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protein expression levels  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology protein expression levels
    Protein Expression Levels, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 46264 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/protein+expression+levels/%CE%B2-Actin+Antibody/pmc12999771-56-0-9
    Average 96 stars, based on 46264 article reviews
    protein expression levels - by Bioz Stars, 2026-09
    96/100 stars

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    Expressing:

    Article Title: Role of AhR-Hsp90-MDM2-mediated VDR ubiquitination in PM2.5-induced renal toxicity.
    Article Snippet: Background and objectives: The kidney is a primary target for the accumulation of particulate matter (PM2.5).. This study aimed to investigate PM2.5-induced renal toxicity mechanisms, focusing on the aryl hydrocarbon receptor (AhR)-Hsp90-MDM2 axis and its impact on vitamin D receptor (VDR) ubiquitination.. Methods: PM2.5’s role in activating the AhR and its downstream pathways was investigated using in vitro and in vivo models.

    Article Title: Targeting EFEMP1 enhances chondrogenesis and inhibits hypertrophic differentiation in a spontaneous osteoarthritis mouse model
    Article Snippet: Following were antibodies and dilution rates used in this study: EFEMP1 (1:1000; GTX111657; GenTex, USA), MMP-13 (1:1000; GTX100665; GenTex, USA), phospho-p70S6K (T421/S424 site) (1:1000; MAB8962; R&D Systems, USA), total p70S6K (1:1000; AF8962-SP; R&D Systems, USA), RUNX2 (1:1000; #12,556; Cell Signaling, USA), and OCN (1:1000; sc-73464; Santa Cruz, USA). .. Protein expression levels were normalized to β-actin (1:2000; sc-47778; Santa Cruz, USA). .. Membranes were then incubated with horseradish peroxidase (HRP)-conjugated secondary antibodies, including anti-rabbit IgG (1:2000; #7074; Cell Signaling Technology, USA) or anti-mouse IgG (1:2000; #7076; Cell Signaling Technology, USA), for 60 min at 25 °C.

    Cell Culture:

    Article Title: Role of AhR-Hsp90-MDM2-mediated VDR ubiquitination in PM2.5-induced renal toxicity.
    Article Snippet: Background and objectives: The kidney is a primary target for the accumulation of particulate matter (PM2.5).. This study aimed to investigate PM2.5-induced renal toxicity mechanisms, focusing on the aryl hydrocarbon receptor (AhR)-Hsp90-MDM2 axis and its impact on vitamin D receptor (VDR) ubiquitination.. Methods: PM2.5’s role in activating the AhR and its downstream pathways was investigated using in vitro and in vivo models.



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    <t>APOC1</t> deficiency inhibits aggressive PTC progression. (A-C) Analyses of APOC1 in PTC tissues (T) and adjacent normal tissues (N). (D) APOC1 protein expression levels in normal and tumor thyroid gland tissues obtained from the Human Protein Atlas database. (E) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by qPCR. (F) CCK8 assay of indicated knockdown APOC1 treatments in TPC-1 and B-CPAP cells. (G) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by Western blot. (H-I) TPC-1 cell proliferation after APOC1 knockdown treatments for 24 h as detected by the EdU assay. Scale bar, 200 μm (J-K) Migration ability of TPC-1 cells after APOC1 knockdown treatment for 24 h as detected by a wound healing assay. (L) Colony formation assay performed on TPC-1 and B-CPAP cells after APOC1 siRNA treatment. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.
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    <t>APOC1</t> deficiency inhibits aggressive PTC progression. (A-C) Analyses of APOC1 in PTC tissues (T) and adjacent normal tissues (N). (D) APOC1 protein expression levels in normal and tumor thyroid gland tissues obtained from the Human Protein Atlas database. (E) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by qPCR. (F) CCK8 assay of indicated knockdown APOC1 treatments in TPC-1 and B-CPAP cells. (G) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by Western blot. (H-I) TPC-1 cell proliferation after APOC1 knockdown treatments for 24 h as detected by the EdU assay. Scale bar, 200 μm (J-K) Migration ability of TPC-1 cells after APOC1 knockdown treatment for 24 h as detected by a wound healing assay. (L) Colony formation assay performed on TPC-1 and B-CPAP cells after APOC1 siRNA treatment. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.
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    <t>APOC1</t> deficiency inhibits aggressive PTC progression. (A-C) Analyses of APOC1 in PTC tissues (T) and adjacent normal tissues (N). (D) APOC1 protein expression levels in normal and tumor thyroid gland tissues obtained from the Human Protein Atlas database. (E) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by qPCR. (F) CCK8 assay of indicated knockdown APOC1 treatments in TPC-1 and B-CPAP cells. (G) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by Western blot. (H-I) TPC-1 cell proliferation after APOC1 knockdown treatments for 24 h as detected by the EdU assay. Scale bar, 200 μm (J-K) Migration ability of TPC-1 cells after APOC1 knockdown treatment for 24 h as detected by a wound healing assay. (L) Colony formation assay performed on TPC-1 and B-CPAP cells after APOC1 siRNA treatment. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.
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    APOC1 deficiency inhibits aggressive PTC progression. (A-C) Analyses of APOC1 in PTC tissues (T) and adjacent normal tissues (N). (D) APOC1 protein expression levels in normal and tumor thyroid gland tissues obtained from the Human Protein Atlas database. (E) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by qPCR. (F) CCK8 assay of indicated knockdown APOC1 treatments in TPC-1 and B-CPAP cells. (G) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by Western blot. (H-I) TPC-1 cell proliferation after APOC1 knockdown treatments for 24 h as detected by the EdU assay. Scale bar, 200 μm (J-K) Migration ability of TPC-1 cells after APOC1 knockdown treatment for 24 h as detected by a wound healing assay. (L) Colony formation assay performed on TPC-1 and B-CPAP cells after APOC1 siRNA treatment. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.

    Journal: Translational Oncology

    Article Title: Apolipoprotein C1 functions as a target of thyroid carcinoma and synergistic effects with promising candidate-cyclopamine

    doi: 10.1016/j.tranon.2025.102617

    Figure Lengend Snippet: APOC1 deficiency inhibits aggressive PTC progression. (A-C) Analyses of APOC1 in PTC tissues (T) and adjacent normal tissues (N). (D) APOC1 protein expression levels in normal and tumor thyroid gland tissues obtained from the Human Protein Atlas database. (E) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by qPCR. (F) CCK8 assay of indicated knockdown APOC1 treatments in TPC-1 and B-CPAP cells. (G) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by Western blot. (H-I) TPC-1 cell proliferation after APOC1 knockdown treatments for 24 h as detected by the EdU assay. Scale bar, 200 μm (J-K) Migration ability of TPC-1 cells after APOC1 knockdown treatment for 24 h as detected by a wound healing assay. (L) Colony formation assay performed on TPC-1 and B-CPAP cells after APOC1 siRNA treatment. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.

    Article Snippet: APOC1 deficiency inhibits aggressive PTC progression. (A-C) Analyses of APOC1 in PTC tissues (T) and adjacent normal tissues (N). (D) APOC1 protein expression levels in normal and tumor thyroid gland tissues obtained from the Human Protein Atlas database. (E) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by qPCR. (F) CCK8 assay of indicated knockdown APOC1 treatments in TPC-1 and B-CPAP cells. (G) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by Western blot. (H-I) TPC-1 cell proliferation after APOC1 knockdown treatments for 24 h as detected by the EdU assay.

    Techniques: Expressing, Knockdown, CCK-8 Assay, Western Blot, EdU Assay, Migration, Wound Healing Assay, Colony Assay, Control

    Expression of APOC1 in PTC and its clinical prevalence. (A-C) Stage-plot analysis of the relationship between APOC1 expression and PTC tumor stages. (D) Age. (E) APOC1 expression in different PTC histological subtypes. (F) Neoplasm locations. (G) Primary neoplasm focus types. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.

    Journal: Translational Oncology

    Article Title: Apolipoprotein C1 functions as a target of thyroid carcinoma and synergistic effects with promising candidate-cyclopamine

    doi: 10.1016/j.tranon.2025.102617

    Figure Lengend Snippet: Expression of APOC1 in PTC and its clinical prevalence. (A-C) Stage-plot analysis of the relationship between APOC1 expression and PTC tumor stages. (D) Age. (E) APOC1 expression in different PTC histological subtypes. (F) Neoplasm locations. (G) Primary neoplasm focus types. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.

    Article Snippet: APOC1 deficiency inhibits aggressive PTC progression. (A-C) Analyses of APOC1 in PTC tissues (T) and adjacent normal tissues (N). (D) APOC1 protein expression levels in normal and tumor thyroid gland tissues obtained from the Human Protein Atlas database. (E) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by qPCR. (F) CCK8 assay of indicated knockdown APOC1 treatments in TPC-1 and B-CPAP cells. (G) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by Western blot. (H-I) TPC-1 cell proliferation after APOC1 knockdown treatments for 24 h as detected by the EdU assay.

    Techniques: Expressing, Control

    Correlation analysis of APOC1 expressions with immune cell infiltration levels and immune checkpoints in PTC. ( A–M ) Correlation between APOC1 expression and infiltration levels of immune cells. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.

    Journal: Translational Oncology

    Article Title: Apolipoprotein C1 functions as a target of thyroid carcinoma and synergistic effects with promising candidate-cyclopamine

    doi: 10.1016/j.tranon.2025.102617

    Figure Lengend Snippet: Correlation analysis of APOC1 expressions with immune cell infiltration levels and immune checkpoints in PTC. ( A–M ) Correlation between APOC1 expression and infiltration levels of immune cells. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.

    Article Snippet: APOC1 deficiency inhibits aggressive PTC progression. (A-C) Analyses of APOC1 in PTC tissues (T) and adjacent normal tissues (N). (D) APOC1 protein expression levels in normal and tumor thyroid gland tissues obtained from the Human Protein Atlas database. (E) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by qPCR. (F) CCK8 assay of indicated knockdown APOC1 treatments in TPC-1 and B-CPAP cells. (G) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by Western blot. (H-I) TPC-1 cell proliferation after APOC1 knockdown treatments for 24 h as detected by the EdU assay.

    Techniques: Expressing, Control

    Molecular docking visualization of APOC1 and drug candidates. ( A ) Farnesylthioacetic-acid; ( B ) Papaverine; ( C ) Hycanthone; ( D ) Indolophenanthridine; ( E ) Nicaraven; ( F ) Methylnorlichexanthone; ( G ) Fananserin, and ( H ) Cyclopamine.

    Journal: Translational Oncology

    Article Title: Apolipoprotein C1 functions as a target of thyroid carcinoma and synergistic effects with promising candidate-cyclopamine

    doi: 10.1016/j.tranon.2025.102617

    Figure Lengend Snippet: Molecular docking visualization of APOC1 and drug candidates. ( A ) Farnesylthioacetic-acid; ( B ) Papaverine; ( C ) Hycanthone; ( D ) Indolophenanthridine; ( E ) Nicaraven; ( F ) Methylnorlichexanthone; ( G ) Fananserin, and ( H ) Cyclopamine.

    Article Snippet: APOC1 deficiency inhibits aggressive PTC progression. (A-C) Analyses of APOC1 in PTC tissues (T) and adjacent normal tissues (N). (D) APOC1 protein expression levels in normal and tumor thyroid gland tissues obtained from the Human Protein Atlas database. (E) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by qPCR. (F) CCK8 assay of indicated knockdown APOC1 treatments in TPC-1 and B-CPAP cells. (G) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by Western blot. (H-I) TPC-1 cell proliferation after APOC1 knockdown treatments for 24 h as detected by the EdU assay.

    Techniques:

    APOC1 deficiency enhances effects of Cyclopamine, inhibits proliferation, and promotes cell death in PTC. ( A ) Cell death after APOC1 knockdown or treatment with 10 μM Cyclopamine for 24 h as analyzed by flow cytometry. ( B ) Colony-forming potential of tumor cells in B-CPAP and TPC-1 cells with APOC1 knockdown or treatment with 10 μM Cyclopamine for 14 days. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.

    Journal: Translational Oncology

    Article Title: Apolipoprotein C1 functions as a target of thyroid carcinoma and synergistic effects with promising candidate-cyclopamine

    doi: 10.1016/j.tranon.2025.102617

    Figure Lengend Snippet: APOC1 deficiency enhances effects of Cyclopamine, inhibits proliferation, and promotes cell death in PTC. ( A ) Cell death after APOC1 knockdown or treatment with 10 μM Cyclopamine for 24 h as analyzed by flow cytometry. ( B ) Colony-forming potential of tumor cells in B-CPAP and TPC-1 cells with APOC1 knockdown or treatment with 10 μM Cyclopamine for 14 days. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the control.

    Article Snippet: APOC1 deficiency inhibits aggressive PTC progression. (A-C) Analyses of APOC1 in PTC tissues (T) and adjacent normal tissues (N). (D) APOC1 protein expression levels in normal and tumor thyroid gland tissues obtained from the Human Protein Atlas database. (E) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by qPCR. (F) CCK8 assay of indicated knockdown APOC1 treatments in TPC-1 and B-CPAP cells. (G) Knockdown efficiencies of APOC1 siRNA into TPC-1 and B-CPAP cells as evaluated by Western blot. (H-I) TPC-1 cell proliferation after APOC1 knockdown treatments for 24 h as detected by the EdU assay.

    Techniques: Knockdown, Flow Cytometry, Control