (ΔRegion 1), region 2 (ΔRegion 2), or both (ΔRegion 1 + 2) (bottom). E. Homology analysis of region 1 and region 2 in the SLC7A3 promoter. F. 143B cells with/without SIRPA knockdown were transfected with plasmids encoding SP1(-500/0)-Luc WT, ΔRegion1, ΔRegion2, and ΔRegion1+2. Then, luciferase levels were measured in extracts after 48 h. G-H. ChIP assay of DNA fragments containing putative region 1 and region 2 within the SLC7A3 promoter region followed by PCR. The SLC7A3 promotor region beyond SP1 regulation (CTR) and the β-actin region <t>(ACTB)</t> were used as negative controls; an anti- histone antibody and rabbit IgG were used as assay controls (G). The histogram shows the relative amount of each DNA fragment binding to SP1 (H). The data are presented as the means±SDs. *P < 0.05, **P < 0.01 by one-way ANOVA.
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    Image Search Results


    Journal: Frontiers in Physiology

    Article Title: Transcriptomic analysis and experimental verification reveal the involvement of PI3K/AKT signaling pathway in high-altitude cognitive dysfunction

    doi: 10.3389/fphys.2026.1781613

    Figure Lengend Snippet: Primer sequences for the genes observed in qRT-PCR.

    Article Snippet: Primary antibody against β -actin were purchased from Zhongshan Golden Bridge Biological Technology Co., Ltd. (Beijing, China).

    Techniques:

    Effects of HH on the BBB integrity in mouse hippocampus. (A) Representative images of EB extravasation in the hippocampus. (B) Quantitative analysis of EB leakage. (C) Representative western blots of ZO-1 and occludin. Quantitative analysis of the ZO-1/β-actin (D) and occludin/β-actin (E) ratios. Data are presented as mean ± SD. Statistical comparisons were performed by Student’s t test. For EB, n = 6 per group; for Western blot analysis, n = 3 per group, ** p < 0.01 vs. Con group.

    Journal: Frontiers in Physiology

    Article Title: Transcriptomic analysis and experimental verification reveal the involvement of PI3K/AKT signaling pathway in high-altitude cognitive dysfunction

    doi: 10.3389/fphys.2026.1781613

    Figure Lengend Snippet: Effects of HH on the BBB integrity in mouse hippocampus. (A) Representative images of EB extravasation in the hippocampus. (B) Quantitative analysis of EB leakage. (C) Representative western blots of ZO-1 and occludin. Quantitative analysis of the ZO-1/β-actin (D) and occludin/β-actin (E) ratios. Data are presented as mean ± SD. Statistical comparisons were performed by Student’s t test. For EB, n = 6 per group; for Western blot analysis, n = 3 per group, ** p < 0.01 vs. Con group.

    Article Snippet: Primary antibody against β -actin were purchased from Zhongshan Golden Bridge Biological Technology Co., Ltd. (Beijing, China).

    Techniques: Western Blot

    Effects of HH on the expression of genes and proteins related to PI3K/AKT signaling pathway in mouse hippocampus. (A) The relative mRNA expression levels of Kdr , Spp1 , Vwf , and Vegfa screened via qRT-PCR. (B) Representative western blots of p-PI3K, PI3K, p-AKT, and AKT. Quantitative analysis of the p-PI3K/PI3K (C) and p-AKT/AKT (D) ratios. (E) Representative western blots of Nrf2, HO-1, p-NF-κB, and NF-κB. Quantitative analysis of the Nrf2/β-actin (F) , HO-1/β-actin (G) , and p-NF-κB/NF-κB (H) ratios. Data are presented as mean ± SD. Statistical comparisons were performed by Student’s t test. For qRT-PCR, n = 6 per group; for Western blot analysis, n = 3 per group, * p < 0.05, ** p < 0.01 vs. Con group.

    Journal: Frontiers in Physiology

    Article Title: Transcriptomic analysis and experimental verification reveal the involvement of PI3K/AKT signaling pathway in high-altitude cognitive dysfunction

    doi: 10.3389/fphys.2026.1781613

    Figure Lengend Snippet: Effects of HH on the expression of genes and proteins related to PI3K/AKT signaling pathway in mouse hippocampus. (A) The relative mRNA expression levels of Kdr , Spp1 , Vwf , and Vegfa screened via qRT-PCR. (B) Representative western blots of p-PI3K, PI3K, p-AKT, and AKT. Quantitative analysis of the p-PI3K/PI3K (C) and p-AKT/AKT (D) ratios. (E) Representative western blots of Nrf2, HO-1, p-NF-κB, and NF-κB. Quantitative analysis of the Nrf2/β-actin (F) , HO-1/β-actin (G) , and p-NF-κB/NF-κB (H) ratios. Data are presented as mean ± SD. Statistical comparisons were performed by Student’s t test. For qRT-PCR, n = 6 per group; for Western blot analysis, n = 3 per group, * p < 0.05, ** p < 0.01 vs. Con group.

    Article Snippet: Primary antibody against β -actin were purchased from Zhongshan Golden Bridge Biological Technology Co., Ltd. (Beijing, China).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot

    Fig. 7. SP1 regulates SLC7A3 expression. A-B. mRNA expression (A) and protein level (B) of SLC7A3 in OS cells with SP1 knockdown or overexpression (n = 3). C. Arginine uptake ratio in OS cells with/without SP1 knockdown upon SLC7A3 overexpression (n = 3). D. Schematic diagram showing possible regulatory sites for SP1 in the SLC7A3 promoter predicted by the JASPAR database (top). Construction of the SLC7A3 luciferase plasmids: wild-type SLC7A3 promoter (WT) and deletion mutants lacking region 1 (ΔRegion 1), region 2 (ΔRegion 2), or both (ΔRegion 1 + 2) (bottom). E. Homology analysis of region 1 and region 2 in the SLC7A3 promoter. F. 143B cells with/without SIRPA knockdown were transfected with plasmids encoding SP1(-500/0)-Luc WT, ΔRegion1, ΔRegion2, and ΔRegion1+2. Then, luciferase levels were measured in extracts after 48 h. G-H. ChIP assay of DNA fragments containing putative region 1 and region 2 within the SLC7A3 promoter region followed by PCR. The SLC7A3 promotor region beyond SP1 regulation (CTR) and the β-actin region (ACTB) were used as negative controls; an anti- histone antibody and rabbit IgG were used as assay controls (G). The histogram shows the relative amount of each DNA fragment binding to SP1 (H). The data are presented as the means±SDs. *P < 0.05, **P < 0.01 by one-way ANOVA.

    Journal: Cancer letters

    Article Title: SIRPA enhances osteosarcoma metastasis by stabilizing SP1 and promoting SLC7A3-mediated arginine uptake.

    doi: 10.1016/j.canlet.2023.216412

    Figure Lengend Snippet: Fig. 7. SP1 regulates SLC7A3 expression. A-B. mRNA expression (A) and protein level (B) of SLC7A3 in OS cells with SP1 knockdown or overexpression (n = 3). C. Arginine uptake ratio in OS cells with/without SP1 knockdown upon SLC7A3 overexpression (n = 3). D. Schematic diagram showing possible regulatory sites for SP1 in the SLC7A3 promoter predicted by the JASPAR database (top). Construction of the SLC7A3 luciferase plasmids: wild-type SLC7A3 promoter (WT) and deletion mutants lacking region 1 (ΔRegion 1), region 2 (ΔRegion 2), or both (ΔRegion 1 + 2) (bottom). E. Homology analysis of region 1 and region 2 in the SLC7A3 promoter. F. 143B cells with/without SIRPA knockdown were transfected with plasmids encoding SP1(-500/0)-Luc WT, ΔRegion1, ΔRegion2, and ΔRegion1+2. Then, luciferase levels were measured in extracts after 48 h. G-H. ChIP assay of DNA fragments containing putative region 1 and region 2 within the SLC7A3 promoter region followed by PCR. The SLC7A3 promotor region beyond SP1 regulation (CTR) and the β-actin region (ACTB) were used as negative controls; an anti- histone antibody and rabbit IgG were used as assay controls (G). The histogram shows the relative amount of each DNA fragment binding to SP1 (H). The data are presented as the means±SDs. *P < 0.05, **P < 0.01 by one-way ANOVA.

    Article Snippet: The membranes were then incubated with diluted (1:1000) primary antibodies against human ACTB (4970; Cell Signaling Technology), SIRPA (47027; Cell Signaling Technology), SLC7A3 (PA5-103721; Invitrogen), RNF4 (12187; Cell Signaling Technology), ubiquitin (3936; Cell Signaling Technology), SP1 (9389; Cell Signaling Technology), p-Thr278-SP1 (PA5-106039; Invitrogen), p-Thr739-SP1 (PA5-104771; Invitrogen), ERK (4695; Cell Signaling Technology), p-ERK (9101; Cell Signaling Technology), AKT (4691; Cell Signaling Technology), p-AKT (4060; Cell Signaling Technology), β-catenin (8480; Cell Signaling Technology), and p-β-catenin (9567; Cell Signaling Technology).

    Techniques: Expressing, Knockdown, Over Expression, Luciferase, Transfection, Binding Assay

    Upper panel represents the effect of pretreatment with either pentagalloyl glucose (PGG) (100 or 200 mg/kg) or famotidine on gastric PECAM-1 level of indomethacin-induced gastric injury. The lower panel represents densitometry analysis of the ratio of PECAM-1 protein over β-actin protein. Data are expressed as mean ± SEM, n = 3. *, @ Statistically significant from control and indomethacin groups of rats, respectively, at p < 0.05 by one-way ANOVA was used for statistical analysis followed by Tukey’s post hoc test.

    Journal: Frontiers in Pharmacology

    Article Title: Pentagalloyl Glucose, a Major Compound in Mango Seed Kernel, Exhibits Distinct Gastroprotective Effects in Indomethacin-Induced Gastropathy in Rats via Modulating the NO/eNOS/iNOS Signaling Pathway

    doi: 10.3389/fphar.2022.800986

    Figure Lengend Snippet: Upper panel represents the effect of pretreatment with either pentagalloyl glucose (PGG) (100 or 200 mg/kg) or famotidine on gastric PECAM-1 level of indomethacin-induced gastric injury. The lower panel represents densitometry analysis of the ratio of PECAM-1 protein over β-actin protein. Data are expressed as mean ± SEM, n = 3. *, @ Statistically significant from control and indomethacin groups of rats, respectively, at p < 0.05 by one-way ANOVA was used for statistical analysis followed by Tukey’s post hoc test.

    Article Snippet: Ten percent SDS-PAGE was used to separate tissue proteins, which were then transferred to nitrocellulose membranes using the Trans-Blot ® semi-dry transfer cell (Bio- Rad, Hercules, CA, United States) at 20 v for 15 min. After blocking with 1 × Tris-buffered saline/0.1% Tween 20 (TBST) with 5% non-fat dry milk for 1 h, rabbit polyclonal antibodies against VEGF (Catalog no: CAB12303; Assay genie, Dublin, Ireland; dilution, 1:500); primary rabbit polyclonal antibodies against PECAM-1 (Catalog no: PA5-96055; Invitrogen, Thermo Fisher Scientific corporation, Massachusetts, United States; dilution, 1:1,000); and primary rabbit monoclonal antibodies against β-actin (Catalog no: M01263; Boster Biological Technology, Pleasanton, CA, United States; diluted at 1:1,000) were all identified by the antibodies used (Sigma-Aldrich, United States).

    Techniques: Control

    Upper panel represents the effect of pretreatment with either pentagalloyl glucose (PGG) (100 or 200 mg/kg) or famotidine on gastric VEGF level of indomethacin-induced gastric injury. The lower panel represents densitometry analysis of the ratio of VEGF protein over β-actin protein. Data are expressed as mean ± SEM, n = 3. * and @ Statistically significant from control or indomethacin groups of rats, respectively, at p < 0.05 by one-way ANOVA was used for statistical analysis followed by Tukey’s post hoc test.

    Journal: Frontiers in Pharmacology

    Article Title: Pentagalloyl Glucose, a Major Compound in Mango Seed Kernel, Exhibits Distinct Gastroprotective Effects in Indomethacin-Induced Gastropathy in Rats via Modulating the NO/eNOS/iNOS Signaling Pathway

    doi: 10.3389/fphar.2022.800986

    Figure Lengend Snippet: Upper panel represents the effect of pretreatment with either pentagalloyl glucose (PGG) (100 or 200 mg/kg) or famotidine on gastric VEGF level of indomethacin-induced gastric injury. The lower panel represents densitometry analysis of the ratio of VEGF protein over β-actin protein. Data are expressed as mean ± SEM, n = 3. * and @ Statistically significant from control or indomethacin groups of rats, respectively, at p < 0.05 by one-way ANOVA was used for statistical analysis followed by Tukey’s post hoc test.

    Article Snippet: Ten percent SDS-PAGE was used to separate tissue proteins, which were then transferred to nitrocellulose membranes using the Trans-Blot ® semi-dry transfer cell (Bio- Rad, Hercules, CA, United States) at 20 v for 15 min. After blocking with 1 × Tris-buffered saline/0.1% Tween 20 (TBST) with 5% non-fat dry milk for 1 h, rabbit polyclonal antibodies against VEGF (Catalog no: CAB12303; Assay genie, Dublin, Ireland; dilution, 1:500); primary rabbit polyclonal antibodies against PECAM-1 (Catalog no: PA5-96055; Invitrogen, Thermo Fisher Scientific corporation, Massachusetts, United States; dilution, 1:1,000); and primary rabbit monoclonal antibodies against β-actin (Catalog no: M01263; Boster Biological Technology, Pleasanton, CA, United States; diluted at 1:1,000) were all identified by the antibodies used (Sigma-Aldrich, United States).

    Techniques: Control