Anti ATM Protein Kinase, phospho Ser1981

DNA damage signaling in X DC patient cells.(A) Immunofluorescence staining of DNA damage proteins. Control X DC 1787 C and patient X DC 1774 P cells were, either not treated ( Bleo) or treated (+Bleo) with bleomycin (10 ug/ml) for 24 hours, fixed and incubated with antibodies against γ H2AX, 53BP1, p ATM or p CHK1 and secondary fluorescent antibodies. Nuclear DNA was counterstained with DAPI (blue). (B). Quantification of γ H2A.X foci, pATM, 53BP1 and pCHK2 associated foci in X DC 1787 C and X DC 1774 P cells. More than 200 cells were analyzed in each cell line and indicated as the average number of foci/cell. Asterisks indicate significant differences in relation to control cells lines or to untreated cells. Average values and standard deviations of two independent experiments are shown. Experiments were repeated 3 times with similar results. Figure provided by CiteAb. Source: PLoS One, PMID: 24987982.

Telomere-initiated senescent cells retain active DDR foci for years after senescence establishment.a. DDR, in the form of ATM pS1981 foci co-localizing with 53BP1 and γH2AX foci, is detectable three years after senescence establishment. Scale bar, 10 um. Below, bar graphs show the percentage of cells positive ± s.e.m. for the indicated DDR markers, in senescent (sen), early passage proliferating (prol) or telomerized proliferating (tel) skin fibroblasts from two independent centenarian donors (cen2 and cen3). Cells were considered positive if bearing more than 3 DDR foci (*** p-value <0.001). b. SA-β-gal staining of the two batches, cen2 and cen3, is shown together with the percentage of BrdU-positive cells. Scale bar, 100 um. Figure provided by CiteAb. Source: PLoS One, PMID: 25340529.

ATM is activated by spermidine in GM00637 cells.GM00637 cells with or without KU55933 pretreatment (a,b), and GM05849 cells (c) were exposed to 50？μM spermidine or CCCP, followed by immunofluorescence analyses of total and p-ATM on Ser-1981. The scale bar is 10？μm. Ratios of cells expressing p-ATM Ser-1981 to cells expressing total ATM were presented (d). 20？45 cells/condition from three experiments were collected. Values are mean？±？SD, *p？<？0.05 vs. control. Figure provided by CiteAb. Source: Sci Rep, PMID: 27089984.

Immunostaining of γH2AX, WT1 and 5mC in patients with IgA nephropathy and controls. Examples of PAS staining and immunostaining with γH2AX (green) and WT1 (red), pATM and 5mC in glomeruli of IgA nephropathy and controls. (A) A control kidney sample of 44-year-old female. Scale bars: 50 μm. Figure provided by CiteAb. Source: Sci Rep, PMID: 31937846.

Immunostaining of γH2AX, WT1 and 5mC in patients with IgA nephropathy and controls. Examples of PAS staining (1) and immunostaining with γH2AX (green) and WT1 (red) (2) , pATM (3) and 5mC (4) in glomeruli of IgA nephropathy and controls. (B) 65-year-old male of IgA nephropathy without podocytopathic features. Arrows indicate γH2AX and WT1 double-positive cells. Scale bars: 50 μm. Figure provided by CiteAb. Source: Sci Rep, PMID: 31937846.

Immunostaining of γH2AX, WT1 and 5mC in patients with IgA nephropathy and controls. Examples of PAS staining (1) and immunostaining with γH2AX (green) and WT1 (red) (2), pATM (3) and 5mC (4) in glomeruli of IgA nephropathy and controls. (C) 55-year-old male of IgA nephropathy with podocytopathic features. Arrows indicate γH2AX and WT1 double-positive cells. Scale bars: 50 μm. Figure provided by CiteAb. Source: Sci Rep, PMID: 31937846.

Generation of Asciz-deficient mice.(A) Schematic comparison of human and mouse ASCIZ. ZF, Zn2+ finger; NLS, nuclear localization signal. Lollipops indicate predicted ATM/ATR phosphorylation sites. (B) Asciz gene structure and targeting strategy, drawn approximately to scale. The four exons (A？D) are indicated by black boxes, as are locations of oligonucleotide primers, ScaI restriction sites and the probe for genotyping, and the positions of loxP sites. (C) Southern blot (top) and PCR genotyping (bottom) of a randomly chosen litter from a heterozygote intercross at weaning. (D) PCR genotyping of a randomly chosen litter at E15.5. (E) Western blot analysis of head extracts of a randomly chosen litter at E12.5 using the indicated antibodies. (F) Western blot analysis of the indicated tissues of an 8-week old male WT mouse, and E15.5 Asciz+/− and Asciz−/− head extracts as antibody specificity controls. Figure provided by CiteAb. Source: PLoS Genet, PMID: 20975950.

Flow Cytometry of Mouse anti-ATMpS1981 antibody. Cells: HEK293. Stimulation: none ？ top image, 0.1mg/ml Zeocin for 3 hr ？ bottom image. Primary antibody: anti-ATM pS1981 antibody at 5 ug/mL for 30 min at 4C. Secondary antibody: anti-mouse IgG FITC at 1ug/ml, 30min at 4C IN THE DARK.

Immunohistochemistry with anti-ATM Antibody. Tissue: Human Bladder Cancer. Fixation: FFPE buffered formalin 10% conc. Ag Retrieval: HIER citrate buffer pH6 (left) or HIER EDTA pH9 (Right). Primary antibody: anti-ATM at 2 ug/ml for 2 hr. Secondary Ab: anti-rabbit polymer HRP for 20min at RT.

Rockland Mouse Anti-ATM Protein Kinase pS1981 Antibody.