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Proteintech anti ca xii
Anti Ca Xii, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/caxii+antibody/CA12+Antibody/pm41418744-157-6-9
Average 93 stars, based on 24 article reviews

anti ca xii - by Bioz Stars, 2026-09

93/100 stars

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Blocking Assay:

Article Title: Preserving the Immune‐Privileged Niche of the Nucleus Pulposus: Safeguarding Intervertebral Discs from Degeneration after Discectomy with Synthetic Mucin Hydrogel Injection
Article Snippet: .. Blocking nonspecific protein binding was carried out using 5% goat serum diluted in PBS for 1 h at room temperature, and Krt19 antibody (1:200, Abclonal, Boston, MA, USA) and CAXII antibody (1:100, Proteintech, Chicago, IL, USA) were incubated overnight at 4 °C. .. Subsequent steps involved treatment with cy3 or FITC‐labeled goat anti‐rabbit secondary antibody (1:800, Beyotime, Shanghai, China), and nuclei were counterstained with DAPI.

Article Title: Preserving the Immune-Privileged Niche of the Nucleus Pulposus: Safeguarding Intervertebral Discs from Degeneration after Discectomy with Synthetic Mucin Hydrogel Injection.
Article Snippet: .. Blocking nonspecific protein binding was carried out using 5% goat serum diluted in PBS for 1 h at room temperature, and Krt19 antibody (1:200, Abclonal, Boston, MA, USA) and CAXII antibody (1:100, Proteintech, Chicago, IL, USA) were incubated overnight at 4 °C. .. Subsequent steps involved treatment with cy3 or FITC-labeled goat antirabbit secondary antibody (1:800, Beyotime, Shanghai, China), and nuclei were counterstained with DAPI.

Protein Binding:

Incubation:

Image Search Results

Figure 1. Membrane expression of CA12 was reduced by histamine treatment in lung cancer cells. Protein expression levels of CA12 after histamine (His) treatment (100 lM, 24 h and 48 h) in both (A) Beas-2B (left panels) and (B) A549 (right panels) cells. b-actin was used as a loading control. (C) The graph indicates relative inten- sity of CA12, normalised by b-actin. The bars represent means ± SEM (n ¼ 4, p < 0.05, p < 0.001). b-actin was used as a loading control. (D) Immunofluorescence staining of CA12 (green) and DAPI (blue) after His treatment (100lM, 24 h) in Beas-2B and A549 cells. The scale bar represents 50 lm. (E) High magnification of immunofluorescence staining of CA12 (green) and DAPI (blue) after His treatment (100 lM, 24 h) in A549 cells. The scale bar represents 10 lm. (F) Immunofluorescence staining of CA12 (green) and DAPI (blue) after His treatment (100 lM, 24h) in CA12-overexpressed H1299 cells. The scale bar represents 10 lm. (G) Surface expression of CA12 after His (100 lM, 24 h) treatment in A549. (H) The graph indicates relative intensity of CA12, normalised by input CA12 and b-actin. The bars represent means ±SEM (n ¼ 3). b-actin was used as a loading control. (I) pHRodo staining (green) after His treatment (100 lM, 24 h) in Beas-2B and A549 cells. The scale bar represents 50 lm. (J) The graph indicates the relative intensity of pHRodo. The bars present means ± SEM (n ¼ 18, p < 0.001).

Journal: Journal of enzyme inhibition and medicinal chemistry

Article Title: Trafficking of carbonic anhydrase 12 and bicarbonate transporters by histamine stimulation mediates intracellular acidic scenario in lung cancer cells.

doi: 10.1080/14756366.2023.2247181

Figure Lengend Snippet: Figure 1. Membrane expression of CA12 was reduced by histamine treatment in lung cancer cells. Protein expression levels of CA12 after histamine (His) treatment (100 lM, 24 h and 48 h) in both (A) Beas-2B (left panels) and (B) A549 (right panels) cells. b-actin was used as a loading control. (C) The graph indicates relative inten- sity of CA12, normalised by b-actin. The bars represent means ± SEM (n ¼ 4, p < 0.05, p < 0.001). b-actin was used as a loading control. (D) Immunofluorescence staining of CA12 (green) and DAPI (blue) after His treatment (100lM, 24 h) in Beas-2B and A549 cells. The scale bar represents 50 lm. (E) High magnification of immunofluorescence staining of CA12 (green) and DAPI (blue) after His treatment (100 lM, 24 h) in A549 cells. The scale bar represents 10 lm. (F) Immunofluorescence staining of CA12 (green) and DAPI (blue) after His treatment (100 lM, 24h) in CA12-overexpressed H1299 cells. The scale bar represents 10 lm. (G) Surface expression of CA12 after His (100 lM, 24 h) treatment in A549. (H) The graph indicates relative intensity of CA12, normalised by input CA12 and b-actin. The bars represent means ±SEM (n ¼ 3). b-actin was used as a loading control. (I) pHRodo staining (green) after His treatment (100 lM, 24 h) in Beas-2B and A549 cells. The scale bar represents 50 lm. (J) The graph indicates the relative intensity of pHRodo. The bars present means ± SEM (n ¼ 18, p < 0.001).

Article Snippet: CA12 (#sc-374314, Santa Cruz Biotechnology, Dallas, TX, USA), NBCn1 (#ab82335, Abcam), AE2, and NBCe1 (#ab56215, Abcam) antibodies (1:100 dilution in 0.5% BSA in DPBS supplemented with 10% goat serum) were treated at 4 C for overnight and cells were washed thrice with 0.5% BSA in DPBS.

Techniques: Membrane, Expressing, Control, Immunofluorescence, Staining

$Figure 2. Histamine treatment reduced NBC activity in A549 cells. (A) NBC activity in response to histamine (His) treatment (100lM) for 24 h in Beas-2B (left panel) and A549 (right panel) cells. (B) The graphs indicate NBC activities of Beas-2B (left panel) and A549(right panel) cells in response to His treatment (100 lM). The bars represent means ± SEM (n ¼ 5 6, p < 0.01). (C, D) Immunofluorescence staining of NBCn1 (red) and DAPI (blue) after His treatment (100 lM, 24 h) in Beas-2B (C) and A549 (D) cells. The scale bar represents 10 lm. (E) The graph indicates the relative intensity of NBCn1 after His treatment (100 lM, 24 h) in Beas-2B cells. The bars represent means ± SEM (n ¼ 8 9). (F) The graph indicates relative intensity of NBCn1 after His treatment (100 lM, 24 h) in A549 cells. The bars represent means ±SEM (n ¼ 10 13, p < 0.001). (G) Immunofluorescence staining of CA12 (green) and NBCn1 (red) after His treatment (100 lM, 24h) in A549 cells. DAPI (nucleus, blue). (H K) The graph indicates relative intensity of CA12-membrane fraction (H), CA12-cytosolic fraction (I), NBCn1-membrane fraction (J), and NBCn1-cytosolic fraction (K) after His treatment (100 lM, 24 h) in A549 cells. The bars represent means ± SEM (n ¼ 6 14, p < 0.05, p < 0.01).$

Journal: Journal of enzyme inhibition and medicinal chemistry

Article Title: Trafficking of carbonic anhydrase 12 and bicarbonate transporters by histamine stimulation mediates intracellular acidic scenario in lung cancer cells.

doi: 10.1080/14756366.2023.2247181

Figure Lengend Snippet: Figure 2. Histamine treatment reduced NBC activity in A549 cells. (A) NBC activity in response to histamine (His) treatment (100lM) for 24 h in Beas-2B (left panel) and A549 (right panel) cells. (B) The graphs indicate NBC activities of Beas-2B (left panel) and A549(right panel) cells in response to His treatment (100 lM). The bars represent means ± SEM (n ¼ 5 6, p < 0.01). (C, D) Immunofluorescence staining of NBCn1 (red) and DAPI (blue) after His treatment (100 lM, 24 h) in Beas-2B (C) and A549 (D) cells. The scale bar represents 10 lm. (E) The graph indicates the relative intensity of NBCn1 after His treatment (100 lM, 24 h) in Beas-2B cells. The bars represent means ± SEM (n ¼ 8 9). (F) The graph indicates relative intensity of NBCn1 after His treatment (100 lM, 24 h) in A549 cells. The bars represent means ±SEM (n ¼ 10 13, p < 0.001). (G) Immunofluorescence staining of CA12 (green) and NBCn1 (red) after His treatment (100 lM, 24h) in A549 cells. DAPI (nucleus, blue). (H K) The graph indicates relative intensity of CA12-membrane fraction (H), CA12-cytosolic fraction (I), NBCn1-membrane fraction (J), and NBCn1-cytosolic fraction (K) after His treatment (100 lM, 24 h) in A549 cells. The bars represent means ± SEM (n ¼ 6 14, p < 0.05, p < 0.01).

Techniques: Activity Assay, Immunofluorescence, Staining, Membrane

Figure 4. Histamine mediated CA12 and AE2 trafficking through the involvement of calcium-dependent calmodulin kinase II. (A) Immunofluorescence staining of CA12 (green) and AE2 (red) after histamine (His) treatment (100lM, 24 h) in A549 cells. DAPI (nucleus, blue). (B) CBE activity in response to His treatment (100 lM) with and without KN62 (10lM) for 24h in A549 cells. (C) The graph indicates CBE activity in response to His treatment (100 lM) with and without KN62 (10lM) for 24 h in A549 cells. The bars represent means ± SEM (n ¼ 4 5, p < 0.05 vs Control and #p < 0.05 vs His-treated group). (D) Surface expression of AE2 and CA12 after His (100 lM) with and without KN62 (10lM) for 24 h in A549 cells. (E) The graph indicates the relative intensity of AE2 normalised by input AE2 and b-actin. The bars rep- resent means ± SEM (n ¼ 5, p < 0.05 vs Control and #p < 0.05 vs His-treated group). b-actin was used as a loading control. (F) The graph indicates the relative inten- sity of CA12 normalised by input CA12 and b-actin. The bars represent means ±SEM (n ¼ 6, p < 0.05 vs Control). b-actin was used as a loading control. (G) pHRodo staining (green) after His treatment (100 lM) with and without KN62 (10lM) for 24 h in A549 cells. The scale bar represents 50 lm. (H) The graph indicates the relative intensity of pHRodo. The bars present means ±SEM (n ¼ 4 6, p < 0.001 vs Control and #p < 0.05 vs His-treated group).

Journal: Journal of enzyme inhibition and medicinal chemistry

Article Title: Trafficking of carbonic anhydrase 12 and bicarbonate transporters by histamine stimulation mediates intracellular acidic scenario in lung cancer cells.

doi: 10.1080/14756366.2023.2247181

Figure Lengend Snippet: Figure 4. Histamine mediated CA12 and AE2 trafficking through the involvement of calcium-dependent calmodulin kinase II. (A) Immunofluorescence staining of CA12 (green) and AE2 (red) after histamine (His) treatment (100lM, 24 h) in A549 cells. DAPI (nucleus, blue). (B) CBE activity in response to His treatment (100 lM) with and without KN62 (10lM) for 24h in A549 cells. (C) The graph indicates CBE activity in response to His treatment (100 lM) with and without KN62 (10lM) for 24 h in A549 cells. The bars represent means ± SEM (n ¼ 4 5, p < 0.05 vs Control and #p < 0.05 vs His-treated group). (D) Surface expression of AE2 and CA12 after His (100 lM) with and without KN62 (10lM) for 24 h in A549 cells. (E) The graph indicates the relative intensity of AE2 normalised by input AE2 and b-actin. The bars rep- resent means ± SEM (n ¼ 5, p < 0.05 vs Control and #p < 0.05 vs His-treated group). b-actin was used as a loading control. (F) The graph indicates the relative inten- sity of CA12 normalised by input CA12 and b-actin. The bars represent means ±SEM (n ¼ 6, p < 0.05 vs Control). b-actin was used as a loading control. (G) pHRodo staining (green) after His treatment (100 lM) with and without KN62 (10lM) for 24 h in A549 cells. The scale bar represents 50 lm. (H) The graph indicates the relative intensity of pHRodo. The bars present means ±SEM (n ¼ 4 6, p < 0.001 vs Control and #p < 0.05 vs His-treated group).

Techniques: Immunofluorescence, Staining, Activity Assay, Control, Expressing

Figure 5. Cellular pH was modulated by CA12 and AE2 trafficking. (A) Surface expression of CA12 and AE2 after histamine (His) (100lM) with and without bafilomycin (Baf; 2 lM) for 24 h in A549 cells. (B) The graph indicates the relative intensity of AE2 normalised by input AE2 and b-actin. The bars represent means ± SEM (n ¼ 6, p < 0.05 vs Control and #p < 0.05 vs His-treated group. (C) The graph indicates the relative intensity of CA12 normalised by input CA12 and b-actin. The bars repre- sent means ± SEM (n ¼ 6, p < 0.05 or p < 0.01 vs Control and #p < 0.05 vs His-treated group). b-actin was used as a loading control. (D) Immunofluorescence stain- ing of CA12 (red) and DAPI (blue) after His treatment (100 lM) with and without Baf (2 lM) for 24 h in A549 cells. (E) Immunofluorescence staining of AE2 (green) and DAPI (blue) after His treatment (100 lM) with and without Baf (2 lM) for 24 h in A549 cells. (F) CBE activity in response to His treatment (100 lM) with or without Baf (2lM) for 24 h in A549 cells. (G) The graph indicates CBE activity in response to His treatment (100 lM) with and without Baf (2 lM) for 24 h in A549 cells. The bars represent the mean ± SEM (n ¼ 3 5, p < 0.01). (H) pHRodo staining (green) after His treatment (100lM) with and without Baf (2 lM) for 24h in A549 cells. The scale bar represents 50 lm. (I) The graph indicates the relative intensity of pHRodo. The bars present means ± SEM (n ¼ 4 5, p < 0.05 vs Control and ##p < 0.01 vs His-treated group).

Journal: Journal of enzyme inhibition and medicinal chemistry

Article Title: Trafficking of carbonic anhydrase 12 and bicarbonate transporters by histamine stimulation mediates intracellular acidic scenario in lung cancer cells.

doi: 10.1080/14756366.2023.2247181

Figure Lengend Snippet: Figure 5. Cellular pH was modulated by CA12 and AE2 trafficking. (A) Surface expression of CA12 and AE2 after histamine (His) (100lM) with and without bafilomycin (Baf; 2 lM) for 24 h in A549 cells. (B) The graph indicates the relative intensity of AE2 normalised by input AE2 and b-actin. The bars represent means ± SEM (n ¼ 6, p < 0.05 vs Control and #p < 0.05 vs His-treated group. (C) The graph indicates the relative intensity of CA12 normalised by input CA12 and b-actin. The bars repre- sent means ± SEM (n ¼ 6, p < 0.05 or p < 0.01 vs Control and #p < 0.05 vs His-treated group). b-actin was used as a loading control. (D) Immunofluorescence stain- ing of CA12 (red) and DAPI (blue) after His treatment (100 lM) with and without Baf (2 lM) for 24 h in A549 cells. (E) Immunofluorescence staining of AE2 (green) and DAPI (blue) after His treatment (100 lM) with and without Baf (2 lM) for 24 h in A549 cells. (F) CBE activity in response to His treatment (100 lM) with or without Baf (2lM) for 24 h in A549 cells. (G) The graph indicates CBE activity in response to His treatment (100 lM) with and without Baf (2 lM) for 24 h in A549 cells. The bars represent the mean ± SEM (n ¼ 3 5, p < 0.01). (H) pHRodo staining (green) after His treatment (100lM) with and without Baf (2 lM) for 24h in A549 cells. The scale bar represents 50 lm. (I) The graph indicates the relative intensity of pHRodo. The bars present means ± SEM (n ¼ 4 5, p < 0.05 vs Control and ##p < 0.01 vs His-treated group).

Techniques: Expressing, Control, Immunofluorescence, Staining, Activity Assay

Figure 6. Schematic illustration of cellular pH regulation through the histamine-mediated acidic scenario. NBCn1 and its associated CA12 co-localize at the plasma membrane. Histamine stimulation induces convergent trafficking of pH-associated proteins such as internalised CA12 and reduced NBCn1 and enhanced expression of AE2 in lung cancer cells. Internalised CA12 and reduced NBCn1 exhausted cytosolic bicarbonate and the enhanced AE2 exacerbates bicarbonate efflux. This histamine receptor activation-induced phenomenon mediated acidic cytosol as termed acidic scenario.

Journal: Journal of enzyme inhibition and medicinal chemistry

Article Title: Trafficking of carbonic anhydrase 12 and bicarbonate transporters by histamine stimulation mediates intracellular acidic scenario in lung cancer cells.

doi: 10.1080/14756366.2023.2247181

Figure Lengend Snippet: Figure 6. Schematic illustration of cellular pH regulation through the histamine-mediated acidic scenario. NBCn1 and its associated CA12 co-localize at the plasma membrane. Histamine stimulation induces convergent trafficking of pH-associated proteins such as internalised CA12 and reduced NBCn1 and enhanced expression of AE2 in lung cancer cells. Internalised CA12 and reduced NBCn1 exhausted cytosolic bicarbonate and the enhanced AE2 exacerbates bicarbonate efflux. This histamine receptor activation-induced phenomenon mediated acidic cytosol as termed acidic scenario.

Techniques: Clinical Proteomics, Membrane, Expressing, Activation Assay

Journal: Oxidative Medicine and Cellular Longevity

Article Title: The Role of the miR-548au-3p/CA12 Axis in Tracheal Chondrogenesis in Congenital Pulmonary Airway Malformations

doi: 10.1155/2023/6428579

Figure Lengend Snippet: Primers for real-time PCR.

Article Snippet: Primary antibodies for this study were specific for CA12 (Boster, Cat. No. A04063, 1 : 1000), LONRF3 (GeneTex, Cat. No. GTX112150, 1 : 2000), MAP2 (Boster, Cat. No. A01201, 1 : 2000), THBS1 (Boster, Cat. No. PB0471, 1 : 2000), PPID, E-cadherin (Beyotime, Cat. No. AF6759, 1 : 1000), N-cadherin (Beyotime, Cat. No. AF5237, 1 : 800), aggrecan (Abcam, Cat. No. ab3778, 1 : 1000), Col2A1 (Boster, Cat. No. A00517, 1 : 2000), MMP13 (Proteintech, Cat. No. 18165-1-AP, 1 : 3000), ADAMTS4 (Proteintech, Cat. No. 11865-1-AP, 1 : 600), and GAPDH (Abcam, Cat. No. ab9485, 1 : 2000).

Techniques:

Identification of DEGs involved in the pathogenesis of CPAM. (a) Flowchart of the study design and samples at each stage of analysis. (b) Scatterplot of mRNA expression variation between diseased CPAM and normal tissues. (c) Hierarchical cluster of gene expression profiles from microarray assays. Expression of CA12, LONRF3, MAP2, THBS1, and PPID at mRNA (d) and protein (e) levels in lung tissues from CPAM and adjacent normal tissues. ∗∗∗ p < 0.001, compared with normal.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: The Role of the miR-548au-3p/CA12 Axis in Tracheal Chondrogenesis in Congenital Pulmonary Airway Malformations

doi: 10.1155/2023/6428579

Figure Lengend Snippet: Identification of DEGs involved in the pathogenesis of CPAM. (a) Flowchart of the study design and samples at each stage of analysis. (b) Scatterplot of mRNA expression variation between diseased CPAM and normal tissues. (c) Hierarchical cluster of gene expression profiles from microarray assays. Expression of CA12, LONRF3, MAP2, THBS1, and PPID at mRNA (d) and protein (e) levels in lung tissues from CPAM and adjacent normal tissues. ∗∗∗ p < 0.001, compared with normal.

Techniques: Expressing, Gene Expression, Microarray

CA12 as a direct target of miR-548au-3p. (a) Binding sites between miR-548au-3p and the 3′-UTR region of CA12 mRNA. (b) HEK-293 cells were cotransfected with miR-548au-3p mimics or NC and wild-type or mutant CA12 3′-UTR, followed by luciferase reporter assay. CA12 mRNA (c) and protein (d) levels in rat tracheal chondrocytes after transfection with miR-548au-3p mimics or inhibitor. ∗∗ p < 0.01 and ∗∗∗ p < 0.001, compared with NC.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: The Role of the miR-548au-3p/CA12 Axis in Tracheal Chondrogenesis in Congenital Pulmonary Airway Malformations

doi: 10.1155/2023/6428579

Figure Lengend Snippet: CA12 as a direct target of miR-548au-3p. (a) Binding sites between miR-548au-3p and the 3′-UTR region of CA12 mRNA. (b) HEK-293 cells were cotransfected with miR-548au-3p mimics or NC and wild-type or mutant CA12 3′-UTR, followed by luciferase reporter assay. CA12 mRNA (c) and protein (d) levels in rat tracheal chondrocytes after transfection with miR-548au-3p mimics or inhibitor. ∗∗ p < 0.01 and ∗∗∗ p < 0.001, compared with NC.

Techniques: Binding Assay, Mutagenesis, Luciferase, Reporter Assay, Transfection

CA12 suppressed rat tracheal chondrocyte proliferation and differentiation. Rat tracheal chondrocytes were transfected with CA12 overexpression plasmid or CA12 siRNA. (a) Transfection efficiency was determined by western blot. (b) Viability of rat tracheal chondrocytes assessed by CCK-8 assay. (c) Cell proliferation ability assessed by EdU staining. Red fluorescence: EdU; blue fluorescence: DAPI (scale bar = 50 μ m). (d) Cell apoptosis levels assessed by TUNEL staining (scale bar = 50 μ m). Red fluorescence: TUNEL; blue fluorescence: DAPI. (e) Cell apoptosis assessed by flow cytometry with Annexin V/propidium iodide staining. (f) Protein expression of E-cadherin and N-cadherin. (g) The effect of miR-548au-3p on differentiation of rat tracheal chondrocytes assessed with Alcian blue staining (scale bar = 100 μ m). (h) Aggrecan, Col2A1, MMP13, and ADAMTS4 protein levels detected by western blot. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001, compared with vector or siRNA NC.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: The Role of the miR-548au-3p/CA12 Axis in Tracheal Chondrogenesis in Congenital Pulmonary Airway Malformations

doi: 10.1155/2023/6428579

Figure Lengend Snippet: CA12 suppressed rat tracheal chondrocyte proliferation and differentiation. Rat tracheal chondrocytes were transfected with CA12 overexpression plasmid or CA12 siRNA. (a) Transfection efficiency was determined by western blot. (b) Viability of rat tracheal chondrocytes assessed by CCK-8 assay. (c) Cell proliferation ability assessed by EdU staining. Red fluorescence: EdU; blue fluorescence: DAPI (scale bar = 50 μ m). (d) Cell apoptosis levels assessed by TUNEL staining (scale bar = 50 μ m). Red fluorescence: TUNEL; blue fluorescence: DAPI. (e) Cell apoptosis assessed by flow cytometry with Annexin V/propidium iodide staining. (f) Protein expression of E-cadherin and N-cadherin. (g) The effect of miR-548au-3p on differentiation of rat tracheal chondrocytes assessed with Alcian blue staining (scale bar = 100 μ m). (h) Aggrecan, Col2A1, MMP13, and ADAMTS4 protein levels detected by western blot. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001, compared with vector or siRNA NC.

Techniques: Transfection, Over Expression, Plasmid Preparation, Western Blot, CCK-8 Assay, Staining, Fluorescence, TUNEL Assay, Flow Cytometry, Expressing

Knockdown of CA12 abolished miR-548au-3p inhibitor mediated effects on rat tracheal chondrocytes. Rat tracheal chondrocytes were cotransfected with CA12 siRNA and miR-548au-3p inhibitor for 48 h. (a) Transfection efficiency was determined by western blot. (b) Viability of rat tracheal chondrocytes assessed by CCK-8 assay. (c) Cell proliferation ability assessed by EdU staining. Red fluorescence: EdU; blue fluorescence: DAPI (scale bar = 50 μ m). (d) Cell apoptosis assessed by TUNEL staining (scale bar = 50 μ m). Red fluorescence: TUNEL; blue fluorescence: DAPI. (e) Cell apoptosis assessed by flow cytometry with Annexin V/propidium iodide staining. (f) E-cadherin and N-cadherin protein levels assessed by western blot. (g) The effect of miR-548au-3p on chondrogenic differentiation of rat tracheal chondrocytes assessed by Alcian blue staining (scale bar = 100 μ m). (h) Aggrecan, Col2A1, MMP13, and ADAMTS4 protein levels assessed by western blot. ∗∗ p < 0.01 and ∗∗∗ p < 0.001, compared with NC or inhibitor siRNA NC.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: The Role of the miR-548au-3p/CA12 Axis in Tracheal Chondrogenesis in Congenital Pulmonary Airway Malformations

doi: 10.1155/2023/6428579

Figure Lengend Snippet: Knockdown of CA12 abolished miR-548au-3p inhibitor mediated effects on rat tracheal chondrocytes. Rat tracheal chondrocytes were cotransfected with CA12 siRNA and miR-548au-3p inhibitor for 48 h. (a) Transfection efficiency was determined by western blot. (b) Viability of rat tracheal chondrocytes assessed by CCK-8 assay. (c) Cell proliferation ability assessed by EdU staining. Red fluorescence: EdU; blue fluorescence: DAPI (scale bar = 50 μ m). (d) Cell apoptosis assessed by TUNEL staining (scale bar = 50 μ m). Red fluorescence: TUNEL; blue fluorescence: DAPI. (e) Cell apoptosis assessed by flow cytometry with Annexin V/propidium iodide staining. (f) E-cadherin and N-cadherin protein levels assessed by western blot. (g) The effect of miR-548au-3p on chondrogenic differentiation of rat tracheal chondrocytes assessed by Alcian blue staining (scale bar = 100 μ m). (h) Aggrecan, Col2A1, MMP13, and ADAMTS4 protein levels assessed by western blot. ∗∗ p < 0.01 and ∗∗∗ p < 0.001, compared with NC or inhibitor siRNA NC.

Techniques: Knockdown, Transfection, Western Blot, CCK-8 Assay, Staining, Fluorescence, TUNEL Assay, Flow Cytometry

Hypoxic TME increases Cis-Pt resistance and CA IX/XII expression levels in HNSCC. A-B Cell viability analysis by MTT assay of FaDu and SCC-011 cells grown in normoxic (21% O 2 ) and hypoxic (1% O 2 ) conditions and incubated with increasing concentrations of Cis-Pt (0–10 µM) for 72 h. All the data are expressed as percentage of viable cells, considering the untreated control cells as 100%. Bars depict mean ± SD of three independent experiments. (*** p < 0.001; ** p < 0.01; * p < 0.1). C HIF-1α, CA IX and CA XII protein levels were analyzed by western blot analysis in FaDu and SCC-011 cell lines grown under normoxia (21% O 2 ) and hypoxia (1% O 2 ) for 72 h. Actin and GADPH were used as loading control. Representative data from one of three experiments are shown. D For CA IX and CA XII mRNA expression analysis in HNSCC patients the Genomics Analysis and Visualization platform (R2: Genomics analysis and visualization platform; http://r2.amc.nl ) was used. The analysis was performed with the following datasets: GSE18674 which includes 22 human normal tissues and GSE42743 which includes 103 oral cavity tumors. The correlation was assessed by one-way analysis of variance (ANOVA), through the R2 platform and presented in box plots. (*** p < 0.0001)

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Inhibition of carbonic anhydrases IX/XII by SLC-0111 boosts cisplatin effects in hampering head and neck squamous carcinoma cell growth and invasion

doi: 10.1186/s13046-022-02345-x

Figure Lengend Snippet: Hypoxic TME increases Cis-Pt resistance and CA IX/XII expression levels in HNSCC. A-B Cell viability analysis by MTT assay of FaDu and SCC-011 cells grown in normoxic (21% O 2 ) and hypoxic (1% O 2 ) conditions and incubated with increasing concentrations of Cis-Pt (0–10 µM) for 72 h. All the data are expressed as percentage of viable cells, considering the untreated control cells as 100%. Bars depict mean ± SD of three independent experiments. (*** p < 0.001; ** p < 0.01; * p < 0.1). C HIF-1α, CA IX and CA XII protein levels were analyzed by western blot analysis in FaDu and SCC-011 cell lines grown under normoxia (21% O 2 ) and hypoxia (1% O 2 ) for 72 h. Actin and GADPH were used as loading control. Representative data from one of three experiments are shown. D For CA IX and CA XII mRNA expression analysis in HNSCC patients the Genomics Analysis and Visualization platform (R2: Genomics analysis and visualization platform; http://r2.amc.nl ) was used. The analysis was performed with the following datasets: GSE18674 which includes 22 human normal tissues and GSE42743 which includes 103 oral cavity tumors. The correlation was assessed by one-way analysis of variance (ANOVA), through the R2 platform and presented in box plots. (*** p < 0.0001)

Article Snippet: Blots were blocked for 1 h with 5% non-fat dry milk and then incubated over night with the following primary antibodies: HIF-1α (BD, Biosciences), CA IX (R&D), CA XII (Santa Cruz), anti-SOX-2 and anti Nanog (CST-9093; Cell Signaling Technology Inc), anti-N-cadherin, anti-E-Cadherin, anti-β-catenin (CST-9782; Cell Signaling Technology Inc), anti-Pro-Caspase-3, anti-cleaved-caspase-3, anti-PARP, anti-cleaved-PARP (CST-9915; Cell Signaling Technology Inc), anti-Stat3 (CST-9139), anti-pStat3 (CST-9138), anti-AKT (CST-9272), anti-pAKT (CST-9271), anti-ERK (CST-9102), anti-pERK (CST-9101), MMP-2 (CST-33437), anti-GADPH (Sigma-G8795), anti-Tubulin (Santa Cruz) and anti-Actin (Sigma-A4700).

Techniques: Expressing, MTT Assay, Incubation, Control, Western Blot

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