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Image Search Results
Journal: Breast Cancer Research and Treatment
Article Title: Targeting ataxia telangiectasia-mutated- and Rad3-related kinase (ATR) in PTEN-deficient breast cancers for personalized therapy
doi: 10.1007/s10549-018-4683-4
Figure Lengend Snippet: Association between PTEN, ATR and pChk1expression in breast cancers
Article Snippet: A further set of slides were incubated for 60 min with the primary
Techniques:
Journal: Breast Cancer Research and Treatment
Article Title: Targeting ataxia telangiectasia-mutated- and Rad3-related kinase (ATR) in PTEN-deficient breast cancers for personalized therapy
doi: 10.1007/s10549-018-4683-4
Figure Lengend Snippet: a Nuclear and cytoplasmic staining of PTEN [a negative staining for both, b negative staining for nuclei and weak for cytoplasm, c some weak staining for nuclei and moderate for cytoplasm d strong staining for both; TMA cores pictures were taken using digital pathology interference at ×100 (left) and ×200 (right)]. Kaplan–Meier plot showing breast cancer-specific survival (BCSS) and b nuclear PTEN level. c combined nuclear PTEN and ATR level. d combined nuclear PTEN and cytoplasmic pCHK1 level. e combined ATR and cytoplasmic pCHK1 level nuclear PTEN negative tumours
Article Snippet: A further set of slides were incubated for 60 min with the primary
Techniques: Staining, Negative Staining
Journal: Journal of Virology
Article Title: The Papillomavirus E1 Helicase Activates a Cellular DNA Damage Response in Viral Replication Foci
doi: 10.1128/jvi.00541-11
Figure Lengend Snippet: FIG. 2. HPV16 E1 activates the pChk1, pChk2, and H2AX proteins. CV-1 cells were transfected with an HPV16 E1 expression plasmid or empty vectors (pMEP9) on coverslips. Cells were stained and with chicken anti-EE (-E1) (in green) and antibodies to various DNA damage response (DDR) proteins, pChk1 (Ser345), pChk2 (Thr68), and histone H2AX (Ser139) (in red).
Article Snippet: The following antibodies and dilutions were used for immunofluorescence: chicken anti-EE (Bethyl Laboratories, Inc., A190-109A; 1:100), M2 mouse and rabbit anti-Flag (Sigma F3165 and F7425; 1:500 and 1:200, respectively), rabbit antiphosphorylated Thr68 Chk2 (Cell Signaling 2661; 1:100), mouse anti-phosphor- on N ovem ber 18, 2012 by U N IV E R S IT Y O F A R IZ O N A LIB R A R Y http://jvi.asm .org/ D ow nloaded from ylated Ser1981 ATM (Abcam ab81292; 1:100), mouse anti-phosphorylated Ser15 p53 (Cell Signaling 9286; 1:100), rabbit anti-phosphorylated Ser139 H2AX (Cell Signaling 2577; 1:100),
Techniques: Transfection, Expressing, Plasmid Preparation, Staining
Journal: Molecular and Cellular Biology
Article Title: Loss of the Epigenetic Tumor Suppressor SNF5 Leads to Cancer without Genomic Instability
doi: 10.1128/mcb.00658-08
Figure Lengend Snippet: FIG. 4. The G2 checkpoint is intact in Snf5-deficient cells. (A) DNA damage signaling is appropriately initiated in Snf5-deficient cells. WT and Snf5-deficient cells were immunoblotted for ATM (serine 1981), p53 (serine 18), phosphorylated Chk1 (pChk1) (serine 317), p21, and Snf5 expression in the absence () or presence () of 2.5 Gy IR. Snf5Fl/Fl, Snf5Flox/Flox. (B and C) The mitotic index of Snf5-deficient cells appropriately decreases following DNA damage and recovers by 6 h. The percentage of pH3-positive cells for unirradiated (IR) or irradiated (IR) WT or Snf5-deficient cells was quantified by fluorescence-activated cell sorting and is noted in each panel. Data represented in panel C are presented as means for at least three independent experiments standard errors.
Article Snippet: Antibodies included anti-SNF5/BAF47 (BD Biosciences and Bethyl Laboratories); anti-Brg1, -p21, -c-jun, and -histone H1 (Santa Cruz Biotechnology);
Techniques: Expressing, Irradiation, FACS