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hrp conjugated β tubulin  (Proteintech)


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    Structured Review

    Proteintech hrp conjugated β tubulin
    Hrp Conjugated β Tubulin, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 50 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hrp+conjugated+%CE%B2+tubulin/HRP-conjugated+beta+Tubulin+Antibody/10__3389_slash_fenvh__2026__1766012-120-10-19
    Average 94 stars, based on 50 article reviews
    hrp conjugated β tubulin - by Bioz Stars, 2026-11
    94/100 stars

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    Related Articles

    Incubation:

    Article Title: Orcinol glucoside ameliorates pulmonary fibrosis by suppressing hyaluronic acid synthesis and macrophage M2 polarization via targeting hyaluronic acid synthase 2
    Article Snippet: Antibodies for Collagen type I α 1 chain (COL1A1; cat. no. 72026; 1:1,000), Phospho-STAT6 (Tyr641; cat. no. 56554S; 1:1,000) and α-smooth muscle actin (α-SMA; cat. no. 19245; 1:1,000) were obtained from Cell Signaling Technology, Inc. .. The HAS2 (cat. no. bs-11290R; 1:1,000) antibody was purchased from BIOSS and HRP-conjugated β-tubulin (cat. no. HRP-66240: 1:20,000) and STAT6 (cat. no. 51073-1-AP; 1:5,000) antibodies were obtained from Proteintech Group, Inc. Membranes were incubated for 1 h at room temperature with an HRP-conjugated secondary antibody (Cell Signaling Technology, Inc.; 1:2,000) following TBS-T (containing 0.05% Tween-20) washing. .. Protein bands were detected using Immobilon Western Chemiluminescent substrate (MilliporeSigma) and imaged with a Tanon 5200 Multi automatic chemiluminescence system (Tanon Science and Technology Co., Ltd.).

    Article Title: Orcinol glucoside ameliorates pulmonary fibrosis by suppressing hyaluronic acid synthesis and macrophage M2 polarization via targeting hyaluronic acid synthase 2.
    Article Snippet: Antibodies for Collagen type I α 1 chain (COL1A1; cat. no. 72026; 1:1,000), Phospho‐STAT6 (Tyr641; cat. no. 56554S; 1:1,000) and α‐smooth muscle actin (α‐SMA; cat. no. 19245; 1:1,000) were obtained from Cell Signaling Technology, Inc. .. The HAS2 (cat. no. bs‐11290R; 1:1,000) antibody was purchased from BIOSS and HRP‐conjugated β‐tubulin (cat. no. HRP‐66240: 1:20,000) and STAT6 (cat. no. 51073‐1‐AP; 1:5,000) antibodies were obtained from Proteintech Group, Inc. Membranes were incubated for 1 h at room temperature with an HRP‐conjugated secondary antibody (Cell Signaling Technology, Inc.; 1:2,000) following TBS‐T (containing 0.05% Tween‐20) washing. .. Protein bands were detected using Immobilon Western Chemiluminescent substrate (MilliporeSigma) and imaged with a Tanon 5200 Multi automatic chemiluminescence system (Tanon Science and Technology Co., Ltd.).

    Article Title: Nano-functionalized probiotic treats atherosclerosis via inhibiting intestinal microbiota-TMA-TMAO axis
    Article Snippet: Then, the membranes containing liver proteins were incubated with corresponding primary antibodies against FMO3 (1:1000, Abcam) and HRP-conjugated GAPDH (1:5000, Proteintech) overnight at 4 °C. .. The membranes containing colon proteins were incubated with corresponding primary antibodies against ZO-1 (1:1000, Abcam), Occludin (1:1000, Abcam), Claudin-1 (1:1000, Abcam), and HRP-conjugated β-tubulin (1:5000, Proteintech) overnight at 4 °C. .. Afterwards, the membranes were incubated with HRP-conjugated secondary anti-rabbit antibody (1:10000, Proteintech) at 37 °C for 2 h. The images of protein bands were developed using a ChemiDoc MP system (BioRad).

    Article Title: Nano-functionalized probiotic treats atherosclerosis via inhibiting intestinal microbiota-TMA-TMAO axis.
    Article Snippet: Subsequently, after being washed with PBS three times, pre-coated LGGwas co-incubatedwithdopamine solution (0.5mgmL−1) or amixture of dopamine solution (0.5mgmL−1) and modified PMF nanoparticles (2.0mgmL−1) for another 1, 2, or 3 h. Following centrifugation and washing, PD@LGG and PDMF@LGG at different incubation timepoints were resuspended and the absorption peaks atA275nmweredetected usingUV-vis (ThermoFisher Scientific) to determine the contents of polydopamine coated on the surface of LGG. .. The membranes containing colon proteins were incubated with corresponding primary antibodies against ZO-1 (1:1000, Abcam), Occludin (1:1000, Abcam), Claudin-1 (1:1000, Abcam), and HRP-conjugated β-tubulin (1:5000, Proteintech) overnight at 4 °C. .. Afterwards, the membranes were incubated with HRPconjugated secondary anti-rabbit antibody (1:10000, Proteintech) at 37 °C for 2 h. The images of protein bands were developed using a ChemiDoc MP system (BioRad).

    Cell-Signaling:

    Article Title: Orcinol glucoside ameliorates pulmonary fibrosis by suppressing hyaluronic acid synthesis and macrophage M2 polarization via targeting hyaluronic acid synthase 2
    Article Snippet: Antibodies for Collagen type I α 1 chain (COL1A1; cat. no. 72026; 1:1,000), Phospho-STAT6 (Tyr641; cat. no. 56554S; 1:1,000) and α-smooth muscle actin (α-SMA; cat. no. 19245; 1:1,000) were obtained from Cell Signaling Technology, Inc. .. The HAS2 (cat. no. bs-11290R; 1:1,000) antibody was purchased from BIOSS and HRP-conjugated β-tubulin (cat. no. HRP-66240: 1:20,000) and STAT6 (cat. no. 51073-1-AP; 1:5,000) antibodies were obtained from Proteintech Group, Inc. Membranes were incubated for 1 h at room temperature with an HRP-conjugated secondary antibody (Cell Signaling Technology, Inc.; 1:2,000) following TBS-T (containing 0.05% Tween-20) washing. .. Protein bands were detected using Immobilon Western Chemiluminescent substrate (MilliporeSigma) and imaged with a Tanon 5200 Multi automatic chemiluminescence system (Tanon Science and Technology Co., Ltd.).

    Transcranial Magnetic Stimulation:

    Article Title: Orcinol glucoside ameliorates pulmonary fibrosis by suppressing hyaluronic acid synthesis and macrophage M2 polarization via targeting hyaluronic acid synthase 2
    Article Snippet: Antibodies for Collagen type I α 1 chain (COL1A1; cat. no. 72026; 1:1,000), Phospho-STAT6 (Tyr641; cat. no. 56554S; 1:1,000) and α-smooth muscle actin (α-SMA; cat. no. 19245; 1:1,000) were obtained from Cell Signaling Technology, Inc. .. The HAS2 (cat. no. bs-11290R; 1:1,000) antibody was purchased from BIOSS and HRP-conjugated β-tubulin (cat. no. HRP-66240: 1:20,000) and STAT6 (cat. no. 51073-1-AP; 1:5,000) antibodies were obtained from Proteintech Group, Inc. Membranes were incubated for 1 h at room temperature with an HRP-conjugated secondary antibody (Cell Signaling Technology, Inc.; 1:2,000) following TBS-T (containing 0.05% Tween-20) washing. .. Protein bands were detected using Immobilon Western Chemiluminescent substrate (MilliporeSigma) and imaged with a Tanon 5200 Multi automatic chemiluminescence system (Tanon Science and Technology Co., Ltd.).



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    TMP restores mitochondrial quality control and activates the AMPK/Sirt1/PGC-1α signaling axis. (A) Representative fluorescence images of intracellular calcium levels detected by Fura-2AM staining (blue). Scale bar: 100 µm. (B) Representative images of mitochondrial membrane potential (ΔΨm) detected by JC-1 staining (Green: monomers/damaged). Scale bar: 100 µm. (C,D) Quantitative analysis of Fura-2AM fluorescence intensity (C) and the percentage of JC-1 monomers (D) (n = 3). (E) Representative Western blot bands showing the levels of energy metabolism-related proteins (PGC-1α, Sirt1, AMPK) and autophagy/mitophagy markers (p62, Beclin1, LC3B, Parkin, p-Parkin) in H9c2 cells treated with Control, Dox, TMP, and Dox + <t>TMP.</t> <t>β-tubulin</t> served as the loading control. (F–M) Quantitative densitometric analysis of relative protein expression from panel E: (F) AMPK, (G) PGC-1α, (H) Sirt1, (I) Beclin1, (J) p-Parkin, (K) Parkin, (L) LC3B-II, and (M) p62. (N) Representative Western blot bands for p62 and LC3B in the autophagic flux assay (cells treated with/without BafA1, 50 nM for 4 h). GAPDH served as the loading control. (O,P) Quantitative densitometric analysis of (O) p62 and (P) LC3B-II relative expression levels from the flux assay. Data are presented as mean ± SD (n = 3). *P < 0.05, P < 0.01, ***P < 0.001, ****P < 0.0001; ns, not significant (P > 0.05).
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    TMP restores mitochondrial quality control and activates the AMPK/Sirt1/PGC-1α signaling axis. (A) Representative fluorescence images of intracellular calcium levels detected by Fura-2AM staining (blue). Scale bar: 100 µm. (B) Representative images of mitochondrial membrane potential (ΔΨm) detected by JC-1 staining (Green: monomers/damaged). Scale bar: 100 µm. (C,D) Quantitative analysis of Fura-2AM fluorescence intensity (C) and the percentage of JC-1 monomers (D) (n = 3). (E) Representative Western blot bands showing the levels of energy metabolism-related proteins (PGC-1α, Sirt1, AMPK) and autophagy/mitophagy markers (p62, Beclin1, LC3B, Parkin, p-Parkin) in H9c2 cells treated with Control, Dox, TMP, and Dox + <t>TMP.</t> <t>β-tubulin</t> served as the loading control. (F–M) Quantitative densitometric analysis of relative protein expression from panel E: (F) AMPK, (G) PGC-1α, (H) Sirt1, (I) Beclin1, (J) p-Parkin, (K) Parkin, (L) LC3B-II, and (M) p62. (N) Representative Western blot bands for p62 and LC3B in the autophagic flux assay (cells treated with/without BafA1, 50 nM for 4 h). GAPDH served as the loading control. (O,P) Quantitative densitometric analysis of (O) p62 and (P) LC3B-II relative expression levels from the flux assay. Data are presented as mean ± SD (n = 3). *P < 0.05, P < 0.01, ***P < 0.001, ****P < 0.0001; ns, not significant (P > 0.05).
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    TMP restores mitochondrial quality control and activates the AMPK/Sirt1/PGC-1α signaling axis. (A) Representative fluorescence images of intracellular calcium levels detected by Fura-2AM staining (blue). Scale bar: 100 µm. (B) Representative images of mitochondrial membrane potential (ΔΨm) detected by JC-1 staining (Green: monomers/damaged). Scale bar: 100 µm. (C,D) Quantitative analysis of Fura-2AM fluorescence intensity (C) and the percentage of JC-1 monomers (D) (n = 3). (E) Representative Western blot bands showing the levels of energy metabolism-related proteins (PGC-1α, Sirt1, AMPK) and autophagy/mitophagy markers (p62, Beclin1, LC3B, Parkin, p-Parkin) in H9c2 cells treated with Control, Dox, TMP, and Dox + <t>TMP.</t> <t>β-tubulin</t> served as the loading control. (F–M) Quantitative densitometric analysis of relative protein expression from panel E: (F) AMPK, (G) PGC-1α, (H) Sirt1, (I) Beclin1, (J) p-Parkin, (K) Parkin, (L) LC3B-II, and (M) p62. (N) Representative Western blot bands for p62 and LC3B in the autophagic flux assay (cells treated with/without BafA1, 50 nM for 4 h). GAPDH served as the loading control. (O,P) Quantitative densitometric analysis of (O) p62 and (P) LC3B-II relative expression levels from the flux assay. Data are presented as mean ± SD (n = 3). *P < 0.05, P < 0.01, ***P < 0.001, ****P < 0.0001; ns, not significant (P > 0.05).
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    TMP restores mitochondrial quality control and activates the AMPK/Sirt1/PGC-1α signaling axis. (A) Representative fluorescence images of intracellular calcium levels detected by Fura-2AM staining (blue). Scale bar: 100 µm. (B) Representative images of mitochondrial membrane potential (ΔΨm) detected by JC-1 staining (Green: monomers/damaged). Scale bar: 100 µm. (C,D) Quantitative analysis of Fura-2AM fluorescence intensity (C) and the percentage of JC-1 monomers (D) (n = 3). (E) Representative Western blot bands showing the levels of energy metabolism-related proteins (PGC-1α, Sirt1, AMPK) and autophagy/mitophagy markers (p62, Beclin1, LC3B, Parkin, p-Parkin) in H9c2 cells treated with Control, Dox, TMP, and Dox + <t>TMP.</t> <t>β-tubulin</t> served as the loading control. (F–M) Quantitative densitometric analysis of relative protein expression from panel E: (F) AMPK, (G) PGC-1α, (H) Sirt1, (I) Beclin1, (J) p-Parkin, (K) Parkin, (L) LC3B-II, and (M) p62. (N) Representative Western blot bands for p62 and LC3B in the autophagic flux assay (cells treated with/without BafA1, 50 nM for 4 h). GAPDH served as the loading control. (O,P) Quantitative densitometric analysis of (O) p62 and (P) LC3B-II relative expression levels from the flux assay. Data are presented as mean ± SD (n = 3). *P < 0.05, P < 0.01, ***P < 0.001, ****P < 0.0001; ns, not significant (P > 0.05).
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    TMP restores mitochondrial quality control and activates the AMPK/Sirt1/PGC-1α signaling axis. (A) Representative fluorescence images of intracellular calcium levels detected by Fura-2AM staining (blue). Scale bar: 100 µm. (B) Representative images of mitochondrial membrane potential (ΔΨm) detected by JC-1 staining (Green: monomers/damaged). Scale bar: 100 µm. (C,D) Quantitative analysis of Fura-2AM fluorescence intensity (C) and the percentage of JC-1 monomers (D) (n = 3). (E) Representative Western blot bands showing the levels of energy metabolism-related proteins (PGC-1α, Sirt1, AMPK) and autophagy/mitophagy markers (p62, Beclin1, LC3B, Parkin, p-Parkin) in H9c2 cells treated with Control, Dox, TMP, and Dox + <t>TMP.</t> <t>β-tubulin</t> served as the loading control. (F–M) Quantitative densitometric analysis of relative protein expression from panel E: (F) AMPK, (G) PGC-1α, (H) Sirt1, (I) Beclin1, (J) p-Parkin, (K) Parkin, (L) LC3B-II, and (M) p62. (N) Representative Western blot bands for p62 and LC3B in the autophagic flux assay (cells treated with/without BafA1, 50 nM for 4 h). GAPDH served as the loading control. (O,P) Quantitative densitometric analysis of (O) p62 and (P) LC3B-II relative expression levels from the flux assay. Data are presented as mean ± SD (n = 3). *P < 0.05, P < 0.01, ***P < 0.001, ****P < 0.0001; ns, not significant (P > 0.05).
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    TMP restores mitochondrial quality control and activates the AMPK/Sirt1/PGC-1α signaling axis. (A) Representative fluorescence images of intracellular calcium levels detected by Fura-2AM staining (blue). Scale bar: 100 µm. (B) Representative images of mitochondrial membrane potential (ΔΨm) detected by JC-1 staining (Green: monomers/damaged). Scale bar: 100 µm. (C,D) Quantitative analysis of Fura-2AM fluorescence intensity (C) and the percentage of JC-1 monomers (D) (n = 3). (E) Representative Western blot bands showing the levels of energy metabolism-related proteins (PGC-1α, Sirt1, AMPK) and autophagy/mitophagy markers (p62, Beclin1, LC3B, Parkin, p-Parkin) in H9c2 cells treated with Control, Dox, TMP, and Dox + <t>TMP.</t> <t>β-tubulin</t> served as the loading control. (F–M) Quantitative densitometric analysis of relative protein expression from panel E: (F) AMPK, (G) PGC-1α, (H) Sirt1, (I) Beclin1, (J) p-Parkin, (K) Parkin, (L) LC3B-II, and (M) p62. (N) Representative Western blot bands for p62 and LC3B in the autophagic flux assay (cells treated with/without BafA1, 50 nM for 4 h). GAPDH served as the loading control. (O,P) Quantitative densitometric analysis of (O) p62 and (P) LC3B-II relative expression levels from the flux assay. Data are presented as mean ± SD (n = 3). *P < 0.05, P < 0.01, ***P < 0.001, ****P < 0.0001; ns, not significant (P > 0.05).
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    TMP restores mitochondrial quality control and activates the AMPK/Sirt1/PGC-1α signaling axis. (A) Representative fluorescence images of intracellular calcium levels detected by Fura-2AM staining (blue). Scale bar: 100 µm. (B) Representative images of mitochondrial membrane potential (ΔΨm) detected by JC-1 staining (Green: monomers/damaged). Scale bar: 100 µm. (C,D) Quantitative analysis of Fura-2AM fluorescence intensity (C) and the percentage of JC-1 monomers (D) (n = 3). (E) Representative Western blot bands showing the levels of energy metabolism-related proteins (PGC-1α, Sirt1, AMPK) and autophagy/mitophagy markers (p62, Beclin1, LC3B, Parkin, p-Parkin) in H9c2 cells treated with Control, Dox, TMP, and Dox + <t>TMP.</t> <t>β-tubulin</t> served as the loading control. (F–M) Quantitative densitometric analysis of relative protein expression from panel E: (F) AMPK, (G) PGC-1α, (H) Sirt1, (I) Beclin1, (J) p-Parkin, (K) Parkin, (L) LC3B-II, and (M) p62. (N) Representative Western blot bands for p62 and LC3B in the autophagic flux assay (cells treated with/without BafA1, 50 nM for 4 h). GAPDH served as the loading control. (O,P) Quantitative densitometric analysis of (O) p62 and (P) LC3B-II relative expression levels from the flux assay. Data are presented as mean ± SD (n = 3). *P < 0.05, P < 0.01, ***P < 0.001, ****P < 0.0001; ns, not significant (P > 0.05).
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    Image Search Results


    TMP restores mitochondrial quality control and activates the AMPK/Sirt1/PGC-1α signaling axis. (A) Representative fluorescence images of intracellular calcium levels detected by Fura-2AM staining (blue). Scale bar: 100 µm. (B) Representative images of mitochondrial membrane potential (ΔΨm) detected by JC-1 staining (Green: monomers/damaged). Scale bar: 100 µm. (C,D) Quantitative analysis of Fura-2AM fluorescence intensity (C) and the percentage of JC-1 monomers (D) (n = 3). (E) Representative Western blot bands showing the levels of energy metabolism-related proteins (PGC-1α, Sirt1, AMPK) and autophagy/mitophagy markers (p62, Beclin1, LC3B, Parkin, p-Parkin) in H9c2 cells treated with Control, Dox, TMP, and Dox + TMP. β-tubulin served as the loading control. (F–M) Quantitative densitometric analysis of relative protein expression from panel E: (F) AMPK, (G) PGC-1α, (H) Sirt1, (I) Beclin1, (J) p-Parkin, (K) Parkin, (L) LC3B-II, and (M) p62. (N) Representative Western blot bands for p62 and LC3B in the autophagic flux assay (cells treated with/without BafA1, 50 nM for 4 h). GAPDH served as the loading control. (O,P) Quantitative densitometric analysis of (O) p62 and (P) LC3B-II relative expression levels from the flux assay. Data are presented as mean ± SD (n = 3). *P < 0.05, P < 0.01, ***P < 0.001, ****P < 0.0001; ns, not significant (P > 0.05).

    Journal: Frontiers in Pharmacology

    Article Title: Tricholoma matsutake polypeptide modulates cardiac metabolism and restores autophagic flux to mitigate doxorubicin-induced senescence

    doi: 10.3389/fphar.2026.1842003

    Figure Lengend Snippet: TMP restores mitochondrial quality control and activates the AMPK/Sirt1/PGC-1α signaling axis. (A) Representative fluorescence images of intracellular calcium levels detected by Fura-2AM staining (blue). Scale bar: 100 µm. (B) Representative images of mitochondrial membrane potential (ΔΨm) detected by JC-1 staining (Green: monomers/damaged). Scale bar: 100 µm. (C,D) Quantitative analysis of Fura-2AM fluorescence intensity (C) and the percentage of JC-1 monomers (D) (n = 3). (E) Representative Western blot bands showing the levels of energy metabolism-related proteins (PGC-1α, Sirt1, AMPK) and autophagy/mitophagy markers (p62, Beclin1, LC3B, Parkin, p-Parkin) in H9c2 cells treated with Control, Dox, TMP, and Dox + TMP. β-tubulin served as the loading control. (F–M) Quantitative densitometric analysis of relative protein expression from panel E: (F) AMPK, (G) PGC-1α, (H) Sirt1, (I) Beclin1, (J) p-Parkin, (K) Parkin, (L) LC3B-II, and (M) p62. (N) Representative Western blot bands for p62 and LC3B in the autophagic flux assay (cells treated with/without BafA1, 50 nM for 4 h). GAPDH served as the loading control. (O,P) Quantitative densitometric analysis of (O) p62 and (P) LC3B-II relative expression levels from the flux assay. Data are presented as mean ± SD (n = 3). *P < 0.05, P < 0.01, ***P < 0.001, ****P < 0.0001; ns, not significant (P > 0.05).

    Article Snippet: HRP-conjugated Goat Anti-Rabbit IgG (Cat. No. AS014) and HRP-conjugated β-tubulin (Cat. No. AC028) were also from Abclonal.

    Techniques: Control, Fluorescence, Staining, Membrane, Western Blot, Expressing, Flux Assay