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96
Vector Biolabs human ift88
Primary cilia are required for GLP-1-potentiated insulin secretion. ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. n = 6 replicates of 50 islets per genotype from 5 mice. ∗p < 0.05, two-way ANOVA with Sidak's multiple comparisons test. ( B ) Quantitative analysis of secretion traces: area under the curve (AUC) during initial glucose stimulation (minutes 10–30), liraglutide stimulation (minutes 30–50), KCl depolarization (minutes 60–70), and total AUC of the entire perifusion (minutes 0–70). βCKO islets secreted significantly less insulin in response to glucose and liraglutide but showed no defect in KCl-induced secretion. Data are mean ± SEM. ∗∗p < 0.01; ns, not significant, unpaired student's t-test. ( C-D ) <t>IFT88</t> knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of three male ( C ) and three female ( D ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not significant; one-way ANOVA with Tukey's multiple comparisons test.
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Thermo Fisher rabbit anti-human ift88 antibody
Primary cilia are required for GLP-1-potentiated insulin secretion. ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. n = 6 replicates of 50 islets per genotype from 5 mice. ∗p < 0.05, two-way ANOVA with Sidak's multiple comparisons test. ( B ) Quantitative analysis of secretion traces: area under the curve (AUC) during initial glucose stimulation (minutes 10–30), liraglutide stimulation (minutes 30–50), KCl depolarization (minutes 60–70), and total AUC of the entire perifusion (minutes 0–70). βCKO islets secreted significantly less insulin in response to glucose and liraglutide but showed no defect in KCl-induced secretion. Data are mean ± SEM. ∗∗p < 0.01; ns, not significant, unpaired student's t-test. ( C-D ) <t>IFT88</t> knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of three male ( C ) and three female ( D ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not significant; one-way ANOVA with Tukey's multiple comparisons test.
Rabbit Anti Human Ift88 Antibody, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ABclonal Biotechnology rabbit anti human ift88 antibody
Primary cilia are required for GLP-1-potentiated insulin secretion. ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. n = 6 replicates of 50 islets per genotype from 5 mice. ∗p < 0.05, two-way ANOVA with Sidak's multiple comparisons test. ( B ) Quantitative analysis of secretion traces: area under the curve (AUC) during initial glucose stimulation (minutes 10–30), liraglutide stimulation (minutes 30–50), KCl depolarization (minutes 60–70), and total AUC of the entire perifusion (minutes 0–70). βCKO islets secreted significantly less insulin in response to glucose and liraglutide but showed no defect in KCl-induced secretion. Data are mean ± SEM. ∗∗p < 0.01; ns, not significant, unpaired student's t-test. ( C-D ) <t>IFT88</t> knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of three male ( C ) and three female ( D ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not significant; one-way ANOVA with Tukey's multiple comparisons test.
Rabbit Anti Human Ift88 Antibody, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Ribobio co sirna targeting human ift88
Primary cilia are required for GLP-1-potentiated insulin secretion. ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. n = 6 replicates of 50 islets per genotype from 5 mice. ∗p < 0.05, two-way ANOVA with Sidak's multiple comparisons test. ( B ) Quantitative analysis of secretion traces: area under the curve (AUC) during initial glucose stimulation (minutes 10–30), liraglutide stimulation (minutes 30–50), KCl depolarization (minutes 60–70), and total AUC of the entire perifusion (minutes 0–70). βCKO islets secreted significantly less insulin in response to glucose and liraglutide but showed no defect in KCl-induced secretion. Data are mean ± SEM. ∗∗p < 0.01; ns, not significant, unpaired student's t-test. ( C-D ) <t>IFT88</t> knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of three male ( C ) and three female ( D ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not significant; one-way ANOVA with Tukey's multiple comparisons test.
Sirna Targeting Human Ift88, supplied by Ribobio co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Addgene inc g human pgk promoter
Primary cilia are required for GLP-1-potentiated insulin secretion. ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. n = 6 replicates of 50 islets per genotype from 5 mice. ∗p < 0.05, two-way ANOVA with Sidak's multiple comparisons test. ( B ) Quantitative analysis of secretion traces: area under the curve (AUC) during initial glucose stimulation (minutes 10–30), liraglutide stimulation (minutes 30–50), KCl depolarization (minutes 60–70), and total AUC of the entire perifusion (minutes 0–70). βCKO islets secreted significantly less insulin in response to glucose and liraglutide but showed no defect in KCl-induced secretion. Data are mean ± SEM. ∗∗p < 0.01; ns, not significant, unpaired student's t-test. ( C-D ) <t>IFT88</t> knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of three male ( C ) and three female ( D ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not significant; one-way ANOVA with Tukey's multiple comparisons test.
G Human Pgk Promoter, supplied by Addgene inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+ift88/MSCV-miRE-shRNA+IFT88-PGK-neo-IRES-GFP+(Plasmid+%2373576)/us11951184-136-67-74
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Thermo Fisher sirna targeting human ift88
IFT88 downregulation increases maturation marker expression with attenuating proliferation activity. (A) cDCs were stimulated with 1 μg/mL Df for 48 h. After immunostaining of acetylated tubulin, the percentage of primary ciliated cells was determined. n = 10 biological replicates (10 donors). The number of observed cells and primary cilium are as follows: no treatment; 8 cilia/1,074 cells. Df; 17 cilia/1,055 cells. The bar indicates the median value. **, p < 0.01 (Mann-Whitney U test). (B) cDCs were stimulated with 1 <g/mL LPS for 24 h. After immunostaining of acetylated tubulin, primary ciliated cDCs were counted and their numbers graphed. n = 15 biological replicates (15 donors). The number of observed cells and primary cilium are as follows: no treatment; 13 cilia/1,679 cells. LPS; 7 cilia/1687 cells. The bar indicates the median rate. *, p < 0.05, Mann-Whitney U test. (C) Five thousand cDCs were stimulated with 1 μg/mL Df for 48 h, then the cell number was calculated by the CCK8/WST-1 assay. To generate the calibration curve, the absorbance values of 3,000, 5,000, and 10,000 cells were measured. Cell numbers in each sample were calculated from the standard curve. Relative cell numbers were calculated by dividing by the untreated sample value. The bar indicates the median value. The Mann-Whitney U test was performed. n = 11 biological replicates (11 donors). (D) Five thousand cDCs were stimulated with 1 μg/mL LPS for 48 h, then relative cell numbers were calculated by performing the CCK8/WST-1 assay. The bar indicates the median value. The Mann Whitney U test was performed. n = 12 biological replicates (12 donors). (E) Five thousand cDCs were stimulated with 10 ng/mL PDGF-A or 10 ng/ml GM-CSF for 48 h. Relative numbers of cDCs were determined by the CCK8/WST-1 assay. For the negative control of PDGF-A stimulation, PDGF-A solvent (4 mM HCl, 0.1% BSA) was added. The bar indicates the median value. Kruskal-Wallis and Dunn’s multiple comparison was used for statistical analysis. *, p < 0.05, **, p < 0.01, n = 15 biological replicates (15 donors). (F) Representative expression of maturation markers in DCs. To differentiate immature DCs, THP1 cells were cultured with 100 ng/ml GM-CSF and 100 ng/mL IL-4 for 5 days. On day 5, cells <t>were</t> <t>electroporated</t> with 20 nM <t>siRNA</t> targeting IFT88 or control siRNA. Two days after electroporation, the expression of cell markers was analyzed by flow cytometry. n = 3 biological replicates. (G) Representative image of IFT88 in THP1-derived immature DC detected by Western blotting. n = 3 biological replicates (3 donors). (H) Immature DCs derived from THP1 were electroporated with 20 nM siRNA. Two days after electroporation, 5,000 cells were stimulated with 10 ng/mL PDGF-A or 10 ng/ml GM-CSF for 48 h. A CCK8/WST-1 assay was performed to calculate the cell number. The bar indicates the median value. **, p < 0.01 (one-way ANOVA, Tukey’s multiple comparison). n = 5 biological replicates.
Sirna Targeting Human Ift88, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech rabbit anti human ift88
Figure 3. Protein loss and motility changes after RNAi. (A) Relative expression of basal body-associated protein BBS8. **P < 0.01 vs the blank group, n = 3. (B) Relative expression of cilia assembly-related protein <t>IFT88.</t> **P < 0.01 vs the blank group, n = 3. (C) Relative expression of basal body protein γ-tubulin. (D) The swimming tracks of Euplotes amieti during RNAi. The swimming speeds (n = 20). The FOPRNAi is the interference group, The Blank is the blank group (E) The swimming speeds of Euplotes amieti during RNAi (n = 20).
Rabbit Anti Human Ift88, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech rabbit anti human intraflagellar transport 88 ift88 antibody
Figure 3. Protein loss and motility changes after RNAi. (A) Relative expression of basal body-associated protein BBS8. **P < 0.01 vs the blank group, n = 3. (B) Relative expression of cilia assembly-related protein <t>IFT88.</t> **P < 0.01 vs the blank group, n = 3. (C) Relative expression of basal body protein γ-tubulin. (D) The swimming tracks of Euplotes amieti during RNAi. The swimming speeds (n = 20). The FOPRNAi is the interference group, The Blank is the blank group (E) The swimming speeds of Euplotes amieti during RNAi (n = 20).
Rabbit Anti Human Intraflagellar Transport 88 Ift88 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Primary cilia are required for GLP-1-potentiated insulin secretion. ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. n = 6 replicates of 50 islets per genotype from 5 mice. ∗p < 0.05, two-way ANOVA with Sidak's multiple comparisons test. ( B ) Quantitative analysis of secretion traces: area under the curve (AUC) during initial glucose stimulation (minutes 10–30), liraglutide stimulation (minutes 30–50), KCl depolarization (minutes 60–70), and total AUC of the entire perifusion (minutes 0–70). βCKO islets secreted significantly less insulin in response to glucose and liraglutide but showed no defect in KCl-induced secretion. Data are mean ± SEM. ∗∗p < 0.01; ns, not significant, unpaired student's t-test. ( C-D ) IFT88 knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of three male ( C ) and three female ( D ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not significant; one-way ANOVA with Tukey's multiple comparisons test.

Journal: Molecular Metabolism

Article Title: Primary cilia regulate GLP-1 signaling in pancreatic β cells

doi: 10.1016/j.molmet.2026.102357

Figure Lengend Snippet: Primary cilia are required for GLP-1-potentiated insulin secretion. ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. n = 6 replicates of 50 islets per genotype from 5 mice. ∗p < 0.05, two-way ANOVA with Sidak's multiple comparisons test. ( B ) Quantitative analysis of secretion traces: area under the curve (AUC) during initial glucose stimulation (minutes 10–30), liraglutide stimulation (minutes 30–50), KCl depolarization (minutes 60–70), and total AUC of the entire perifusion (minutes 0–70). βCKO islets secreted significantly less insulin in response to glucose and liraglutide but showed no defect in KCl-induced secretion. Data are mean ± SEM. ∗∗p < 0.01; ns, not significant, unpaired student's t-test. ( C-D ) IFT88 knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of three male ( C ) and three female ( D ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not significant; one-way ANOVA with Tukey's multiple comparisons test.

Article Snippet: IFT88 knockdown in human islets: Healthy non-diabetic human islets were transduced with adenoviral vectors encoding either GFP-tagged shRNA targeting human IFT88 (Ad-GFP-h-IFT88-shRNA) or scrambled control (Ad-GFP-U6-scrmb-shRNA, #1122N; Vector Biolabs).

Techniques: Knock-Out, Knockdown, Transduction, Control, shRNA, Incubation

IFT88 downregulation increases maturation marker expression with attenuating proliferation activity. (A) cDCs were stimulated with 1 μg/mL Df for 48 h. After immunostaining of acetylated tubulin, the percentage of primary ciliated cells was determined. n = 10 biological replicates (10 donors). The number of observed cells and primary cilium are as follows: no treatment; 8 cilia/1,074 cells. Df; 17 cilia/1,055 cells. The bar indicates the median value. **, p < 0.01 (Mann-Whitney U test). (B) cDCs were stimulated with 1 <g/mL LPS for 24 h. After immunostaining of acetylated tubulin, primary ciliated cDCs were counted and their numbers graphed. n = 15 biological replicates (15 donors). The number of observed cells and primary cilium are as follows: no treatment; 13 cilia/1,679 cells. LPS; 7 cilia/1687 cells. The bar indicates the median rate. *, p < 0.05, Mann-Whitney U test. (C) Five thousand cDCs were stimulated with 1 μg/mL Df for 48 h, then the cell number was calculated by the CCK8/WST-1 assay. To generate the calibration curve, the absorbance values of 3,000, 5,000, and 10,000 cells were measured. Cell numbers in each sample were calculated from the standard curve. Relative cell numbers were calculated by dividing by the untreated sample value. The bar indicates the median value. The Mann-Whitney U test was performed. n = 11 biological replicates (11 donors). (D) Five thousand cDCs were stimulated with 1 μg/mL LPS for 48 h, then relative cell numbers were calculated by performing the CCK8/WST-1 assay. The bar indicates the median value. The Mann Whitney U test was performed. n = 12 biological replicates (12 donors). (E) Five thousand cDCs were stimulated with 10 ng/mL PDGF-A or 10 ng/ml GM-CSF for 48 h. Relative numbers of cDCs were determined by the CCK8/WST-1 assay. For the negative control of PDGF-A stimulation, PDGF-A solvent (4 mM HCl, 0.1% BSA) was added. The bar indicates the median value. Kruskal-Wallis and Dunn’s multiple comparison was used for statistical analysis. *, p < 0.05, **, p < 0.01, n = 15 biological replicates (15 donors). (F) Representative expression of maturation markers in DCs. To differentiate immature DCs, THP1 cells were cultured with 100 ng/ml GM-CSF and 100 ng/mL IL-4 for 5 days. On day 5, cells were electroporated with 20 nM siRNA targeting IFT88 or control siRNA. Two days after electroporation, the expression of cell markers was analyzed by flow cytometry. n = 3 biological replicates. (G) Representative image of IFT88 in THP1-derived immature DC detected by Western blotting. n = 3 biological replicates (3 donors). (H) Immature DCs derived from THP1 were electroporated with 20 nM siRNA. Two days after electroporation, 5,000 cells were stimulated with 10 ng/mL PDGF-A or 10 ng/ml GM-CSF for 48 h. A CCK8/WST-1 assay was performed to calculate the cell number. The bar indicates the median value. **, p < 0.01 (one-way ANOVA, Tukey’s multiple comparison). n = 5 biological replicates.

Journal: Frontiers in Molecular Biosciences

Article Title: Dendritic cell proliferation by primary cilium in atopic dermatitis

doi: 10.3389/fmolb.2023.1149828

Figure Lengend Snippet: IFT88 downregulation increases maturation marker expression with attenuating proliferation activity. (A) cDCs were stimulated with 1 μg/mL Df for 48 h. After immunostaining of acetylated tubulin, the percentage of primary ciliated cells was determined. n = 10 biological replicates (10 donors). The number of observed cells and primary cilium are as follows: no treatment; 8 cilia/1,074 cells. Df; 17 cilia/1,055 cells. The bar indicates the median value. **, p < 0.01 (Mann-Whitney U test). (B) cDCs were stimulated with 1

Article Snippet: After 5 days of differentiation, cells were electroporated with 20 nM siRNA targeting human IFT88 (Life Technologies), or siRNA Control (AM4611, Invitrogen) with the Neon Transfection System (Thermo Fisher Scientific).

Techniques: Marker, Expressing, Activity Assay, Immunostaining, MANN-WHITNEY, WST-1 Assay, Negative Control, Solvent, Comparison, Cell Culture, Control, Electroporation, Flow Cytometry, Derivative Assay, Western Blot

Figure 3. Protein loss and motility changes after RNAi. (A) Relative expression of basal body-associated protein BBS8. **P < 0.01 vs the blank group, n = 3. (B) Relative expression of cilia assembly-related protein IFT88. **P < 0.01 vs the blank group, n = 3. (C) Relative expression of basal body protein γ-tubulin. (D) The swimming tracks of Euplotes amieti during RNAi. The swimming speeds (n = 20). The FOPRNAi is the interference group, The Blank is the blank group (E) The swimming speeds of Euplotes amieti during RNAi (n = 20).

Journal: Acta Protozoologica

Article Title: The function of ciliopathy protein FOP on cilia and cortical microtubule cytoskeleton in Euplotes amieti

doi: 10.4467/16890027ap.23.005.18868

Figure Lengend Snippet: Figure 3. Protein loss and motility changes after RNAi. (A) Relative expression of basal body-associated protein BBS8. **P < 0.01 vs the blank group, n = 3. (B) Relative expression of cilia assembly-related protein IFT88. **P < 0.01 vs the blank group, n = 3. (C) Relative expression of basal body protein γ-tubulin. (D) The swimming tracks of Euplotes amieti during RNAi. The swimming speeds (n = 20). The FOPRNAi is the interference group, The Blank is the blank group (E) The swimming speeds of Euplotes amieti during RNAi (n = 20).

Article Snippet: Subsequently, the membranes were blocked in TBST buffer with 1 % skimmed milk for 2 hours at RT and respectively incubated with rabbit anti-human FOP (1:2000, Proteintech, China), rabbit anti-human β-tubulin (1:10000, Abcam, USA), rabbit anti-human BBS8 (1:500, Proteintech, China), rabbit anti-human IFT88 (1:1500, Proteintech, China), mouse anti-human γ-tubulin (1:10000, Sigma-Aldrich, USA), rabbit anti-human β-actin (1:10000, Proteintech, China) overnight at 4 °C, followed by peroxidase-conjugated sheep anti-rabbit/ mouse IgG secondary antibody (1:2000, Thermo Fisher Scientific, USA) for 2 hours at RT, respectively.

Techniques: Expressing