Journal: BMC Cancer

Article Title: CCL1 is a major regulatory T cell attracting factor in human breast cancer

doi: 10.1186/s12885-018-5117-8

Figure Lengend Snippet: CCL1 and FoxP3 are intensively expressed in human invasive breast cancer. Tissue microarrays (TMAs) of mammary carcinoma and non-malignant control samples have been immunohistochemically stained for the indicated proteins. Representative sections for ( a ) CCL1, ( b ) CCL22 and ( c ) FoxP3 are shown. ( d ) TMAs of breast cancer and healthy breast tissue were analyzed for the number of positive cells/mm 2 . For statistical analysis the Mann-Whitney-U-Test was used

Article Snippet: Primary antibodies against CCL22 (Peprotech, Hamburg, Germany), FoxP3 (Abcam, Cambridge, USA) and CCL1 (Atlas antibodies, Stockholm, Sweden) were incubated for 16 h at 4 °C.

Techniques: Control, Staining, MANN-WHITNEY

Journal: BMC Cancer

Article Title: CCL1 is a major regulatory T cell attracting factor in human breast cancer

doi: 10.1186/s12885-018-5117-8

Figure Lengend Snippet: Correlation between chemokine expression and density of FoxP3+ cells

Article Snippet: Primary antibodies against CCL22 (Peprotech, Hamburg, Germany), FoxP3 (Abcam, Cambridge, USA) and CCL1 (Atlas antibodies, Stockholm, Sweden) were incubated for 16 h at 4 °C.

Techniques: Expressing

Journal: BMC Cancer

Article Title: CCL1 is a major regulatory T cell attracting factor in human breast cancer

doi: 10.1186/s12885-018-5117-8

Figure Lengend Snippet: Association between chemokine expression and pathological features

Article Snippet: Primary antibodies against CCL22 (Peprotech, Hamburg, Germany), FoxP3 (Abcam, Cambridge, USA) and CCL1 (Atlas antibodies, Stockholm, Sweden) were incubated for 16 h at 4 °C.

Techniques: Expressing

Journal: BMC Cancer

Article Title: CCL1 is a major regulatory T cell attracting factor in human breast cancer

doi: 10.1186/s12885-018-5117-8

Figure Lengend Snippet: Effect of intratumoral CCL1 on patient survival. Tumor samples have been divided into CCL1 high-expressing ( n = 88) and CCL1 low-expressing tumors ( n = 87) based on the median CCL1-positive cell number/mm 2 (median = 10.14 cells/mm 2 ). Survival in both groups was then compared with a log-rank test ( p = 0.149)

Article Snippet: Primary antibodies against CCL22 (Peprotech, Hamburg, Germany), FoxP3 (Abcam, Cambridge, USA) and CCL1 (Atlas antibodies, Stockholm, Sweden) were incubated for 16 h at 4 °C.

Techniques: Expressing

Journal: Frontiers in Immunology

Article Title: FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/β-Catenin Pathway in a Murine Model of Lupus Nephritis

doi: 10.3389/fimmu.2019.00784

Figure Lengend Snippet: Primers used for real-time PCR analysis.

Article Snippet: After transfer, 5% bovine serum albumin (in TBST buffer; Beijing Solarbio Science) was used to block the membrane at room temperature for 1 h. Then, the membranes were pre-incubated with the primary antibodies anti-FKN (Lot: GR18924-38, Abcam, 1:1,000 dilution), anti-α-SMA (Lot: GR282976-20, Abcam, 1:1,000 dilution), anti-vimentin (Lot: GR3186827-2, Abcam, 1:1,000 dilution), anti-E-cadherin (Lot: GR3184955-1, Abcam, 1:1,000 dilution), Wnt-4 (SC-3762, SantaCruz, 1:500 dilution), c-Myc (Cat#10828-1-AP, Proteintech, 1:1,000 dilution), anti-cyclin D1 (Lot: GR312543-18, Abcam, 1:1,000 dilution), P-NF-κB –p65 (S536, Cell signaling,1:1,000 dilution), NF-κB –p65 (D14E12, Cell signaling,1:1,000 dilution), TGFβ (Lot: SC-146, SantaCruz, 1:500 dilution), F4/80 (Lot:GR3250648-1, Abcam, 1:1000 dilution), CCL22 (Cat#: DF7781, Affinity, 1:1,000 dilution) and anti-GAPDH (cat#6-004-1-1g, Proteintech, 1:1500 dilution) at 4°C overnight and then incubated with secondary antibody following washing with TBST three times.

Techniques: Real-time Polymerase Chain Reaction, Sequencing

Journal: Frontiers in Immunology

Article Title: FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/β-Catenin Pathway in a Murine Model of Lupus Nephritis

doi: 10.3389/fimmu.2019.00784

Figure Lengend Snippet: Twelve-week-old MRL/lpr mice were IP injected with isotype antibody, recombinant-FKN protein, and anti-FKN antibody for 7 days. In kidney sections of MRL/lpr mice stained by IHC (original magnification, ×400). (a) Control group; (b) IgG group; (c) rFKN group; (d) anti-FKN group. (A) Expression of FKN as examined by IHC staining in the renal tissues. (B) Expression of Wnt-4 as examined by IHC staining in the renal tissues. (C) Expression of CCL22 as examined by IHC staining in the renal tissues. (D) Expression of F4/80 as examined by IHC staining in the renal tissues. (E) The column diagram indicates the statistical of (A-D) . * p < 0.05 compared with the control group. No significant differences between IgG compared to the control group are indicated as * p > 0.05. Significant differences among the rFKN group and anti-FKN groups are indicated as # p < 0.05. Data are expressed as the means ± standard deviation ( n = 3). Statistical analyses were performed using one-way ANOVA.

Article Snippet: After transfer, 5% bovine serum albumin (in TBST buffer; Beijing Solarbio Science) was used to block the membrane at room temperature for 1 h. Then, the membranes were pre-incubated with the primary antibodies anti-FKN (Lot: GR18924-38, Abcam, 1:1,000 dilution), anti-α-SMA (Lot: GR282976-20, Abcam, 1:1,000 dilution), anti-vimentin (Lot: GR3186827-2, Abcam, 1:1,000 dilution), anti-E-cadherin (Lot: GR3184955-1, Abcam, 1:1,000 dilution), Wnt-4 (SC-3762, SantaCruz, 1:500 dilution), c-Myc (Cat#10828-1-AP, Proteintech, 1:1,000 dilution), anti-cyclin D1 (Lot: GR312543-18, Abcam, 1:1,000 dilution), P-NF-κB –p65 (S536, Cell signaling,1:1,000 dilution), NF-κB –p65 (D14E12, Cell signaling,1:1,000 dilution), TGFβ (Lot: SC-146, SantaCruz, 1:500 dilution), F4/80 (Lot:GR3250648-1, Abcam, 1:1000 dilution), CCL22 (Cat#: DF7781, Affinity, 1:1,000 dilution) and anti-GAPDH (cat#6-004-1-1g, Proteintech, 1:1500 dilution) at 4°C overnight and then incubated with secondary antibody following washing with TBST three times.

Techniques: Injection, Recombinant, Staining, Control, Expressing, Immunohistochemistry, Standard Deviation

Journal: Frontiers in Immunology

Article Title: FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/β-Catenin Pathway in a Murine Model of Lupus Nephritis

doi: 10.3389/fimmu.2019.00784

Figure Lengend Snippet: FKN is involved EMT and fibrosis via the Wnt/β-catenin pathway in the kidney of MRL/lpr mice. Histopathological features of renal tissue in the MRL/lpr mice model were studied by PASM staining (original magnification, ×400). (a) Control group;(b) IgG group; (c) rFKN group; (d) anti-FKN group. (A1) Assessment of glomerular and renal interstitial pathologies stained with PASM. Glomerular pathology was graded from the sum of scores for glomerular inflammation, thickness of basement membrane, epithelial cell reactivity, crescent formation, and necrosis. Interstitial pathology was graded using the sum of scores for perivascular inflammation and inflammatory cell infiltration. Scores were graded as 0 to 4 (0, none; 1 mild; 2 moderate; 3 moderate-high; 4 high). (A2 ) the sum of score by PASM staining in the renal glomerular inflammation. (A3) the sum of score by PASM staining in the renal glomerular inflammation. Renal tissue extract (~50 μg) was resolved on SDS-PAGE and western blot analysis was performed using antibodies against FKN, vimentin, α-SMA, E-cadherin, Wnt-4, β-catenin, cyclinD1, and c-Myc. GAPDH was used as an internal control. Total RNA were extracted from renal tissue of mice. Then the RNA was reverse-transcribed into cDNA and the transcripts were quantified using real-time PCR. GAPDH was used as an internal control. NF-kB-P65 was used as an internal control group of P- NF-kB-P65. Western blotting (B) and qRT-PCR (C) was used to detect the protein and mRNA levels of FKN, vimentin, α-SMA, E-cadherin, Wnt-4, β-catenin, cyclinD1, c-Myc, P- NF-kB -P65, CCL22 and F4/80 in renal tissues. * p < 0.05 compared with the control group. No significant differences between IgG compared to the control group are indicated as * p > 0.05. Significant differences among the rFKN group and anti-FKN groups are indicated as # p < 0.05. Data are expressed as the means ± standard deviation ( n = 3). Statistical analyses were performed using one-way ANOVA.

Article Snippet: After transfer, 5% bovine serum albumin (in TBST buffer; Beijing Solarbio Science) was used to block the membrane at room temperature for 1 h. Then, the membranes were pre-incubated with the primary antibodies anti-FKN (Lot: GR18924-38, Abcam, 1:1,000 dilution), anti-α-SMA (Lot: GR282976-20, Abcam, 1:1,000 dilution), anti-vimentin (Lot: GR3186827-2, Abcam, 1:1,000 dilution), anti-E-cadherin (Lot: GR3184955-1, Abcam, 1:1,000 dilution), Wnt-4 (SC-3762, SantaCruz, 1:500 dilution), c-Myc (Cat#10828-1-AP, Proteintech, 1:1,000 dilution), anti-cyclin D1 (Lot: GR312543-18, Abcam, 1:1,000 dilution), P-NF-κB –p65 (S536, Cell signaling,1:1,000 dilution), NF-κB –p65 (D14E12, Cell signaling,1:1,000 dilution), TGFβ (Lot: SC-146, SantaCruz, 1:500 dilution), F4/80 (Lot:GR3250648-1, Abcam, 1:1000 dilution), CCL22 (Cat#: DF7781, Affinity, 1:1,000 dilution) and anti-GAPDH (cat#6-004-1-1g, Proteintech, 1:1500 dilution) at 4°C overnight and then incubated with secondary antibody following washing with TBST three times.

Techniques: Staining, Control, Membrane, SDS Page, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Standard Deviation

Journal:

Article Title: Expression of CCL28 by Reed-Sternberg Cells Defines a Major Subtype of Classical Hodgkin's Disease with Frequent Infiltration of Eosinophils and/or Plasma Cells

doi:

Figure Lengend Snippet: Summary of the Primers Used for RT-PCR

Article Snippet: Sections were then incubated at 4°C overnight with monoclonal mouse anti-LMP-1 (CS1-4; DAKO Japan), goat anti-TARC/CCL17 (Genzyme/Techne, Cambridge, MA), rabbit anti-MDC/CCL22 (Peprotech EC, London, England), mouse anti-eotaxin/CCL11 (43911.11; R&D), goat anti-MEC/CCL28 (DAKO Japan), mouse anti-CCR4 (KM-2160; Kyowa Hakko, Tokyo, Japan), rabbit anti-CCR10 (Biocarta, San Diego, CA), or anti-CD138/syndecan-1 (B-B4; Immunotech, Marseille, France).

Techniques:

Journal:

Article Title: Expression of CCL28 by Reed-Sternberg Cells Defines a Major Subtype of Classical Hodgkin's Disease with Frequent Infiltration of Eosinophils and/or Plasma Cells

doi:

Figure Lengend Snippet: Chemotactic response of HD-derived cell lines to CXCL16 and CCL27. Indicated HD-derived cell lines were examined for chemotactic responses to CXCL16, the ligand for CXCR6 (A), or to CCL27, the monospecific ligand for CCR10 (B), both at nM. For details, see Materials and Methods. Representative results from at least two separate assays are shown.

Article Snippet: Sections were then incubated at 4°C overnight with monoclonal mouse anti-LMP-1 (CS1-4; DAKO Japan), goat anti-TARC/CCL17 (Genzyme/Techne, Cambridge, MA), rabbit anti-MDC/CCL22 (Peprotech EC, London, England), mouse anti-eotaxin/CCL11 (43911.11; R&D), goat anti-MEC/CCL28 (DAKO Japan), mouse anti-CCR4 (KM-2160; Kyowa Hakko, Tokyo, Japan), rabbit anti-CCR10 (Biocarta, San Diego, CA), or anti-CD138/syndecan-1 (B-B4; Immunotech, Marseille, France).

Techniques: Derivative Assay

Journal:

Article Title: Expression of CCL28 by Reed-Sternberg Cells Defines a Major Subtype of Classical Hodgkin's Disease with Frequent Infiltration of Eosinophils and/or Plasma Cells

doi:

Figure Lengend Snippet: Immunohistochemical analysis of HD tissues. Classical HD tissue specimens were examined with the following reagents: A, anti-LMP-1 (case 6); B, anti-TARC/CCL17 (case 6); C, anti-MDC/CCL22 (case 6); D, anti-CCR4 (case 13); E, anti-MEC/CCL28 (case 7); F, anti-MEC/CCL28 (case 5); G, anti-CCR10 (case 7); H, anti-CCR10 (case 6); I, anti-eotaxin/CCL11 (case 13); J, a representative isotype control (case 5); K, H&E staining (case 5); L, anti-CD138/syndecan-1 (case 6). For details, see Materials and Methods. All experiments were done at least twice and representative results are shown. Asterisks indicate H-RS cells. Original magnifications, ×1000.

Article Snippet: Sections were then incubated at 4°C overnight with monoclonal mouse anti-LMP-1 (CS1-4; DAKO Japan), goat anti-TARC/CCL17 (Genzyme/Techne, Cambridge, MA), rabbit anti-MDC/CCL22 (Peprotech EC, London, England), mouse anti-eotaxin/CCL11 (43911.11; R&D), goat anti-MEC/CCL28 (DAKO Japan), mouse anti-CCR4 (KM-2160; Kyowa Hakko, Tokyo, Japan), rabbit anti-CCR10 (Biocarta, San Diego, CA), or anti-CD138/syndecan-1 (B-B4; Immunotech, Marseille, France).

Techniques: Immunohistochemical staining, Staining

Journal:

Article Title: Expression of CCL28 by Reed-Sternberg Cells Defines a Major Subtype of Classical Hodgkin's Disease with Frequent Infiltration of Eosinophils and/or Plasma Cells

doi:

Figure Lengend Snippet: Results of Immunohistochemical Staining of Classical HD Tissue Specimens

Article Snippet: Sections were then incubated at 4°C overnight with monoclonal mouse anti-LMP-1 (CS1-4; DAKO Japan), goat anti-TARC/CCL17 (Genzyme/Techne, Cambridge, MA), rabbit anti-MDC/CCL22 (Peprotech EC, London, England), mouse anti-eotaxin/CCL11 (43911.11; R&D), goat anti-MEC/CCL28 (DAKO Japan), mouse anti-CCR4 (KM-2160; Kyowa Hakko, Tokyo, Japan), rabbit anti-CCR10 (Biocarta, San Diego, CA), or anti-CD138/syndecan-1 (B-B4; Immunotech, Marseille, France).

Techniques: Immunohistochemical staining, Staining

Journal: Frontiers in immunology

Article Title: FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/β-Catenin Pathway in a Murine Model of Lupus Nephritis.

doi: 10.3389/fimmu.2019.00784

Figure Lengend Snippet: FIGURE 3 | FKN participates in the EMT process of HK-2 cells via the Wnt/β-catenin signaling pathway. To detect the protein and mRNA levels of FKN, EMT markers (vimentin, α-SMA, E-cadherin) and Wnt/β-catenin pathway targets (Wnt-4, β-catenin, cyclinD1, and c-Myc) in different groups of HK-2 cells, cells were incubated for (Continued)

Article Snippet: The sections were incubated with individually primary antibodies against FKN (1:200) (Lot: GR18924-38, Abcam), Wnt-4 (1:200) (SC-3762, Santa Cruz Technologies), F4/80 (Lot: GR3250648-1, Abcam, 1:200 dilution), and CCL22 (Cat#: DF7781, Affinity, 1:200 dilution) overnight at 4◦C, then incubated with goat polyclonal secondary antibody for 20min at 37◦C.

Techniques: Incubation

Journal: Frontiers in immunology

Article Title: FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/β-Catenin Pathway in a Murine Model of Lupus Nephritis.

doi: 10.3389/fimmu.2019.00784

Figure Lengend Snippet: FIGURE 4 | The effects of FKN on the levels of blood urea nitrogen, serum creatinine, 24 h urinary protein, ANA, anti-ds-DNA, and anti-ds-Sm determined at the end of 13 weeks. (A) Level of serum creatinine. (B) Level of blood urea nitrogen. (C) Level of 24 h urinary protein. (D) Level of ANA, anti-ds-DNA, and anti-ds-Sm. Control, MRL/lpr mice; IgG, MRL/lpr mice treated with isotype antibody; rFKN, MRL/lpr mice treated with recombinant-FKN antibody; anti-FKN, MRL/lpr mice treated with anti-FKN antibody. *p < 0.05 compared with the control group. No significant differences between IgG compared to the control group are indicated as *p > 0.05. Significant differences among the rFKN group and anti-FKN groups are indicated as #p < 0.05. Data are expressed as the means ± standard deviation (n = 3). Statistical analyses were performed using one-way ANOVA.

Article Snippet: The sections were incubated with individually primary antibodies against FKN (1:200) (Lot: GR18924-38, Abcam), Wnt-4 (1:200) (SC-3762, Santa Cruz Technologies), F4/80 (Lot: GR3250648-1, Abcam, 1:200 dilution), and CCL22 (Cat#: DF7781, Affinity, 1:200 dilution) overnight at 4◦C, then incubated with goat polyclonal secondary antibody for 20min at 37◦C.

Techniques: Control, Recombinant, Standard Deviation

Journal: Frontiers in immunology

Article Title: FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/β-Catenin Pathway in a Murine Model of Lupus Nephritis.

doi: 10.3389/fimmu.2019.00784

Figure Lengend Snippet: FIGURE 5 | Twelve-week-old MRL/lpr mice were IP injected with isotype antibody, recombinant-FKN protein, and anti-FKN antibody for 7 days. In kidney sections of MRL/lpr mice stained by IHC (original magnification, ×400). (a) Control group; (b) IgG group; (c) rFKN group; (d) anti-FKN group. (A) Expression of FKN as examined by IHC staining in the renal tissues. (B) Expression of Wnt-4 as examined by IHC staining in the renal tissues. (C) Expression of CCL22 as examined by IHC staining in the renal tissues. (D) Expression of F4/80 as examined by IHC staining in the renal tissues. (E) The column diagram indicates the statistical of (A-D). *p < 0.05 compared with the control group. No significant differences between IgG compared to the control group are indicated as *p > 0.05. Significant differences among the rFKN group and anti-FKN groups are indicated as #p < 0.05. Data are expressed as the means ± standard deviation (n = 3). Statistical analyses were performed using one-way ANOVA.

Article Snippet: The sections were incubated with individually primary antibodies against FKN (1:200) (Lot: GR18924-38, Abcam), Wnt-4 (1:200) (SC-3762, Santa Cruz Technologies), F4/80 (Lot: GR3250648-1, Abcam, 1:200 dilution), and CCL22 (Cat#: DF7781, Affinity, 1:200 dilution) overnight at 4◦C, then incubated with goat polyclonal secondary antibody for 20min at 37◦C.

Techniques: Injection, Recombinant, Staining, Control, Expressing, Immunohistochemistry, Standard Deviation

Journal: Frontiers in immunology

Article Title: FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/β-Catenin Pathway in a Murine Model of Lupus Nephritis.

doi: 10.3389/fimmu.2019.00784

Figure Lengend Snippet: FIGURE 6 | FKN is involved EMT and fibrosis via the Wnt/β-catenin pathway in the kidney of MRL/lpr mice. Histopathological features of renal tissue in the MRL/lpr mice model were studied by PASM staining (original magnification, ×400). (a) Control group;(b) IgG group; (c) rFKN group; (d) anti-FKN group. (A1) Assessment of glomerular and renal interstitial pathologies stained with PASM. Glomerular pathology was graded from the sum of scores for glomerular inflammation, thickness of basement membrane, epithelial cell reactivity, crescent formation, and necrosis. Interstitial pathology was graded using the sum of scores for perivascular inflammation and inflammatory cell infiltration. Scores were graded as 0 to 4 (0, none; 1 mild; 2 moderate; 3 moderate-high; 4 high). (A2) the sum of score by PASM staining in the renal glomerular inflammation. (A3) the sum of score by PASM staining in the renal glomerular inflammation. Renal tissue extract (∼50 µg) was resolved on SDS-PAGE and western blot analysis was performed using antibodies against FKN, vimentin, α-SMA, E-cadherin, Wnt-4, β-catenin, cyclinD1, and c-Myc. GAPDH was used as an internal control. Total RNA were extracted from renal tissue of mice. Then the RNA was reverse-transcribed into cDNA and the transcripts were quantified using real-time PCR. GAPDH was used as an internal control. NF-kB-P65 was used as an internal control group of P- NF-kB-P65. Western blotting (B) and qRT-PCR (C) was used to detect the protein and mRNA levels of FKN, vimentin, α-SMA, E-cadherin, Wnt-4, β-catenin, cyclinD1, c-Myc, P- NF-kB -P65, CCL22 and F4/80 in renal tissues. *p < 0.05 compared with the control group. No significant differences between IgG compared to the control group are indicated as *p > 0.05. Significant differences among the rFKN group and anti-FKN groups are indicated as #p < 0.05. Data are expressed as the means ± standard deviation (n = 3). Statistical analyses were performed using one-way ANOVA.

Article Snippet: The sections were incubated with individually primary antibodies against FKN (1:200) (Lot: GR18924-38, Abcam), Wnt-4 (1:200) (SC-3762, Santa Cruz Technologies), F4/80 (Lot: GR3250648-1, Abcam, 1:200 dilution), and CCL22 (Cat#: DF7781, Affinity, 1:200 dilution) overnight at 4◦C, then incubated with goat polyclonal secondary antibody for 20min at 37◦C.

Techniques: Staining, Control, Membrane, SDS Page, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Standard Deviation

Journal: Oncotarget

Article Title: Enhancement of adoptive T cell transfer with single low dose pretreatment of doxorubicin or paclitaxel in mice

doi:

Figure Lengend Snippet: The E.G7 tumor-bearing mice were established on day -7 and treated with or without single low dose of Dox or Tax on day -1 (tumor volume about 100 mm 3 ) followed by ACT on day 0. All mice were sacrificed on day 3. A. - B. Proteins extracted from tumors of Dox- or Tax-treated mice were analyzed with Western blotting. TGF-β, IDO, CCL2, VEGF, CCL22, COX-2 and IL-10 were significantly decreased in a dose-dependent manner. C. Nuclear proteins extracted from tumors of mice of each group were analyzed with EMSA. NF-κB/DNA binding activity was decreased by single low dose treatment of Dox and Tax, respectively, in a dose-dependent manner. D. Percentages of Tregs in TDLN and spleen were significantly decreased in mice treated with single low dose of Dox or Tax. E. Percentages of MDSCs in bone marrow and spleen were significantly decreased in mice treated with single low dose of Dox or Tax. F. IL-12 levels in the serum assayed by ELISA were increased in a dose-dependent manner in mice treated with single low dose of Dox or Tax. (* p < 0.05, ** p < 0.01 compared with that of the control).

Article Snippet: The membranes were incubated with primary antibodies against anti-IDO, anti-COX-2 (Millipore), TGF-β, CCL2, (Cell Signaling), anti-MDC (CCL22), anti-VEGF, anti-IL-10 and β-actin (Abcam) at 4°C overnight.

Techniques: Western Blot, Binding Assay, Activity Assay, Enzyme-linked Immunosorbent Assay, Control