Description: Rabbit polyclonal antibody to ATG4C Immunogen: KLH-conjugated synthetic peptide encompassing a sequence within the N-term region of human ATG4C. The exact sequence is proprietary. Purification: The antibody was purified by immunogen affinity chromatography. Clonality: Polyclonal Form: Liquid in 0.42% Potassium phosphate, 0.87% Sodium chloride, pH 7.3, 30% glycerol, and 0.01% sodium azide. Dilution: WB (1/500 - 1/1000), IH (1/100 - 1/200), IF/IC (1/100 - 1/500) Gene Symbol: ATG4C Alternative Names: APG4C; AUTL1; AUTL3; Cysteine protease ATG4C; AUT-like 3 cysteine endopeptidase; Autophagin-3; Autophagy-related cysteine endopeptidase 3; Autophagy-related protein 4 homolog CEntrez Gene (Human): 84938SwissProt (Human): Q96DT6Storage/Stability : Shipped at 4°C. Upon delivery aliquot and store at -20°C for one year. Avoid freeze/thaw cycles.
-
Western blot analysis of ATG4C expression in AML12 (A), rat testis (B), MCF7 (C), LO2 (D) whole cell lysates.
-
Immunohistochemical analysis of ATG4C staining in human prostate cancer formalin fixed paraffin embedded tissue section. The section was pre-treated using heat mediated antigen retrieval with sodium citrate buffer (pH 6.0). The section was then incubated with the antibody at room temperature and detected using an HRP conjugated compact polymer system. DAB was used as the chromogen. The section was then counterstained with haematoxylin and mounted with DPX.
-
Immunofluorescent analysis of ATG4C staining in K562 cells. Formalin-fixed cells were permeabilized with 0.1% Triton X-100 in TBS for 5-10 minutes and blocked with 3% BSA-PBS for 30 minutes at room temperature. Cells were probed with the primary antibody in 3% BSA-PBS and incubated overnight at 4 °C in a hidified chamber. Cells were washed with PBST and incubated with a DyLight 594-conjugated secondary antibody (red) in PBS at room temperature in the dark. DAPI was used to stain the cell nuclei (blue).
Disruption of a Sirt1-dependent autophagy checkpoint in the prostate results in prostatic intraepithelial neoplasia lesion formation