Cell death following DNA damage occurs from cells arrested in G1 or at the G1/S boundary. Cell death following DNA damage occurs from cells arrested in.

Slides:

Advertisements

Similar presentations

Figure S1 A MRC5 Control Chk1 TdR(h): γH2AX Cleaved casp3 RPA34

Advertisements

E2 GSCE2 bulkG7 GSCG7 bulk Mean SF4Gy (95% CI) 0.78 (0.72, 0.83) 0.56 (0.47, 0.64) 0.65 (0.57,0.72) 0.43 (0.34,0.51) T test of meansp = 0.001p =

Volume 314, Issue 1, Pages (January 2012)

Volume 14, Issue 2, Pages (August 2008)

Figure 5. FK866 caused apoptosis in MCF-7 cells while nicotinamide adenine dinucleotide (NAD+) reversed FK866-induced apoptosis. (A) Representative quadrant.

Kassardjian A, Rizkallah R, Riman S, Renfro SH, Alexander KE, et al

B) A) ** ** ** ** Cell count (h)

DNA content flow cytometric histograms of propidium iodide–stained A549 cells. DNA content flow cytometric histograms of propidium iodide–stained A549.

A stochastic feedback loop model predicts the kinetics of DDR and growth arrest at the single cell level. A stochastic feedback loop model predicts the.

A culture‐induced TE‐like subpopulation

Figure 1. Artemisinin derivatives inhibited EOC growth and arrested the cell cycle at the G2/M phase (A) SKOV3 and primary epithelial ovarian cancer (EOC)

Induction of apoptosis by CDIP expression.

DNA damage induces complex signal activation dynamics across many signaling pathways. DNA damage induces complex signal activation dynamics across many.

(a) (b) SUPPLEMENTARY FIGURE 1:

Aurora kinase inhibitory VX-680 increases Bax/Bcl-2 ratio and induces apoptosis in Aurora-A-high acute myeloid leukemia by Xue-Fei Huang, Shao-Kai Luo,

Drug-resistant T-lymphoid tumors undergo apoptosis selectively in response to an antimicrotubule agent, EM011 by Ritu Aneja, Jun Zhou, Surya N. Vangapandu,

Anthony J. Cesare, Makoto T. Hayashi, Laure Crabbe, Jan Karlseder

Log T = 0 T = 2.5 T = 5 T = 7.5 T = 10 T = 12.5 T = 15 T = 17.5 T = 20

TNF enhances dose‐dependent cell death following doxorubicin‐induced DNA damage with minimal affect on dose‐dependent cell‐cycle arrest. TNF enhances dose‐dependent.

Intracellular noise in the cAMP circuit drives observed population behaviors Firing rate phase diagrams for single cells in a population (top) and the.

Characterization of promoters relative to pAGA1

Valentina Manfé, Edyta Biskup, Peter Johansen, Maria R

SUPPLEMENTAL TABLE 1. Cell cycle profiles of HeLa cells treated

A p53-Dependent Checkpoint Pathway Prevents Rereplication

Volume 13, Issue 8, Pages (November 2015)

The Mammalian UV Response

Volume 21, Issue 6, Pages (June 2012)

Consequences of reducing SF3B2 expression.

Lag time to division depends on the frequency of pulsed glucose for a subpopulation Lag time to division depends on the frequency of pulsed glucose for.

Changes to the growth conditions break the circuit by changing host gene expression Changes to the growth conditions break the circuit by changing host.

Prediction of novel cell cycle inhibitors based on CODIM1.

Volume 9, Issue 2, Pages (October 2014)

The cell cycle influences circadian phase progression Circadian intervals with divisions (p1,d1,p2) last 21.95 ± 3.8 h (n = 1,926) and are significantly.

Chemical inhibitors of microtubule function attenuate signal but do not affect pathway variability Chemical inhibitors of microtubule function attenuate.

The Tumor Suppressor MIG6 Controls Mitotic Progression and the G2/M DNA Damage Checkpoint by Stabilizing the WEE1 Kinase Mari Sasaki, Takeshi Terabayashi,

A Genetic Screen Identifies TCF3/E2A and TRIAP1 as Pathway-Specific Regulators of the Cellular Response to p53 Activation Zdenek Andrysik, Jihye Kim,

Safety profile of reversibly immortalised human mesoangioblasts

José Antonio Tercero, Maria Pia Longhese, John F.X Diffley

Volume 15, Issue 6, Pages (September 2004)

Arsenic Induces Tumor Necrosis Factor α Release and Tumor Necrosis Factor Receptor 1 Signaling in T Helper Cell Apoptosis Hsin-Su Yu, Gwo-Shing Chen

An integrated NHR network.

Feedback loop signalling is necessary and sufficient to maintain proliferation arrest during establishment of irreversible cell senescence. Feedback loop.

Differential stress sensitivity of the dividing versus non‐dividing cells. Differential stress sensitivity of the dividing versus non‐dividing cells. (A)

Distinct collagen structures in the upper and lower neonatal dermis (related to Fig 1)‏ Distinct collagen structures in the upper and lower neonatal dermis.

New Histone Incorporation Marks Sites of UV Repair in Human Cells

Characterising dermis expansion and gene expression changes during mouse development (related to Fig 1)‏ Characterising dermis expansion and gene expression.

Palbociclib increases proteasome activity and the clearance of protein aggregates without significant effects on autophagy Palbociclib increases proteasome.

Time‐course analysis of NICD degradation.

Volume 41, Issue 5, Pages (November 2004)

Volume 18, Issue 12, Pages (December 2010)

Glucose pulses incorporate directly into the de novo biomass in non‐dividing cells Glucose pulses incorporate directly into the de novo biomass in non‐dividing.

Microenvironment‐dependent differentiation and morphology.

Silvia Selleri, Holger Seltmann, Silvia Gariboldi, Yuri F

Volume 16, Issue 19, Pages (October 2006)

SEMA3C regulates prostate cancer cell growth

MK-8628 augments T lymphocyte apoptosis.

Association of NM-HA and NM-GFP with SGs is transient.

CYP1A1 knockdown increases cell death.

Figure 1. Effects of Gal-4 on apoptosis and proliferation of monocytes

Volume 14, Issue 2, Pages (August 2008)

Combined experimental and computational analysis of DNA damage signaling reveals context‐dependent roles for Erk in apoptosis and G1/S arrest after genotoxic.

Regulation of a transcription factor network by Cdk1 coordinates late cell cycle gene expression A, B Cells expressing differentially tagged WT TFs (TOS4‐3FLAG.

Effects of PS-341 on apoptosis in orthotopic human pancreatic tumors.

Effects of knockdown of ANRIL on NSCLC cell cycle and apoptosis in vitro. Effects of knockdown of ANRIL on NSCLC cell cycle and apoptosis in vitro. A,

Combined experimental and computational analysis of DNA damage signaling reveals context‐dependent roles for Erk in apoptosis and G1/S arrest after genotoxic.

Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. A.

A, P causes G2-M arrest with apoptosis in asynchronous population of PC-3 when exposed to 1.5 and 5 μmol/L P for various time points. A, P

SY-1425 induces maturation in RARA-high AML

RA-9 induces G2–M cell-cycle arrest and caspase-mediated apoptosis in ovarian cancer cells. RA-9 induces G2–M cell-cycle arrest and caspase-mediated apoptosis.

Yun-Gui Yang, Tomas Lindahl, Deborah E. Barnes Cell

Presentation transcript:

Cell death following DNA damage occurs from cells arrested in G1 or at the G1/S boundary. Cell death following DNA damage occurs from cells arrested in G1 or at the G1/S boundary. (A) Representative flow cytometry profiles showing DNA content for cells exposed to 0 (black) or 2 μM (gray) doxorubicin, at time points between 3 and 42 h following treatment. Treatment with low‐dose doxorubicin (gray traces) results in an accumulation in the G1 population (2 N DNA content) as compared with untreated cells (black traces) by as early as 3 h following treatment. This accumulation persists through at least 15 h. By 24 h following treatment, the accumulation in G1 is completely abrogated and an accumulation in the S‐phase population is apparent, suggesting synchronous release into S‐phase. (B) Representative scatter plots showing DNA content and cleaved caspase‐3 in cells treated with 2 μM Dox (left) or 2 μM Dox+TNFα (right) at 24 h following treatment. The majority of cells staining positively for cleaved caspase‐3 have 2 N DNA content (red box), consistent with apoptosis in G1 or at the G1/S boundary. (C) Cells were synchronized in late G1 and at the G1/S boundary via a double thymidine block and released directly into aphidicolin‐containing media to block progression through S‐phase. Cells were treated with or without 2 μM Dox 1 h later and analyzed 8 h later for apoptosis by flow cytometry (top). The percentage of cells staining positively for both apoptotic markers is indicated from two biological replicates in each of two independent experiments (bottom). (D) Cells treated with either 0 or 2 μM Dox were pulsed with BrdU for 4 h beginning 15 h following treatment. At 48 h following treatment, cells were analyzed by flow cytometry for DNA content and BrdU incorporation (top). Overlays of the cell cycle/BrdU distributions from cells treated with either 0 (black) or 2 μM (gray) Dox reveal an accumulation of BrdU‐positive cells with 4 N DNA content in populations treated with 2 μM doxorubicin, indicating that the population of cells synchronously released from a G1 or G1/S arrest into S between 12 and 24 h following treatment is the same population that accumulates in G2/M by 48 h following treatment. No BrdU‐positive cells re‐entered the G1 population by 48 h after 2 μM Dox, consistent with a persistent G2/M arrest. Left and right panels are identical, with the Dox‐treated cells shown either behind (left) or in front of (right) the untreated controls. (E) Cells treated with 0 or 2 μM Dox as in (D) were collected at 48 h following treatment and analyzed for DNA content and the mitotic marker, pHH3. Mitotic cells are boxed, indicating stable G2 arrest after doxorubicin treatment. (F) A model for the early G1/S decision point. Source data is available for this figure in the Supplementary Information. Andrea R Tentner et al. Mol Syst Biol 2012;8:568 © as stated in the article, figure or figure legend