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Proteintech cct3

<t>CCT3</t> expression is associated with unfavorable clinical outcomes in clear cell renal carcinoma (ccRCC) (A) Bar graph depicts the protein expression levels of CCT3 in selected cancer types and their respective normal tissues. Data were obtained from the Clinical Proteomic Tumor Analysis Consortium (CPTAC) unpaired sample analysis. (B) Upregulated expression of CCT3 in clear cell renal carcinoma (ccRCC) compared to normal kidney tissues, as determined by the UALCAN online database analysis. (C) Analysis of the impact of CCT3 expression on the p53/Rb pathway in ccRCC, derived from the CPTAC database. (D) Correlation analysis between CCT3 mRNA expression levels and the mRNA expression levels of key genes involved in the p53/Rb pathway (TP53, Rb1, CDK4, and E2F3) using Spearman correlation, as analyzed by GEPIA. (E and F) Kaplan-Meier survival curves illustrating the association between CCT3 expression and overall survival (OS) and progression-free survival (PFS) in patients with ccRCC. Patients were stratified into low and high CCT3 expression groups. Statistical significance is indicated as ∗ p < 0.05, ∗∗ p < 0.01, ∗ p < 0.001, and ns for non-significant differences. Data in A are presented as mean ± standard deviation (SD). Two-tailed Student’s t test.

Cct3, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 18 article reviews

cct3 - by Bioz Stars, 2026-05

93/100 stars

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1) Product Images from "CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma"

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

Journal: iScience

doi: 10.1016/j.isci.2026.114840

CCT3 expression is associated with unfavorable clinical outcomes in clear cell renal carcinoma (ccRCC) (A) Bar graph depicts the protein expression levels of CCT3 in selected cancer types and their respective normal tissues. Data were obtained from the Clinical Proteomic Tumor Analysis Consortium (CPTAC) unpaired sample analysis. (B) Upregulated expression of CCT3 in clear cell renal carcinoma (ccRCC) compared to normal kidney tissues, as determined by the UALCAN online database analysis. (C) Analysis of the impact of CCT3 expression on the p53/Rb pathway in ccRCC, derived from the CPTAC database. (D) Correlation analysis between CCT3 mRNA expression levels and the mRNA expression levels of key genes involved in the p53/Rb pathway (TP53, Rb1, CDK4, and E2F3) using Spearman correlation, as analyzed by GEPIA. (E and F) Kaplan-Meier survival curves illustrating the association between CCT3 expression and overall survival (OS) and progression-free survival (PFS) in patients with ccRCC. Patients were stratified into low and high CCT3 expression groups. Statistical significance is indicated as ∗ p < 0.05, ∗∗ p < 0.01, ∗ p < 0.001, and ns for non-significant differences. Data in A are presented as mean ± standard deviation (SD). Two-tailed Student’s t test.

Figure Legend Snippet: CCT3 expression is associated with unfavorable clinical outcomes in clear cell renal carcinoma (ccRCC) (A) Bar graph depicts the protein expression levels of CCT3 in selected cancer types and their respective normal tissues. Data were obtained from the Clinical Proteomic Tumor Analysis Consortium (CPTAC) unpaired sample analysis. (B) Upregulated expression of CCT3 in clear cell renal carcinoma (ccRCC) compared to normal kidney tissues, as determined by the UALCAN online database analysis. (C) Analysis of the impact of CCT3 expression on the p53/Rb pathway in ccRCC, derived from the CPTAC database. (D) Correlation analysis between CCT3 mRNA expression levels and the mRNA expression levels of key genes involved in the p53/Rb pathway (TP53, Rb1, CDK4, and E2F3) using Spearman correlation, as analyzed by GEPIA. (E and F) Kaplan-Meier survival curves illustrating the association between CCT3 expression and overall survival (OS) and progression-free survival (PFS) in patients with ccRCC. Patients were stratified into low and high CCT3 expression groups. Statistical significance is indicated as ∗ p < 0.05, ∗∗ p < 0.01, ∗ p < 0.001, and ns for non-significant differences. Data in A are presented as mean ± standard deviation (SD). Two-tailed Student’s t test.

Techniques Used: Expressing, Derivative Assay, Standard Deviation, Two Tailed Test

The depletion of CCT3 impairs the abilities of proliferation, migration, and invasion in ccRCC cells (A) Western blot analysis was performed to assess the protein expression of CCT3 in four pairs of clear cell renal cell carcinoma tissues (T) and their corresponding adjacent normal tissues (N). ( n = 4). (B) The immunohistochemical results of CCT3 in ccRCC and normal renal tissue in the HPA database. (C) Western blot was used to assess the effects of two distinct CCT3 knockdown sequences in 786-O and 769-P cells. (D and E) Wound-healing assay indicates that CCT3 knockdown suppresses the viability of 786-O and 769-P cells. (F and G) Transwell assay indicates impaired abilities of migration and invasion of 769-P and 786-O cells. (H and I) The proliferative abilities of stably CCT3-depleted 769-P and 786-O cells were measured with an EdU staining assay. (Scale bars, 100 μm. Data in C-I are presented as the means ± SDs ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). Two-tailed Student’s t test for A, Student’s t test for C-I.

Figure Legend Snippet: The depletion of CCT3 impairs the abilities of proliferation, migration, and invasion in ccRCC cells (A) Western blot analysis was performed to assess the protein expression of CCT3 in four pairs of clear cell renal cell carcinoma tissues (T) and their corresponding adjacent normal tissues (N). ( n = 4). (B) The immunohistochemical results of CCT3 in ccRCC and normal renal tissue in the HPA database. (C) Western blot was used to assess the effects of two distinct CCT3 knockdown sequences in 786-O and 769-P cells. (D and E) Wound-healing assay indicates that CCT3 knockdown suppresses the viability of 786-O and 769-P cells. (F and G) Transwell assay indicates impaired abilities of migration and invasion of 769-P and 786-O cells. (H and I) The proliferative abilities of stably CCT3-depleted 769-P and 786-O cells were measured with an EdU staining assay. (Scale bars, 100 μm. Data in C-I are presented as the means ± SDs ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). Two-tailed Student’s t test for A, Student’s t test for C-I.

Techniques Used: Migration, Western Blot, Expressing, Immunohistochemical staining, Knockdown, Wound Healing Assay, Transwell Assay, Stable Transfection, Staining, Two Tailed Test

The reduction of CCT3 induces cellular senescence in ccRCC cells (A) Western blot analysis was performed to assess the protein expression of CDK4, CyclinD, p-Rb (Ser807/811), and p21 in CCT3 knockdown cells. (B) The mRNA expression levels of senescence-associated genes, including interleukin 1 A, TNF, CDK2, CDK4, and CDK6 in CCT3-depleted cells were examined by qRT-PCR. (C) Changes of SA-β-gal activity in CCT3-knockdown cells. Data represent the percentage of cells staining positive for SA-β-gal ±SD. (D) Cell cycle analysis calculated the distribution of the cells in G1, S, and G2/M phases. (E) Representative immunofluorescent staining of p21 and p-Rb (Ser807/811) in each cell. (F) Western blot analysis was performed to assess the protein expression of CDK4, CyclinD, p-Rb (Ser807/811), and p21 in CCT3 overexpressed cells. (G) Wound-healing assay indicates that the overexpression of CCT3 enhances the proliferation capacity of A498 cells. (H) The Transwell assay demonstrated that the overexpression of CCT3 enhances the migratory and invasive capabilities of A498 cells. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). Student’s t test.

Figure Legend Snippet: The reduction of CCT3 induces cellular senescence in ccRCC cells (A) Western blot analysis was performed to assess the protein expression of CDK4, CyclinD, p-Rb (Ser807/811), and p21 in CCT3 knockdown cells. (B) The mRNA expression levels of senescence-associated genes, including interleukin 1 A, TNF, CDK2, CDK4, and CDK6 in CCT3-depleted cells were examined by qRT-PCR. (C) Changes of SA-β-gal activity in CCT3-knockdown cells. Data represent the percentage of cells staining positive for SA-β-gal ±SD. (D) Cell cycle analysis calculated the distribution of the cells in G1, S, and G2/M phases. (E) Representative immunofluorescent staining of p21 and p-Rb (Ser807/811) in each cell. (F) Western blot analysis was performed to assess the protein expression of CDK4, CyclinD, p-Rb (Ser807/811), and p21 in CCT3 overexpressed cells. (G) Wound-healing assay indicates that the overexpression of CCT3 enhances the proliferation capacity of A498 cells. (H) The Transwell assay demonstrated that the overexpression of CCT3 enhances the migratory and invasive capabilities of A498 cells. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). Student’s t test.

Techniques Used: Western Blot, Expressing, Knockdown, Quantitative RT-PCR, Activity Assay, Staining, Cell Cycle Assay, Wound Healing Assay, Over Expression, Transwell Assay

Knockdown of XPO1 inhibited the invasion and migration abilities of ccRCC cells (A) The Venn diagram obtained by taking the intersection of the relevant gene sets of CCT3 and RB1 after screening. (B) Expression level of XPO1 in clear cell RCC from the TCGA database. (C) The immunohistochemical results of XPO1 in ccRCC and normal renal tissue in the HPA database. (D) A Kaplan-Meier curve illustrates OS in patients with ccRCC from low and high XPO1 expression groups. (E) The promoter methylation level of XPO1 in KIRC from the TCGA database. (F) Western blot analysis was performed to assess the protein expression of XPO1 in CCT3-depleted cells. (G) Using Spearman correlation analysis, the correlation between Gene CCT3 and XPO1 expression, and the correlation between XPO1 and RB1 expression. (H) Wound-healing assay indicates that XPO1 knockdown suppresses the viability of 786-O and 769-P cells. (I) Transwell assay indicates impaired abilities of migration and invasion of 769-P and 786-O cells. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). Two-tailed Student’s t test for B and E. Student’s t test for F, H, and I.

Figure Legend Snippet: Knockdown of XPO1 inhibited the invasion and migration abilities of ccRCC cells (A) The Venn diagram obtained by taking the intersection of the relevant gene sets of CCT3 and RB1 after screening. (B) Expression level of XPO1 in clear cell RCC from the TCGA database. (C) The immunohistochemical results of XPO1 in ccRCC and normal renal tissue in the HPA database. (D) A Kaplan-Meier curve illustrates OS in patients with ccRCC from low and high XPO1 expression groups. (E) The promoter methylation level of XPO1 in KIRC from the TCGA database. (F) Western blot analysis was performed to assess the protein expression of XPO1 in CCT3-depleted cells. (G) Using Spearman correlation analysis, the correlation between Gene CCT3 and XPO1 expression, and the correlation between XPO1 and RB1 expression. (H) Wound-healing assay indicates that XPO1 knockdown suppresses the viability of 786-O and 769-P cells. (I) Transwell assay indicates impaired abilities of migration and invasion of 769-P and 786-O cells. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). Two-tailed Student’s t test for B and E. Student’s t test for F, H, and I.

Techniques Used: Knockdown, Migration, Expressing, Immunohistochemical staining, Methylation, Western Blot, Wound Healing Assay, Transwell Assay, Two Tailed Test

CCT3 regulates RB1 activity by influencing the stability of the XPO1 protein (A) The Co-IP was performed to analyze the endogenous interaction between CCT3 and XPO1 in ccRCC cells. protein pellets were analyzed by Western blot with anti-CCT3 and anti-XPO1 antibodies. (B) Pull-down of CCT3, XPO1, and CCT3 with GST-tagged was analyzed by Western Blot. (C) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with CHX for the times indicated. (D) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with BafA1. (E) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with MG132. (F) Visualization results of the CCT3 and XPO1 molecular docking. (All data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). One-way ANOVA for C, Student’s t test for D and E.

Figure Legend Snippet: CCT3 regulates RB1 activity by influencing the stability of the XPO1 protein (A) The Co-IP was performed to analyze the endogenous interaction between CCT3 and XPO1 in ccRCC cells. protein pellets were analyzed by Western blot with anti-CCT3 and anti-XPO1 antibodies. (B) Pull-down of CCT3, XPO1, and CCT3 with GST-tagged was analyzed by Western Blot. (C) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with CHX for the times indicated. (D) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with BafA1. (E) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with MG132. (F) Visualization results of the CCT3 and XPO1 molecular docking. (All data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). One-way ANOVA for C, Student’s t test for D and E.

Techniques Used: Activity Assay, Co-Immunoprecipitation Assay, Western Blot, Control, Knockdown

$Rescue experiments demonstrate the effects of CCT3 overexpression and XPO1 knockdown on cell function (A) Western blot was used to detect the expression of RB1 and Cyclin D in nuclear and cytoplasmic fractions of cells. (B) Western blot analysis was performed to assess the protein expression of Cyclin D, p-Rb (Ser807/811) in the rescue assay. (C) Senescence β-Galactosidase Staining in rescue assay. (D) A healing assay was performed in the rescue assay. (E) Transwell assay was performed in the rescue assay. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). One-way ANOVA for D, E.$
Figure Legend Snippet: Rescue experiments demonstrate the effects of CCT3 overexpression and XPO1 knockdown on cell function (A) Western blot was used to detect the expression of RB1 and Cyclin D in nuclear and cytoplasmic fractions of cells. (B) Western blot analysis was performed to assess the protein expression of Cyclin D, p-Rb (Ser807/811) in the rescue assay. (C) Senescence β-Galactosidase Staining in rescue assay. (D) A healing assay was performed in the rescue assay. (E) Transwell assay was performed in the rescue assay. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). One-way ANOVA for D, E.

Techniques Used: Over Expression, Knockdown, Cell Function Assay, Western Blot, Expressing, Rescue Assay, Staining, Transwell Assay

Knockdown of CCT3 combined with a selective XPO1 inhibitor can promote cellular senescence to suppress tumor progression in vivo (A) Nude mice were used to establish a tumor xenograft model utilizing CCT3 knockdown cell lines and the selective XPO1 inhibitor, Selinexor. (B and C) The tumor volumes and tumor weight of each group. (D) Western blot analysis was performed to assess the protein expression of p53, Cyclin D, CDK4, and PCNA in tissue. (E and F) The immunohistochemistry and immunofluorescence assays of Ki67. (Scale bars, 100 μm. All data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). Repeated measures ANOVA for B and C. One-way ANOVA for D and E.

Figure Legend Snippet: Knockdown of CCT3 combined with a selective XPO1 inhibitor can promote cellular senescence to suppress tumor progression in vivo (A) Nude mice were used to establish a tumor xenograft model utilizing CCT3 knockdown cell lines and the selective XPO1 inhibitor, Selinexor. (B and C) The tumor volumes and tumor weight of each group. (D) Western blot analysis was performed to assess the protein expression of p53, Cyclin D, CDK4, and PCNA in tissue. (E and F) The immunohistochemistry and immunofluorescence assays of Ki67. (Scale bars, 100 μm. All data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). Repeated measures ANOVA for B and C. One-way ANOVA for D and E.

Techniques Used: Knockdown, In Vivo, Western Blot, Expressing, Immunohistochemistry, Immunofluorescence

Image Search Results

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: CCT3 expression is associated with unfavorable clinical outcomes in clear cell renal carcinoma (ccRCC) (A) Bar graph depicts the protein expression levels of CCT3 in selected cancer types and their respective normal tissues. Data were obtained from the Clinical Proteomic Tumor Analysis Consortium (CPTAC) unpaired sample analysis. (B) Upregulated expression of CCT3 in clear cell renal carcinoma (ccRCC) compared to normal kidney tissues, as determined by the UALCAN online database analysis. (C) Analysis of the impact of CCT3 expression on the p53/Rb pathway in ccRCC, derived from the CPTAC database. (D) Correlation analysis between CCT3 mRNA expression levels and the mRNA expression levels of key genes involved in the p53/Rb pathway (TP53, Rb1, CDK4, and E2F3) using Spearman correlation, as analyzed by GEPIA. (E and F) Kaplan-Meier survival curves illustrating the association between CCT3 expression and overall survival (OS) and progression-free survival (PFS) in patients with ccRCC. Patients were stratified into low and high CCT3 expression groups. Statistical significance is indicated as ∗ p < 0.05, ∗∗ p < 0.01, ∗ p < 0.001, and ns for non-significant differences. Data in A are presented as mean ± standard deviation (SD). Two-tailed Student’s t test.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Expressing, Derivative Assay, Standard Deviation, Two Tailed Test

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: The depletion of CCT3 impairs the abilities of proliferation, migration, and invasion in ccRCC cells (A) Western blot analysis was performed to assess the protein expression of CCT3 in four pairs of clear cell renal cell carcinoma tissues (T) and their corresponding adjacent normal tissues (N). ( n = 4). (B) The immunohistochemical results of CCT3 in ccRCC and normal renal tissue in the HPA database. (C) Western blot was used to assess the effects of two distinct CCT3 knockdown sequences in 786-O and 769-P cells. (D and E) Wound-healing assay indicates that CCT3 knockdown suppresses the viability of 786-O and 769-P cells. (F and G) Transwell assay indicates impaired abilities of migration and invasion of 769-P and 786-O cells. (H and I) The proliferative abilities of stably CCT3-depleted 769-P and 786-O cells were measured with an EdU staining assay. (Scale bars, 100 μm. Data in C-I are presented as the means ± SDs ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). Two-tailed Student’s t test for A, Student’s t test for C-I.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Migration, Western Blot, Expressing, Immunohistochemical staining, Knockdown, Wound Healing Assay, Transwell Assay, Stable Transfection, Staining, Two Tailed Test

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: The reduction of CCT3 induces cellular senescence in ccRCC cells (A) Western blot analysis was performed to assess the protein expression of CDK4, CyclinD, p-Rb (Ser807/811), and p21 in CCT3 knockdown cells. (B) The mRNA expression levels of senescence-associated genes, including interleukin 1 A, TNF, CDK2, CDK4, and CDK6 in CCT3-depleted cells were examined by qRT-PCR. (C) Changes of SA-β-gal activity in CCT3-knockdown cells. Data represent the percentage of cells staining positive for SA-β-gal ±SD. (D) Cell cycle analysis calculated the distribution of the cells in G1, S, and G2/M phases. (E) Representative immunofluorescent staining of p21 and p-Rb (Ser807/811) in each cell. (F) Western blot analysis was performed to assess the protein expression of CDK4, CyclinD, p-Rb (Ser807/811), and p21 in CCT3 overexpressed cells. (G) Wound-healing assay indicates that the overexpression of CCT3 enhances the proliferation capacity of A498 cells. (H) The Transwell assay demonstrated that the overexpression of CCT3 enhances the migratory and invasive capabilities of A498 cells. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). Student’s t test.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Western Blot, Expressing, Knockdown, Quantitative RT-PCR, Activity Assay, Staining, Cell Cycle Assay, Wound Healing Assay, Over Expression, Transwell Assay

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: Knockdown of XPO1 inhibited the invasion and migration abilities of ccRCC cells (A) The Venn diagram obtained by taking the intersection of the relevant gene sets of CCT3 and RB1 after screening. (B) Expression level of XPO1 in clear cell RCC from the TCGA database. (C) The immunohistochemical results of XPO1 in ccRCC and normal renal tissue in the HPA database. (D) A Kaplan-Meier curve illustrates OS in patients with ccRCC from low and high XPO1 expression groups. (E) The promoter methylation level of XPO1 in KIRC from the TCGA database. (F) Western blot analysis was performed to assess the protein expression of XPO1 in CCT3-depleted cells. (G) Using Spearman correlation analysis, the correlation between Gene CCT3 and XPO1 expression, and the correlation between XPO1 and RB1 expression. (H) Wound-healing assay indicates that XPO1 knockdown suppresses the viability of 786-O and 769-P cells. (I) Transwell assay indicates impaired abilities of migration and invasion of 769-P and 786-O cells. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). Two-tailed Student’s t test for B and E. Student’s t test for F, H, and I.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Knockdown, Migration, Expressing, Immunohistochemical staining, Methylation, Western Blot, Wound Healing Assay, Transwell Assay, Two Tailed Test

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: CCT3 regulates RB1 activity by influencing the stability of the XPO1 protein (A) The Co-IP was performed to analyze the endogenous interaction between CCT3 and XPO1 in ccRCC cells. protein pellets were analyzed by Western blot with anti-CCT3 and anti-XPO1 antibodies. (B) Pull-down of CCT3, XPO1, and CCT3 with GST-tagged was analyzed by Western Blot. (C) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with CHX for the times indicated. (D) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with BafA1. (E) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with MG132. (F) Visualization results of the CCT3 and XPO1 molecular docking. (All data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). One-way ANOVA for C, Student’s t test for D and E.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Activity Assay, Co-Immunoprecipitation Assay, Western Blot, Control, Knockdown

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: Rescue experiments demonstrate the effects of CCT3 overexpression and XPO1 knockdown on cell function (A) Western blot was used to detect the expression of RB1 and Cyclin D in nuclear and cytoplasmic fractions of cells. (B) Western blot analysis was performed to assess the protein expression of Cyclin D, p-Rb (Ser807/811) in the rescue assay. (C) Senescence β-Galactosidase Staining in rescue assay. (D) A healing assay was performed in the rescue assay. (E) Transwell assay was performed in the rescue assay. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). One-way ANOVA for D, E.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Over Expression, Knockdown, Cell Function Assay, Western Blot, Expressing, Rescue Assay, Staining, Transwell Assay

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: Knockdown of CCT3 combined with a selective XPO1 inhibitor can promote cellular senescence to suppress tumor progression in vivo (A) Nude mice were used to establish a tumor xenograft model utilizing CCT3 knockdown cell lines and the selective XPO1 inhibitor, Selinexor. (B and C) The tumor volumes and tumor weight of each group. (D) Western blot analysis was performed to assess the protein expression of p53, Cyclin D, CDK4, and PCNA in tissue. (E and F) The immunohistochemistry and immunofluorescence assays of Ki67. (Scale bars, 100 μm. All data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). Repeated measures ANOVA for B and C. One-way ANOVA for D and E.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Knockdown, In Vivo, Western Blot, Expressing, Immunohistochemistry, Immunofluorescence

CCT3 is upregulated in lung cancer tissues and cell lines. (A–F) CCT3 expression in: (A,B) NSCLC ( GSE10072 , GSE19801), (C,D) TCGA-LUAD/LUSC (by stage), (E,F) SCLC ( GSE40419 , GSE30219 ) versus normal tissues (***P < 0.0001); (G) qPCR (left) and Western blot (right) of CCT3 in BEAS-2B versus lung cancer cell lines (GAPDH control, ***P < 0.0001, ns: not significant); (H,I) IHC staining of CCT3 in (H) LUAD and (I) LUSC tissues at 40×/400× magnification.

Journal: Technology in Cancer Research & Treatment

Article Title: CCT3 Facilitates the Malignant Progression of NSCLC and SCLC via PI3 K/AKT-EMT Axis and Emerges as a Novel Serum Diagnostic Biomarker

doi: 10.1177/15330338251412203

Figure Lengend Snippet: CCT3 is upregulated in lung cancer tissues and cell lines. (A–F) CCT3 expression in: (A,B) NSCLC ( GSE10072 , GSE19801), (C,D) TCGA-LUAD/LUSC (by stage), (E,F) SCLC ( GSE40419 , GSE30219 ) versus normal tissues (***P < 0.0001); (G) qPCR (left) and Western blot (right) of CCT3 in BEAS-2B versus lung cancer cell lines (GAPDH control, ***P < 0.0001, ns: not significant); (H,I) IHC staining of CCT3 in (H) LUAD and (I) LUSC tissues at 40×/400× magnification.

Article Snippet: Sections were incubated overnight at 4 °C with primary antibodies against CCT3 (Santa Cruz, sc-271336; dilution:1:200) and Ki-67 (Servicebio,GB111499-100; dilution:1:500), followed by HRP-conjugated secondary antibodies.

Techniques: Expressing, Western Blot, Control, Immunohistochemistry

Effects of CCT3 modulation on proliferation, colony formation, and metastasis of lung cancer cells. (A–C) Cell proliferation (CCK-8, A), colony formation (B, images and quantification), and migration/invasion (Transwell, C, images and quantification) in NCI-H1703, DMS114, and NCI-H446 cells transfected with control siRNA (NC), CCT3-targeting siRNAs (si-CCT3#1, si-CCT3#2), empty vector (Vector), or CCT3-overexpressing vector (OE-CCT3); (D) Representative images of xenograft tumors, (E) tumor volume quantification, (F) tumor weight measurement, and (G) IHC analysis of CCT3 and Ki67 expression in tumor tissues from BALB/c nude mice injected with control (shNC) or CCT3-knockdown (shCCT3) NCI-H446 cells; ***P < 0.001, ****P < 0.0001 versus respective controls (NC for siRNA, Vector for OE-CCT3).

Journal: Technology in Cancer Research & Treatment

Article Title: CCT3 Facilitates the Malignant Progression of NSCLC and SCLC via PI3 K/AKT-EMT Axis and Emerges as a Novel Serum Diagnostic Biomarker

doi: 10.1177/15330338251412203

Figure Lengend Snippet: Effects of CCT3 modulation on proliferation, colony formation, and metastasis of lung cancer cells. (A–C) Cell proliferation (CCK-8, A), colony formation (B, images and quantification), and migration/invasion (Transwell, C, images and quantification) in NCI-H1703, DMS114, and NCI-H446 cells transfected with control siRNA (NC), CCT3-targeting siRNAs (si-CCT3#1, si-CCT3#2), empty vector (Vector), or CCT3-overexpressing vector (OE-CCT3); (D) Representative images of xenograft tumors, (E) tumor volume quantification, (F) tumor weight measurement, and (G) IHC analysis of CCT3 and Ki67 expression in tumor tissues from BALB/c nude mice injected with control (shNC) or CCT3-knockdown (shCCT3) NCI-H446 cells; ***P < 0.001, ****P < 0.0001 versus respective controls (NC for siRNA, Vector for OE-CCT3).

Techniques: CCK-8 Assay, Migration, Transfection, Control, Plasmid Preparation, Expressing, Injection, Knockdown

Exploration of CCT3-interacting proteins and downstream signaling pathways in lung cancer. (A) CCT3 protein-protein interaction network (STRING database prediction, Cytoscape visualization; nodes: proteins, edges: interactions); (B) GO enrichment (biological process, cellular component, molecular function) and KEGG pathway analysis of CCT3-interacting proteins (significant enrichment in PI3K-AKT pathway highlighted); (C–E) Western blot analysis of PI3K-AKT pathway components (p-PI3 K, PI3 K, p-AKT, AKT) and EMT markers (N-cadherin, E-cadherin, Vimentin) in NCI-H1703 (C), DMS114 (D), and NCI-H446 (E) cells transfected with control siRNA (NC), CCT3-targeting siRNAs (si-CCT3#1–#2), empty vector (Vector), or CCT3-overexpressing vector (OE-CCT3) (GAPDH loading control).

Journal: Technology in Cancer Research & Treatment

Article Title: CCT3 Facilitates the Malignant Progression of NSCLC and SCLC via PI3 K/AKT-EMT Axis and Emerges as a Novel Serum Diagnostic Biomarker

doi: 10.1177/15330338251412203

Figure Lengend Snippet: Exploration of CCT3-interacting proteins and downstream signaling pathways in lung cancer. (A) CCT3 protein-protein interaction network (STRING database prediction, Cytoscape visualization; nodes: proteins, edges: interactions); (B) GO enrichment (biological process, cellular component, molecular function) and KEGG pathway analysis of CCT3-interacting proteins (significant enrichment in PI3K-AKT pathway highlighted); (C–E) Western blot analysis of PI3K-AKT pathway components (p-PI3 K, PI3 K, p-AKT, AKT) and EMT markers (N-cadherin, E-cadherin, Vimentin) in NCI-H1703 (C), DMS114 (D), and NCI-H446 (E) cells transfected with control siRNA (NC), CCT3-targeting siRNAs (si-CCT3#1–#2), empty vector (Vector), or CCT3-overexpressing vector (OE-CCT3) (GAPDH loading control).

Techniques: Protein-Protein interactions, Western Blot, Transfection, Control, Plasmid Preparation

Rescue assays confirm PI3K-AKT signaling mediates CCT3-regulated lung cancer cell phenotypes. (A) CCK-8 proliferation curves, (B) colony formation (images and quantification), and (C) migration/invasion (Transwell, images and quantification) in NCI-H1703, DMS114, and NCI-H446 cells transfected with control siRNA (NC), CCT3-targeting siRNA (si_CCT3), or si_CCT3 plus PI3 K agonist 740Y-P (si_CCT3 + 740Y-P); ****P < 0.0001 for si_CCT3 versus NC or si_CCT3 + 740Y-P versus si_CCT3.

Journal: Technology in Cancer Research & Treatment

Article Title: CCT3 Facilitates the Malignant Progression of NSCLC and SCLC via PI3 K/AKT-EMT Axis and Emerges as a Novel Serum Diagnostic Biomarker

doi: 10.1177/15330338251412203

Figure Lengend Snippet: Rescue assays confirm PI3K-AKT signaling mediates CCT3-regulated lung cancer cell phenotypes. (A) CCK-8 proliferation curves, (B) colony formation (images and quantification), and (C) migration/invasion (Transwell, images and quantification) in NCI-H1703, DMS114, and NCI-H446 cells transfected with control siRNA (NC), CCT3-targeting siRNA (si_CCT3), or si_CCT3 plus PI3 K agonist 740Y-P (si_CCT3 + 740Y-P); ****P < 0.0001 for si_CCT3 versus NC or si_CCT3 + 740Y-P versus si_CCT3.

Techniques: CCK-8 Assay, Migration, Transfection, Control

CCT3-related functional validation, clinical significance, and mechanistic insights in lung cancer. (A–C) Western blot analysis of PI3 K - AKT pathway proteins (p-PI3 K, PI3 K, p-AKT, AKT) and EMT markers (N-cadherin, E-cadherin, Vimentin) in (A) NCI - H1703, (B) DMS114, and (C) NCI - H446 cells transfected with NC, si_CCT3, or si_CCT3 + 740Y - P. (D–F) Serum CCT3 concentrations in normal controls (NC), pulmonary nodules (PN), non-small cell lung cancer (NSCLC), and small cell lung cancer (SCLC) (**P < 0.01, ***P < 0.001, ****P < 0.0001); CCT3 levels in (E) NSCLC and (F) SCLC patients stratified by tumor stage (I–IV) and lymph node metastasis (N0 vs N1). (G–J) ROC curves: (G) CCT3 alone for PN/NSCLC/SCLC diagnosis; (H–I) Other tumor markers (eg, CEA, NSE) for NSCLC and SCLC diagnosis, respectively; (J) CCT3 combined with other markers for NSCLC/SCLC diagnosis. (K) Bootstrap internal validation (1000 iterations) for the CCT3 diagnostic model. (L–M) Decision-curve analysis (DCA) evaluating the net clinical benefit of CCT3-based models across different threshold probabilities for (L) NSCLC and (M) SCLC. (N) Schematic model summarizing the role of CCT3 in promoting lung cancer proliferation and metastasis via activation of the PI3K-AKT pathway and induction of epithelial-mesenchymal transition (EMT), integrating experimental and clinical findings.

Journal: Technology in Cancer Research & Treatment

Article Title: CCT3 Facilitates the Malignant Progression of NSCLC and SCLC via PI3 K/AKT-EMT Axis and Emerges as a Novel Serum Diagnostic Biomarker

doi: 10.1177/15330338251412203

Figure Lengend Snippet: CCT3-related functional validation, clinical significance, and mechanistic insights in lung cancer. (A–C) Western blot analysis of PI3 K - AKT pathway proteins (p-PI3 K, PI3 K, p-AKT, AKT) and EMT markers (N-cadherin, E-cadherin, Vimentin) in (A) NCI - H1703, (B) DMS114, and (C) NCI - H446 cells transfected with NC, si_CCT3, or si_CCT3 + 740Y - P. (D–F) Serum CCT3 concentrations in normal controls (NC), pulmonary nodules (PN), non-small cell lung cancer (NSCLC), and small cell lung cancer (SCLC) (**P < 0.01, ***P < 0.001, ****P < 0.0001); CCT3 levels in (E) NSCLC and (F) SCLC patients stratified by tumor stage (I–IV) and lymph node metastasis (N0 vs N1). (G–J) ROC curves: (G) CCT3 alone for PN/NSCLC/SCLC diagnosis; (H–I) Other tumor markers (eg, CEA, NSE) for NSCLC and SCLC diagnosis, respectively; (J) CCT3 combined with other markers for NSCLC/SCLC diagnosis. (K) Bootstrap internal validation (1000 iterations) for the CCT3 diagnostic model. (L–M) Decision-curve analysis (DCA) evaluating the net clinical benefit of CCT3-based models across different threshold probabilities for (L) NSCLC and (M) SCLC. (N) Schematic model summarizing the role of CCT3 in promoting lung cancer proliferation and metastasis via activation of the PI3K-AKT pathway and induction of epithelial-mesenchymal transition (EMT), integrating experimental and clinical findings.

Techniques: Functional Assay, Biomarker Discovery, Western Blot, Transfection, Diagnostic Assay, Activation Assay

( A ) Overexpression of ANKRD55 and TCP1 in HEK293T cells followed by co-IP analysis to determine their interaction. ( B ) Protein extraction from Jurkat cells with subsequent co-IP assay to determine the interaction between ANKRD55 and TCP1. ( C ) PLA experiment in Jurkat cells to assess the interaction between ANKRD55 and TCP1. Cells were fixed and incubated with primary antibodies against ANKRD55 and TCP1, followed by PLA probe ligation and amplification. Red fluorescent puncta indicate close proximity (<40 nm) between ANKRD55 and TCP1, suggesting a direct or complex-mediated interaction. Nuclei were counterstained with DAPI (blue). Representative images are shown. Scale bars: 2 μm (top), 5 μm (bottom). ( D ) Immunofluorescent staining of Jurkat cells to analyze the colocalization of ANKRD55 and TCP1. Scale bars: 2 μm. ( E – K ) Co-IP assays were performed using HEK293T cells to investigate the interactions between ANKRD55 and individual CCT subunits, including CCT2, CCT3, CCT4, CCT5, CCT6, CCT7, and CCT8. ( L ) Immunofluorescent staining of Jurkat cells to assess colocalization between ANKRD55 and specific CCT subunits (CCT2, CCT3, CCT4, and CCT7). Scale bars: 2 μm (first 4 panels), 1 μm (fifth panel). ( M ) Immunofluorescent staining of Jurkat cells to visualize the subcellular localization of ANKRD55, TCP1, and pericentrin. Scale bars: 5 μm. ( N – P ) Immunoblotting analysis of TCP1 ( N ), CCT3 ( O ), and CCT6 ( P ) expression levels in Jurkat cells following ANKRD55 knockdown.

Journal: The Journal of Clinical Investigation

Article Title: ANKRD55 is a key regulator of T cell inflammation in multiple sclerosis

doi: 10.1172/JCI195214

Figure Lengend Snippet: ( A ) Overexpression of ANKRD55 and TCP1 in HEK293T cells followed by co-IP analysis to determine their interaction. ( B ) Protein extraction from Jurkat cells with subsequent co-IP assay to determine the interaction between ANKRD55 and TCP1. ( C ) PLA experiment in Jurkat cells to assess the interaction between ANKRD55 and TCP1. Cells were fixed and incubated with primary antibodies against ANKRD55 and TCP1, followed by PLA probe ligation and amplification. Red fluorescent puncta indicate close proximity (<40 nm) between ANKRD55 and TCP1, suggesting a direct or complex-mediated interaction. Nuclei were counterstained with DAPI (blue). Representative images are shown. Scale bars: 2 μm (top), 5 μm (bottom). ( D ) Immunofluorescent staining of Jurkat cells to analyze the colocalization of ANKRD55 and TCP1. Scale bars: 2 μm. ( E – K ) Co-IP assays were performed using HEK293T cells to investigate the interactions between ANKRD55 and individual CCT subunits, including CCT2, CCT3, CCT4, CCT5, CCT6, CCT7, and CCT8. ( L ) Immunofluorescent staining of Jurkat cells to assess colocalization between ANKRD55 and specific CCT subunits (CCT2, CCT3, CCT4, and CCT7). Scale bars: 2 μm (first 4 panels), 1 μm (fifth panel). ( M ) Immunofluorescent staining of Jurkat cells to visualize the subcellular localization of ANKRD55, TCP1, and pericentrin. Scale bars: 5 μm. ( N – P ) Immunoblotting analysis of TCP1 ( N ), CCT3 ( O ), and CCT6 ( P ) expression levels in Jurkat cells following ANKRD55 knockdown.

Article Snippet: TCP1 antibody (catalog 10320 and 68183), CCT2 antibody (catalog 68214), CCT3 antibody (catalog 60264), CCT4 antibody (catalog 67455), CCT5 antibody (catalog 67400), CCT6 antibody (catalog 19793), CCT7 antibody (catalog 68214), DYKDDDDK tag polyclonal antibody (catalog 20543), HA tag polyclonal antibody (catalog 51064), phospho-ERK1/2 (Thr202/Tyr204) polyclonal antibody (catalog 28733), CD247 polyclonal antibody (catalog 12837), and phospho-LCK-Y394 rabbit antibody (catalog AP0182) were purchased from Proteintech.

Techniques: Over Expression, Co-Immunoprecipitation Assay, Protein Extraction, Incubation, Ligation, Amplification, Staining, Western Blot, Expressing, Knockdown

( A and B ) α-Tubulin immunoblotting in lysates and pellet determined by microtubule sedimentation assay in Jurkat cells with TCP1 ( A ) or ANKRD55 ( B ) knocked down. ( C ) TCP1 degradation rate analyzed via immunoblot after cycloheximide (CHX; 70 μM) treatment for 0–48 hours in control and Jurkat cells overexpressing ANKRD55. ( D – F ) Co-IP detection of interactions between CCT5 and TCP1 ( D ), CCT3 ( E ), or CCT6 ( F ) at varying concentrations of ANKRD55 in HEK293T. ( G ) Immunofluorescence analysis of immune synapse formation between Jurkat and Raji cells. Jurkat cells were prelabeled with CMAC. Raji cells were stimulated with SEE for 30 minutes. The 2 cell types were then cocultured for 30 minutes. Cells were stained with antibodies against ANKRD55, TCP1, pericentrin, and α-tubulin to visualize protein localization at the immune synapse. Scale bars: 2 μm. BF, bright-field; CMAC, CellTracker blue fluorescent probe. ( H ) Flow cytometry–based immune synapse (IS) pattern analysis. ( I and J ) Raji cells (APCs) stained with CFSE and stimulated with SEE for 30 minutes at 37°C and Jurkat cells (T cells) stained with CMTPX. T cell conjugation with APCs after 20 minutes of contact was analyzed by flow cytometry. Conjugate percentages were determined for Jurkat cells with ANKRD55 or TCP1 knocked down ( I ) and pretreatment with HSF1A (50 μM) for 2 hours ( J ). ( K ) Mean clinical score of EAE in mice injected intraperitoneally with PBS or HSF1A (20 mg/mL) ( n = 7 or 8 mice per group), induced by active immunization with MOG 35–55 . ( L ) Immunoblot analysis of TCR signaling in Jurkat cells. Cells included vector control, a stable ANKRD55-overexpressing cell line, and ANKRD55-overexpressing cells pretreated with HSF1A (50 μM, 2 hours). All groups were stimulated on plates coated with anti-CD3 and anti-CD28. Lysates were collected at the indicated time points (1, 2, 15, and 30 minutes) and probed for TCR signaling–associated proteins. ( M ) H&E and Luxol fast blue (LFB) staining of spinal cord sections at the peak of EAE disease. Arrows indicate areas of demyelination. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, by 2-way ANOVA with Tukey’s multiple-comparison test. Data are shown as mean ± SEM.

Journal: The Journal of Clinical Investigation

Article Title: ANKRD55 is a key regulator of T cell inflammation in multiple sclerosis

doi: 10.1172/JCI195214

Figure Lengend Snippet: ( A and B ) α-Tubulin immunoblotting in lysates and pellet determined by microtubule sedimentation assay in Jurkat cells with TCP1 ( A ) or ANKRD55 ( B ) knocked down. ( C ) TCP1 degradation rate analyzed via immunoblot after cycloheximide (CHX; 70 μM) treatment for 0–48 hours in control and Jurkat cells overexpressing ANKRD55. ( D – F ) Co-IP detection of interactions between CCT5 and TCP1 ( D ), CCT3 ( E ), or CCT6 ( F ) at varying concentrations of ANKRD55 in HEK293T. ( G ) Immunofluorescence analysis of immune synapse formation between Jurkat and Raji cells. Jurkat cells were prelabeled with CMAC. Raji cells were stimulated with SEE for 30 minutes. The 2 cell types were then cocultured for 30 minutes. Cells were stained with antibodies against ANKRD55, TCP1, pericentrin, and α-tubulin to visualize protein localization at the immune synapse. Scale bars: 2 μm. BF, bright-field; CMAC, CellTracker blue fluorescent probe. ( H ) Flow cytometry–based immune synapse (IS) pattern analysis. ( I and J ) Raji cells (APCs) stained with CFSE and stimulated with SEE for 30 minutes at 37°C and Jurkat cells (T cells) stained with CMTPX. T cell conjugation with APCs after 20 minutes of contact was analyzed by flow cytometry. Conjugate percentages were determined for Jurkat cells with ANKRD55 or TCP1 knocked down ( I ) and pretreatment with HSF1A (50 μM) for 2 hours ( J ). ( K ) Mean clinical score of EAE in mice injected intraperitoneally with PBS or HSF1A (20 mg/mL) ( n = 7 or 8 mice per group), induced by active immunization with MOG 35–55 . ( L ) Immunoblot analysis of TCR signaling in Jurkat cells. Cells included vector control, a stable ANKRD55-overexpressing cell line, and ANKRD55-overexpressing cells pretreated with HSF1A (50 μM, 2 hours). All groups were stimulated on plates coated with anti-CD3 and anti-CD28. Lysates were collected at the indicated time points (1, 2, 15, and 30 minutes) and probed for TCR signaling–associated proteins. ( M ) H&E and Luxol fast blue (LFB) staining of spinal cord sections at the peak of EAE disease. Arrows indicate areas of demyelination. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, by 2-way ANOVA with Tukey’s multiple-comparison test. Data are shown as mean ± SEM.

Techniques: Western Blot, Microtubule Sedimentation Assay, Control, Co-Immunoprecipitation Assay, Immunofluorescence, Staining, Flow Cytometry, Conjugation Assay, Injection, Plasmid Preparation, Comparison

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