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Proteintech β tubulin

Validation of key pathways and antioxidative effect mediated by the composite stent. (A) Western blot analysis of OXPHOS pathway-related proteins in each <t>group;</t> <t>β-Tubulin</t> was used as a loading control. (B) Quantification of the five mitochondrial OXPHOS complexes expression from Western blot bands, normalized to the loading control. (C) Western blot analysis of PI3K-Akt and HIF-1 pathway-related proteins in each group; β-Tubulin was used as a loading control. (D) Quantification of total Akt and HIF-1α expression from Western blot bands, normalized to the loading control. (E) Quantitative analysis of p-Akt normalized to total Akt expression. (F) Representative immunofluorescence images of tissue sections stained for Occludin to assess tight junctions and CD31 to visualize endothelial cells. (G) Quantification of Occludin and CD31 fluorescence intensity. (H) MDA levels, and SOD activity. Data were presented as mean ± SD (n = 3, biological replicates). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

β Tubulin, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 2478 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+%CE%B2+tubulin/beta+Tubulin+Antibody/pmc12857289-338-8-17
Average 96 stars, based on 2478 article reviews

β tubulin - by Bioz Stars, 2026-10

96/100 stars

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1) Product Images from "Integrated fabrication of a shape-adaptable, antioxidative composite stent for effective closure and biological repair of enteroatmospheric fistula"

Article Title: Integrated fabrication of a shape-adaptable, antioxidative composite stent for effective closure and biological repair of enteroatmospheric fistula

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.01.014

Figure Legend Snippet: Validation of key pathways and antioxidative effect mediated by the composite stent. (A) Western blot analysis of OXPHOS pathway-related proteins in each group; β-Tubulin was used as a loading control. (B) Quantification of the five mitochondrial OXPHOS complexes expression from Western blot bands, normalized to the loading control. (C) Western blot analysis of PI3K-Akt and HIF-1 pathway-related proteins in each group; β-Tubulin was used as a loading control. (D) Quantification of total Akt and HIF-1α expression from Western blot bands, normalized to the loading control. (E) Quantitative analysis of p-Akt normalized to total Akt expression. (F) Representative immunofluorescence images of tissue sections stained for Occludin to assess tight junctions and CD31 to visualize endothelial cells. (G) Quantification of Occludin and CD31 fluorescence intensity. (H) MDA levels, and SOD activity. Data were presented as mean ± SD (n = 3, biological replicates). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Techniques Used: Biomarker Discovery, Western Blot, Control, Expressing, Immunofluorescence, Staining, Fluorescence, Activity Assay

other:

Article Title: Hepatic cavernous hemangioma decellularized extracellular matrix/GelMA composite hydrogel promotes angiogenesis via the ITGA9–FAK–ERK1/2 axis
Article Snippet: Primary antibodies included: anti-VEGFA (1:10,000, Proteintech, China), anti-PDGF-BB (1:1,000, Proteintech, China), anti-ITGA9 (1:1,000, Proteintech, China), anti-FAK (1:1,000, Proteintech, China), anti-phospho-FAK (1:1,000, Cell Signaling Technology, USA), anti-ERK1/2 (1:10,000, Proteintech, China), anti-phospho-ERK1/2 (1:5,000, Proteintech, China), and anti-β-Tubulin (1:10,000, Proteintech, China).

Article Title: PKM2 Lactylation Promotes Colorectal Cancer Vasculogenic Mimicry and Bevacizumab Resistance by Facilitating FOSL1 Super-Enhancer Formation
Article Snippet: Primary 15 antibodies used in this study are used in this study are anti-Pan Kla (Jingjie, PTM-1401RM), 16 anti-PKM2 (Cell Signaling Technology, 4053), anti-PKM2 K206 lactylation (Jingjie, in this paper), 17 anti-AARS1 (Abclonal, A15017), anti-c-Myc (Cell Signaling Technology, 5605), anti-SOX2 18 (Abcam, ab93689), anti-NANOG (Cell Signaling Technology, 4903), anti-OCT4 (Cell Signaling 19 Technology, 2750), anti-Snail (Cell Signaling Technology, 3879), anti-E-cadherin (Cell Signaling 20 Technology, 3195), anti-Vimentin (Cell Signaling Technology, 5741), anti-PARP (Cell Signaling 21 Technology, 9532), anti-phospho-PKM2 (ThermoFisher, PA5105500), anti-ERK1/2 (Cell 22 Signaling Technology, 4695), anti-phospho-ERK1/2 (Cell Signaling Technology, 4370), 23 anti-Importin α5 (Abcam, ab187175), anti-HK2 (Cell Signaling Technology, 2867), anti-PFKFB3 24 (Abcam, ab181861), anti-LDHA (Proteintech, 19987-1-AP), anti-SLC16A3 (Proteintech, 25 22787-1-AP), anti-FOSL1 (Abcam, ab252421), anti-Pan Kac (Cell Signaling Technology, 9441), 26 anti-P300 (Abcam, ab275378), anti-SIRT1 (Cell Signaling Technology, 8469), anti-SNAI2 (Cell 27 Signaling Technology, 9585), anti-MAZ (Cell Signaling Technology, 90940), anti-FLAG tag 28 (Proteintech, 60002-1-Ig), anti-HA tag (Proteintech, 51064-2-AP), anti-Lamin A (Proteintech, 29 10298-1-AP) and anti-β-tubulin (Proteintech, 10068-1-AP).

Article Title: PSAT1 Promotes NSCLC Progression via the De Novo Serine Synthesis Pathway and Represents a Therapeutic Vulnerability
Article Snippet: The antibodies and dilution ratios used were as follows: Anti‐PSAT1 (10,501–1‐AP, at 1:5000 dilution, Proteintech), anti‐β‐Tubulin (10,094–1‐AP, at 1:2000 dilution, Proteintech), anti‐phosphorylated NF‐κB (p‐NF‐κB) (AP1294, at 1:1000 dilution, ABclonal), anti‐NF‐κB (10,745–1‐AP, at 1:1000 dilution, Proteintech), anti‐Cysteine‐dependent Aspartate‐specific Protease 3 (Caspase 3) (A19654, at 1:1000 dilution, ABclonal), anti‐B‐cell lymphoma‐2 (Bcl‐2) (A19693, at 1:1000 dilution, ABclonal), anti‐Bcl‐2‐Associated X protein (Bax) (A20227, at 1:1000 dilution, ABclonal), anti‐Cytochrome C (A4912, at 1:1000 dilution, ABclonal).

Article Title: PSAT1 Promotes NSCLC Progression via the De Novo Serine Synthesis Pathway and Represents a Therapeutic Vulnerability.
Article Snippet: The antibodies and dilution ratios used were as follows: Anti- PSAT1 (10,501–1- AP, at 1:5000 dilution, Proteintech), anti- β- Tubulin (10,094–1- AP, at 1:2000 dilution, Proteintech), anti- phosphorylated NF- κB (p- NF- κB) (AP1294, at 1:1000 dilution, ABclonal), anti- NF- κB (10,745–1- AP, at 1:1000 dilution, Proteintech), anti- Cysteinedependent Aspartate- specific Protease 3 (Caspase 3) (A19654, at 1:1000 dilution, ABclonal), anti- B- cell lymphoma- 2 (Bcl- 2) (A19693, at 1:1000 dilution, ABclonal), anti- Bcl- 2- Associated X protein (Bax) (A20227, at 1:1000 dilution, ABclonal), antiCytochrome C (A4912, at 1:1000 dilution, ABclonal).

Incubation:

Article Title: Rosmarinic Acid Targets AKR1B1 to Ameliorate Atherosclerosis via Vascular Endothelial Cell Energy Metabolism Regulation
Article Snippet: Proteins were then separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) (CW2384, CWBIO, Taizhou, China) on an 8–10% gradient gel, followed by the transfer to a polyvinylidene difluoride (PVDF) membranes (MerckMillipore, Burlington, MA, USA). .. The membranes were blocked with skim milk for one https://doi.org/10.3390/biom16030403 hour at 37 ◦C and incubated overnight at 4 ◦C with the following primary antibodies: anti-AKR1B1 (A22132, 1:5000, Abclonal Technology, Wuhan, China), anti-SIRT3 (ab189860, 1:1000, Abcam, Cambridge, UK), anti-PFKFB3 (ab181861, 1:1000, Abcam, Cambridge, UK), anti-β-tubulin (10068-1-AP, Proteintech, Wuhan, China), and anti-β-actin (20536-1-AP, Proteintech, Wuhan, China). .. Subsequently, the membranes were incubated for one hour with goat anti-mouse (1:10000, Proteintech, Wuhan, China) and goat anti-rabbit (1:10000, Proteintech, Wuhan, China) at 37 ◦C.

Article Title: Rosmarinic Acid Targets AKR1B1 to Ameliorate Atherosclerosis via Vascular Endothelial Cell Energy Metabolism Regulation
Article Snippet: Proteins were then separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) (CW2384, CWBIO, Taizhou, China) on an 8–10% gradient gel, followed by the transfer to a polyvinylidene difluoride (PVDF) membranes (Merck-Millipore, Burlington, MA, USA). .. The membranes were blocked with skim milk for one hour at 37 °C and incubated overnight at 4 °C with the following primary antibodies: anti-AKR1B1 (A22132, 1:5000, Abclonal Technology, Wuhan, China), anti-SIRT3 (ab189860, 1:1000, Abcam, Cambridge, UK), anti-PFKFB3 (ab181861, 1:1000, Abcam, Cambridge, UK), anti-β-tubulin (10068-1-AP, Proteintech, Wuhan, China), and anti-β-actin (20536-1-AP, Proteintech, Wuhan, China). .. Subsequently, the membranes were incubated for one hour with goat anti-mouse (1:10000, Proteintech, Wuhan, China) and goat anti-rabbit (1:10000, Proteintech, Wuhan, China) at 37 °C.

Western Blot:

Article Title: NCOA4-Mediated Ferritinophagy Induces Ferroptosis and Enriches Ferritin-Containing EVs via Ferritin Phase Separation to Promote Mechanical Ventilation-Induced Pulmonary Fibrosis
Article Snippet: Following three washes with 1 × TBST, membranes were then probed with HRP-conjugated secondary antibodies diluted 1:4000 at room temperature for 1 h. Blots were visualized using Image Lab TM software (Biorad, USA) with the enhanced chemiluminescence (ECL) system (Vazyme, China). .. The primary antibodies used for immunoblotting included anti-Fibronectin (ab268020, Abcam, USA), anti-alpha smooth muscle Actin (ab5694, Abcam, USA), anti-β-tubulin (HRP-66240, Proteintech, China), anti-GPX4 (ab125066, Abcam, USA), anti-SLC7A11 (ab307601, Abcam, USA), anti-FTH1 (4393S, CST, USA), anti-Alix (ab186429, Abcam, USA), anti-CD63 (ab217345, Abcam, USA), anti-NCOA4 (PA5-96398, Thermofisher, USA), anti-AGTR1 (NBP1-77078, Novus Biologicals, USA), and anti-Angiotensin II (ab259823, Abcam, USA). .. The HRP-conjugated secondary antibodies used included Anti-rabbit IgG (A0208, Beyotime, China) and Anti-mouse IgG (A0216, Beyotime, China).

Membrane:

Article Title: Small peptides derived from the autoinhibitory XY linker of phospholipase C-β isoforms inhibit enzyme activity and reduce inflammation.
Article Snippet: Separated proteins were transferred onto a 0.45 μm nitrocellulose membrane (Bio-Rad) using a wet blotting system for 2 h at 100 V and 4 ◦C in transfer buffer (25 mM Tris-Base, 190 mM glycine, 0.1% SDS, 20% methanol, pH 8.4). .. Thereafter, the membrane was blocked with 5% BSATBST for 1 h. Isoform PLCβ3, β-tubulin and α-actin were probed with specific primary antibodies anti-PLCβ3 (1:100 in 1% BSA-TBST; sc133231, Santa Cruz Biotechnology), anti-β-tubulin (1:1000 in 2.5% BSA-TBST; 10094–1-AP, Proteintech) and anti-α-actin (1:1000 in 2.5% BSA-TBST; A2066, Sigma-Aldrich). .. Additionally, integrin α6/β1 was probed as a membrane-fraction control with the anti-integrin antibody (1:2000 in 1%BSA-TBST; ab181551, Abcam) [43].

Image Search Results

Melatonin dose modulates NSCs lineage commitment, viability, oxidative stress, and mitochondrial membrane potential at day 5. (A) Representative immunofluorescence images of TUJ1 with Nestin in NSCs cultured within the cell-laden MT/BEM matrix and exposed to melatonin (0, 25, 50, 75, 100 μM) for 5 days (scale bar, 50 μm). (B) Representative images of GFAP with Nestin under the same conditions (scale bar, 50 μm). (C) Representative images of Olig2 with Nestin (scale bar, 50 μm). (D) Percentages of TUJ1(+), GFAP (+), and Olig2(+) cells relative to total nuclei (DAPI) (n = 10 fields/group). (E) RT-qPCR of TUJ1, GFAP, and Olig2 normalized to GAPDH and expressed as fold change versus control (ΔΔCt) (n = 6). (F) Live/Dead staining (Calcein AM/EthD-1) at day 5. (G) Western blots of TUJ1 and GFAP with GAPDH loading control. (H) Densitometry of TUJ1/GAPDH and GFAP/GAPDH (n = 3 independent experiments). (I) ROS staining by DCFH-DA with Rosup as the positive control. (J) Quantification of ROS fluorescence intensity (n = 10 fields/group, compared to control). (K) JC-1 staining of mitochondrial membrane potential (ΔΨm) with CCCP as the positive control for depolarization. (L) JC-1 red/green ratio (n = 10 fields/group, compared to control). Statistical analysis: Data are presented as mean ± SD. one-way ANOVA with Holm–Sidak's multiple comparisons for multi-group datasets (D, E, J, L); unpaired two-tailed t -test for the two-group comparison (H). Significance: ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Journal: Bioactive Materials

Article Title: Melatonin-incorporated brain extracellular matrix hydrogel enhances NSCs mitochondrial metabolism to promote neuroregeneration via the AMPK-PGC-1α-NRF1/TFAM axis after spinal cord injury

doi: 10.1016/j.bioactmat.2026.04.006

Figure Lengend Snippet: Melatonin dose modulates NSCs lineage commitment, viability, oxidative stress, and mitochondrial membrane potential at day 5. (A) Representative immunofluorescence images of TUJ1 with Nestin in NSCs cultured within the cell-laden MT/BEM matrix and exposed to melatonin (0, 25, 50, 75, 100 μM) for 5 days (scale bar, 50 μm). (B) Representative images of GFAP with Nestin under the same conditions (scale bar, 50 μm). (C) Representative images of Olig2 with Nestin (scale bar, 50 μm). (D) Percentages of TUJ1(+), GFAP (+), and Olig2(+) cells relative to total nuclei (DAPI) (n = 10 fields/group). (E) RT-qPCR of TUJ1, GFAP, and Olig2 normalized to GAPDH and expressed as fold change versus control (ΔΔCt) (n = 6). (F) Live/Dead staining (Calcein AM/EthD-1) at day 5. (G) Western blots of TUJ1 and GFAP with GAPDH loading control. (H) Densitometry of TUJ1/GAPDH and GFAP/GAPDH (n = 3 independent experiments). (I) ROS staining by DCFH-DA with Rosup as the positive control. (J) Quantification of ROS fluorescence intensity (n = 10 fields/group, compared to control). (K) JC-1 staining of mitochondrial membrane potential (ΔΨm) with CCCP as the positive control for depolarization. (L) JC-1 red/green ratio (n = 10 fields/group, compared to control). Statistical analysis: Data are presented as mean ± SD. one-way ANOVA with Holm–Sidak's multiple comparisons for multi-group datasets (D, E, J, L); unpaired two-tailed t -test for the two-group comparison (H). Significance: ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: Following blocking, membranes were incubated overnight at 4 °C with the following primary antibodies: GFAP (1:1000; #80788, CST, USA), TUJ1 (1:1000; #YA586, MCE, China), GAPDH (1:1000; #2118, CST, USA), phospho-ACC (Ser79) (1:1000; #11818, CST, USA), Acetyl-CoA Carboxylase (C83B10) (1:1000; #3676, CST, USA), Total OXPHOS Rodent WB Antibody Cocktail (1:1000; #ab110413, Abcam, UK), phospho-AMPKα (Thr172) (1:1000; #2535, CST, USA), and total AMPKα (1:1000; #2532, CST, USA).

Techniques: Membrane, Immunofluorescence, Cell Culture, Quantitative RT-PCR, Control, Staining, Western Blot, Positive Control, Fluorescence, Two Tailed Test, Comparison

Three-dimensional immunofluorescence and transcriptomic profiling of melatonin-treated NSCs. (A) Representative 3D confocal reconstructions of NSCs networks cultured for 5 days in BEM or MT/BEM hydrogels, immunostained for Nestin, TUJ1, GFAP and OLIG2 with DAPI nuclear counterstain. Scale bar: 50 μm. (B-C) Quantification of neurite outgrowth showing total neurite length (μm) (B) and neurite filament area (μm 2 ) (C) per field of view. (D) Quantification of astroglial differentiation expressed as GFAP + area (% of ROI). (E) Quantification of oligodendroglial lineage commitment expressed as OLIG2 + cells (% of DAPI + nuclei). Data are presented as mean ± SD. Statistical significance was assessed using an unpaired two-tailed t -test; ∗p < 0.05, ∗∗p < 0.01 versus NSCs@BEM.

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.04.006

Figure Lengend Snippet: Three-dimensional immunofluorescence and transcriptomic profiling of melatonin-treated NSCs. (A) Representative 3D confocal reconstructions of NSCs networks cultured for 5 days in BEM or MT/BEM hydrogels, immunostained for Nestin, TUJ1, GFAP and OLIG2 with DAPI nuclear counterstain. Scale bar: 50 μm. (B-C) Quantification of neurite outgrowth showing total neurite length (μm) (B) and neurite filament area (μm 2 ) (C) per field of view. (D) Quantification of astroglial differentiation expressed as GFAP + area (% of ROI). (E) Quantification of oligodendroglial lineage commitment expressed as OLIG2 + cells (% of DAPI + nuclei). Data are presented as mean ± SD. Statistical significance was assessed using an unpaired two-tailed t -test; ∗p < 0.05, ∗∗p < 0.01 versus NSCs@BEM.

Techniques: Immunofluorescence, Cell Culture, Two Tailed Test

Molecular validation of neural repair and mechanism activation in spinal cord tissue. Western blot and qPCR analyses of spinal cord tissue lysates from Sham, SCI, BEM, NSCs@BEM, and NSCs@MT/BEM groups. (A) Representative Western blots for the neuronal marker TUJ1 and the glial scar marker GFAP. (B) Representative Western blots for phosphorylated AMPK (p-AMPK), phosphorylated ACC (p-ACC), and their respective total proteins. (C) Representative Western blots for the five oxidative phosphorylation (OXPHOS) complex subunits. (D) Densitometric quantification of TUJ1 and GFAP protein levels. (E) Densitometric quantification of the p-AMPK/total AMPK and p-ACC/total ACC ratios. (F) Densitometric quantification of OXPHOS complex protein levels. (G) Relative mRNA expression of neural markers (TUJ1, GFAP, Olig2) and key mitochondrial biogenesis regulators (Ppargc1a, Tfam) determined by qPCR. Data are presented as mean ± SD. Statistical significance was determined by one-way ANOVA with Holm–Sidak's multiple comparisons test. (∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.04.006

Figure Lengend Snippet: Molecular validation of neural repair and mechanism activation in spinal cord tissue. Western blot and qPCR analyses of spinal cord tissue lysates from Sham, SCI, BEM, NSCs@BEM, and NSCs@MT/BEM groups. (A) Representative Western blots for the neuronal marker TUJ1 and the glial scar marker GFAP. (B) Representative Western blots for phosphorylated AMPK (p-AMPK), phosphorylated ACC (p-ACC), and their respective total proteins. (C) Representative Western blots for the five oxidative phosphorylation (OXPHOS) complex subunits. (D) Densitometric quantification of TUJ1 and GFAP protein levels. (E) Densitometric quantification of the p-AMPK/total AMPK and p-ACC/total ACC ratios. (F) Densitometric quantification of OXPHOS complex protein levels. (G) Relative mRNA expression of neural markers (TUJ1, GFAP, Olig2) and key mitochondrial biogenesis regulators (Ppargc1a, Tfam) determined by qPCR. Data are presented as mean ± SD. Statistical significance was determined by one-way ANOVA with Holm–Sidak's multiple comparisons test. (∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).

Techniques: Biomarker Discovery, Activation Assay, Western Blot, Marker, Phospho-proteomics, Expressing

Journal: Bioactive Materials

Article Title: Integrated fabrication of a shape-adaptable, antioxidative composite stent for effective closure and biological repair of enteroatmospheric fistula

doi: 10.1016/j.bioactmat.2026.01.014

Figure Lengend Snippet: Validation of key pathways and antioxidative effect mediated by the composite stent. (A) Western blot analysis of OXPHOS pathway-related proteins in each group; β-Tubulin was used as a loading control. (B) Quantification of the five mitochondrial OXPHOS complexes expression from Western blot bands, normalized to the loading control. (C) Western blot analysis of PI3K-Akt and HIF-1 pathway-related proteins in each group; β-Tubulin was used as a loading control. (D) Quantification of total Akt and HIF-1α expression from Western blot bands, normalized to the loading control. (E) Quantitative analysis of p-Akt normalized to total Akt expression. (F) Representative immunofluorescence images of tissue sections stained for Occludin to assess tight junctions and CD31 to visualize endothelial cells. (G) Quantification of Occludin and CD31 fluorescence intensity. (H) MDA levels, and SOD activity. Data were presented as mean ± SD (n = 3, biological replicates). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: Antibodies against mitochondrial oxidative phosphorylation complexes (OXPHOS cocktail), β-Tubulin, total Akt, p-Akt, and HIF-1α were purchased from Proteintech (Chicago, IL).

Techniques: Biomarker Discovery, Western Blot, Control, Expressing, Immunofluorescence, Staining, Fluorescence, Activity Assay

Expression of vimentin, E-cadherin, and GSK3β under IL-17A or TGF-β stimulation in CRC cells. HCT116 cells were either untreated or treated with recombinant IL-17A (25 ng/mL) or recombinant TGF-β (20 ng/mL) for 48 hours. The mRNA expression levels of vimentin (A), E-cadherin (B), and GSK3β (C) were analyzed by RT-qPCR using GAPDH as an internal control. (D) Protein expression levels of vimentin, E-cadherin, and GSK3β were analyzed by western blotting with specific antibodies. GAPDH was used as the internal control for detecting vimentin and GSK3β, while β-tubulin served as the loading control for E-cadherin. All experiments were independently repeated 2 to 3 times using biological replicates, with similar results obtained. *P<0.05, as determined by a two-sided paired Student’s t-test compared to the NC; **, P<0.01. CRC, colorectal cancer; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; IL-17A, interleukin-17A; NC, negative control; RT-qPCR, reverse transcription quantitative real-time polymerase chain reaction; TGF-β, transforming growth factor-beta.

Journal: Translational Cancer Research

Article Title: Immune-driven induction of miR-501-5p by IL-17A enhances colorectal cancer progression

doi: 10.21037/tcr-2025-1-2843

Figure Lengend Snippet: Expression of vimentin, E-cadherin, and GSK3β under IL-17A or TGF-β stimulation in CRC cells. HCT116 cells were either untreated or treated with recombinant IL-17A (25 ng/mL) or recombinant TGF-β (20 ng/mL) for 48 hours. The mRNA expression levels of vimentin (A), E-cadherin (B), and GSK3β (C) were analyzed by RT-qPCR using GAPDH as an internal control. (D) Protein expression levels of vimentin, E-cadherin, and GSK3β were analyzed by western blotting with specific antibodies. GAPDH was used as the internal control for detecting vimentin and GSK3β, while β-tubulin served as the loading control for E-cadherin. All experiments were independently repeated 2 to 3 times using biological replicates, with similar results obtained. *P<0.05, as determined by a two-sided paired Student’s t-test compared to the NC; **, P<0.01. CRC, colorectal cancer; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; IL-17A, interleukin-17A; NC, negative control; RT-qPCR, reverse transcription quantitative real-time polymerase chain reaction; TGF-β, transforming growth factor-beta.

Article Snippet: The primary antibodies used included anti-beta tubulin antibody (mouse mAb, #GB15140, Servicebio, Wuhan, China), anti-actin monoclonal antibody (mouse mAb, #GB15001, Servicebio), anti- glycogen synthase kinase 3 beta (GAPDH) monoclonal antibody (mouse mAb, #GB12002, Servicebio), anti-vimentin (Rabbit mAb, #5741T, Cell Signaling, Danvers, USA), GSK-3β (Rabbit mAb, #12456T, Cell Signaling), and anti-E-Cadherin (Rabbit mAb #3195, Cell Signaling).

Techniques: Expressing, Recombinant, Quantitative RT-PCR, Control, Western Blot, Negative Control, Reverse Transcription, Real-time Polymerase Chain Reaction

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β tubulin (Proteintech)

Structured Review

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1) Product Images from "Integrated fabrication of a shape-adaptable, antioxidative composite stent for effective closure and biological repair of enteroatmospheric fistula"

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