rabbit polyclonal antibodies against cgas  (Boster Bio)

Journal: Virology Journal

Article Title: Pseudorabies virus UL38 attenuates the cGAS-STING signaling pathway by recruiting Tollip to promote STING for autophagy degradation

doi: 10.1186/s12985-024-02379-x

Figure Lengend Snippet: UL38 promotes decreasing of STING. PK15 cells were transfected with pCMV-Myc (1 µg) or Myc-UL38 (1 µg) for 24 h, then cells were stimulated with 1 MOI PRV ( A ), poly(dA: dT) (1 µg/mL) ( B ) or 2’3’-cGAMP (2 mg/mL) ( C ) respectively for another 12 h. Cells were collected for western blotting analysis. The expression of cGAS, STING, TBK1, IRF3 and phosphorylated IRF3 were detected. For all experiments, β-actin serves as a loading control

Article Snippet: Sangon Biotech (Shanghai, China) provided the following antibodies: rabbit polyclonal antibody against the FLAG tag (D191041), rabbit polyclonal antibody against the HA tag (D110004), rabbit polyclonal antibody against cGAS (D163570), HRP-conjugated Goat Anti-Rabbit IgG (D110058) and HRP-conjugated Goat Anti-Mouse IgG (D110087).

Techniques: Transfection, Western Blot, Expressing, Control

Journal: Cancers

Article Title: Nectin-1 Expression Correlates with the Susceptibility of Malignant Melanoma to Oncolytic Herpes Simplex Virus In Vitro and In Vivo

doi: 10.3390/cancers13123058

Figure Lengend Snippet: Correlation of the oncolytic activity of T-VEC with the expression of stimulator of interferon genes (STING) and cyclic GMP-AMP synthase (cGAS) in a panel of melanoma cell lines. ( A ) Western Blot analysis of STING and cGAS with respect to housekeeping protein ß-actin using lysates of 20 melanoma cell lines. ( B ) Densitometric quantification of STING and cGAS, normalized for ß-actin and shown as the mean and standard error of three independent Western blot experiments. ( C ) Spearman correlation coefficient, ( D ) box plot, and ( E ) ROC curve analyses of all responder and non-responder cell lines with respect to STING (upper part) and cGAS expression (lower part) and corresponding susceptibility to T-VEC induced cell death. p values for box plots were calculated using the Mann–Whitney test; ROC curves analyzed the area under the curve (AUC).

Article Snippet: The following primary antibodies were used: Rabbit monoclonal antibody against STING (D2P2F, Cell Signaling; dilution for patient samples 1:50, dilution for cell lines 1:200), murine monoclonal antibody against Nectin-1 (R1.302.12, Santa Cruz, Heidelberg, Germany; dilution for patient samples 1:50), rabbit polyclonal antibody against Nectin-1 (AB_2736197, Invitrogen/Thermo Fisher; dilution for cell lines 1:100), murine monoclonal antibody against HVEM (CW10, Santa Cruz; dilution 1:500 for patient samples and cell lines), rabbit polyclonal antibody against cGAS (NBP1-86761, Novus Biologicals/Bio-Techne, Wiesbaden Nordenstadt, Germany; dilution for patient samples 1:200), and rabbit monoclonal antibody against cGAS (D1D3G) (Cell Signaling; dilution for cell lines 1:200).

Techniques: Activity Assay, Expressing, Western Blot, MANN-WHITNEY

Journal: Cancers

Article Title: Nectin-1 Expression Correlates with the Susceptibility of Malignant Melanoma to Oncolytic Herpes Simplex Virus In Vitro and In Vivo

doi: 10.3390/cancers13123058

Figure Lengend Snippet: Correlation of biomarkers evaluated by flow cytometry, Western blot, and immunohistochemistry with the oncolytic activity of T-VEC in melanoma cell lines. Spearman correlation coefficient analysis for ( A ) Nectin-1 and HVEM expression, measured by flow cytometry (FACS) and immunohistochemistry (IHC), ( B ) STING and cGAS expression, evaluated by Western blot (WB) and immunohistochemistry, and ( C ) expression of all four biomarkers in immunohistochemistry with the oncolytic activity of T-VEC in 20 melanoma cell lines. Data show the mean of three independent experiments for each biomarker and MTT assay.

Article Snippet: The following primary antibodies were used: Rabbit monoclonal antibody against STING (D2P2F, Cell Signaling; dilution for patient samples 1:50, dilution for cell lines 1:200), murine monoclonal antibody against Nectin-1 (R1.302.12, Santa Cruz, Heidelberg, Germany; dilution for patient samples 1:50), rabbit polyclonal antibody against Nectin-1 (AB_2736197, Invitrogen/Thermo Fisher; dilution for cell lines 1:100), murine monoclonal antibody against HVEM (CW10, Santa Cruz; dilution 1:500 for patient samples and cell lines), rabbit polyclonal antibody against cGAS (NBP1-86761, Novus Biologicals/Bio-Techne, Wiesbaden Nordenstadt, Germany; dilution for patient samples 1:200), and rabbit monoclonal antibody against cGAS (D1D3G) (Cell Signaling; dilution for cell lines 1:200).

Techniques: Flow Cytometry, Western Blot, Immunohistochemistry, Activity Assay, Expressing, Biomarker Discovery, MTT Assay

Journal: Cancers

Article Title: Nectin-1 Expression Correlates with the Susceptibility of Malignant Melanoma to Oncolytic Herpes Simplex Virus In Vitro and In Vivo

doi: 10.3390/cancers13123058

Figure Lengend Snippet: Oncolytic effect of T-VEC upon injection into 35 malignant melanoma lesions. ( A ) Waterfall plot showing the response rate of each individual lesion as increase or decrease of the tumor volume, calculated as (length × width × thickness)/2 when the maximum anti-tumor effect had been achieved. ( B ) Based on this criterion, 14 and 21 lesions were respectively categorized as non-responders (+129.89% to −29%) and responders (−30% to −100%). ( C ) Representative example of Nectin-1, HVEM, STING, and cGAS immunostaining in a melanoma lesion responding (upper panel) or not responding (lower panel) to intratumoral T-VEC injection. Images provide an overview and details at higher magnification (inserts); corresponding size bars are included. ( D ) Spearman correlation coefficient analysis of Nectin-1, HVEM, STING, and cGAS immunostaining with the oncolytic activity of T-VEC inoculated into the respective lesion. ( E ) Box plots (with median, interquartile ranges, minimum, and maximum values) and ( F ) ROC curve analysis of responder and non-responder lesions with respect to Nectin-1, HVEM, STING, and cGAS immunostaining. p values for box plots were calculated using the Mann–Whitney test; p values for ROC curves analyzed the area under the curve.

Article Snippet: The following primary antibodies were used: Rabbit monoclonal antibody against STING (D2P2F, Cell Signaling; dilution for patient samples 1:50, dilution for cell lines 1:200), murine monoclonal antibody against Nectin-1 (R1.302.12, Santa Cruz, Heidelberg, Germany; dilution for patient samples 1:50), rabbit polyclonal antibody against Nectin-1 (AB_2736197, Invitrogen/Thermo Fisher; dilution for cell lines 1:100), murine monoclonal antibody against HVEM (CW10, Santa Cruz; dilution 1:500 for patient samples and cell lines), rabbit polyclonal antibody against cGAS (NBP1-86761, Novus Biologicals/Bio-Techne, Wiesbaden Nordenstadt, Germany; dilution for patient samples 1:200), and rabbit monoclonal antibody against cGAS (D1D3G) (Cell Signaling; dilution for cell lines 1:200).

Techniques: Injection, Immunostaining, Activity Assay, MANN-WHITNEY

Journal: The EMBO Journal

Article Title: Zika virus elicits inflammation to evade antiviral response by cleaving cGAS via NS 1‐caspase‐1 axis

doi: 10.15252/embj.201899347

Figure Lengend Snippet: ZIKV non‐structural proteins NS1 enhance inflammasome activation to benefit its infection by recruiting USP8 to cleave K11‐linked poly‐ubiquitin chains from caspase‐1 at Lys134. NS1‐mediated stabilization of caspase‐1 further promotes the cleavage of cGAS, thus inhibiting type I IFN signaling as well as antiviral innate immunity.

Article Snippet: Rabbit polyclonal antibodies against murine cGAS (R3252‐1) were from Abiocode.

Techniques: Activation Assay, Infection, Ubiquitin Proteomics