Separation-of-function mutations in ATM dictate responses to DNA damage and oxidative stress. Separation-of-function mutations in ATM dictate responses.

Slides:



Advertisements
Similar presentations
Increased levels of ATRi-induced replication stress in AMLMLL cells.
Advertisements

Volume 11, Issue 2, Pages (April 2015)
Volume 65, Issue 1, Pages (January 2017)
IFN-γ antagonizes TGF-β in vivo.
Cytotoxicity of MSP samples to normal and cancer cell lines.
TPAD controller performance for three force components.
FIP200 maintains microRNA1198-5p expression via Ago2 in naïve T cells.
Three different types of transfer functions with a codomain of [0,1].
TPAD training protocol.
CCR2+ monocytes are a relevant source of type I IFN in response to Af.
Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. (A)
Memory CD8+ T cells that become terminally differentiated by multiple antigen encounters lose core 2 O-glycan synthesis activity. Memory CD8+ T cells that.
Comparative analysis of the nuclear F-actin networks in A3
Protein sequence alignment of the NS3 helicase–encoding region of 63 flaviviruses demonstrates conservation of a KIR2DS2-binding peptide. Protein sequence.
Ex vivo testing of the soft robotic devices.
Human PBMC-derived MERS-CoV–specific T cells are multifunctional.
Group data during free walking between sessions 1 and 16.
Virus-specific T cell responses are detected in all MERS survivors.
Volume 54, Issue 6, Pages (June 2014)
Platelets are required for hFcγRIIA-induced anaphylaxis.
Comparison of repertoire distributions to baseline.
Enhanced expression of TLR7 protein in PBMCs from women.
Characterization of the light-responsive transdermal MNs.
Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells. Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells.
SYCE2 potentiates the steady-state DNA repair activity without affecting the cell cycle checkpoint. SYCE2 potentiates the steady-state DNA repair activity.
Protein sequence alignment of the NS3 helicase–encoding region of 63 flaviviruses demonstrates conservation of a KIR2DS2-binding peptide. Protein sequence.
IFN-γ antagonizes TGF-β in vivo.
Neutrophil depletion ameliorates colitis in Cx3cr1cre:Il10rafl/fl BM chimeras. Neutrophil depletion ameliorates colitis in Cx3cr1cre:Il10rafl/fl BM chimeras.
Immune cell recruitment after the NIR-boosted and MN-mediated cancer immunotherapy. Immune cell recruitment after the NIR-boosted and MN-mediated cancer.
Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. (A)
AMPK-mediated mTORC2 signaling does not require mTOR Ser1261phosphorylation. AMPK-mediated mTORC2 signaling does not require mTOR Ser1261phosphorylation.
AMPK directly increases mTORC2 catalytic activity.
FIP200 maintains microRNA1198-5p expression via Ago2 in naïve T cells.
Antitumor effect of local cancer immunotherapy treatment in various tumor models. Antitumor effect of local cancer immunotherapy treatment in various tumor.
Fig. 2 AcPGP induces IL-8 and G-CSF release from human bronchial epithelial cells. AcPGP induces IL-8 and G-CSF release from human bronchial epithelial.
Cell viability tests. Cell viability tests. SEM images of (A) MC3T3-E1 cells and (B) MSCs on days 1, 3, and 5 of culture. (C) Survival rates of MC3T3-E1.
Fig. 1 TET2 is a coactivator of ERα.
Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. (A)
Fig. 3 E2F1 interacts with components of the splicing machinery.
Fig. 3. BET inhibition reduces homologous recombination.
Immune evasion occurs through loss of TNF, IFN-γ, or antigen presentation pathways. Immune evasion occurs through loss of TNF, IFN-γ, or antigen presentation.
Fig. 1 meR marks on E2F1 confer genome-wide effects.
Global analysis of RV[S/T]F motif phosphorylation during mitosis.
Inhibition of CDK9 by UNC drives MYC loss.
MYC degradation screen identifies a compound that stabilizes MYC protein. MYC degradation screen identifies a compound that stabilizes MYC protein. (A)
Ado loss drives TNF-dependent immune evasion.
Fig. 3 BMS blocks functional responses in primary immune cells driven by IL-23 and IL-12. BMS blocks functional responses in primary immune.
Fig. 7 BMS reduces the elevated expression of type I IFN–regulated genes both ex vivo in blood from patients with lupus and in a phase 1 study of.
BMS blocks functional responses in primary immune cells driven by IFNα
Fig. 4 HRI regulates BCL11A levels.
Fig. 2 HRI depletion elevates γ-globin in HUDEP2 cells.
by Emilie Clement, Hiroyuki Inuzuka, Naoe T
Sensitivity analysis of cellular responses to perturbation of the DNA damage response signaling in the presence of chemotherapies. Sensitivity analysis.
Type I and III IFNR expression on hematopoietic cells is required for protection against IA. Type I and III IFNR expression on hematopoietic cells is required.
Fig. 3 Proteomic analysis and Western blot analysis of protein cargos of various EVs. Proteomic analysis and Western blot analysis of protein cargos of.
Fig. 5 Simultaneous absence of caspase-3 and -7 is required for significant decrease of caspase-8 and -9 activation in intrinsic apoptosis. Simultaneous.
AEGIS autonomous targeting process.
H19 was essential for cancer metastasis.
Fig. 6 Multivalent DNA vaccine and protein antigen delivery by T4-AAV nanoparticles. Multivalent DNA vaccine and protein antigen delivery by T4-AAV nanoparticles.
Fig. 2 Viperin promotes methionine oxidation of KSHV helicase.
SIRT7-mediated ATM deacetylation is essential for its deactivation and DNA damage repair by Ming Tang, Zhiming Li, Chaohua Zhang, Xiaopeng Lu, Bo Tu, Ziyang.
UNC drives MYC protein loss.
Human basophils are unresponsive to contact-dependent or contact-independent inhibition by Tregs. Human basophils are unresponsive to contact-dependent.
Wip1 Phosphatase Modulates ATM-Dependent Signaling Pathways
Fig. 3 Effects of ASO and eGLP1-ASO conjugates on gene expression and protein levels in vitro in cell lines and primary mouse islet cells. Effects of ASO.
NE cleaves and activates GSDMD.
Afatinib rapidly destabilizes endogenous TRIB2 and specifically induces caspase 3 cleavage and U937 cytotoxicity. Afatinib rapidly destabilizes endogenous.
Fig. 3 TBK1 phosphorylates RAB7AS72 but not the equivalent residue in other RABs in vitro. TBK1 phosphorylates RAB7AS72 but not the equivalent residue.
Fig. 1 Cellular PFAS negatively regulates RTA-dependent transcriptional activation. Cellular PFAS negatively regulates RTA-dependent transcriptional activation.
CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis. CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis.
Presentation transcript:

Separation-of-function mutations in ATM dictate responses to DNA damage and oxidative stress. Separation-of-function mutations in ATM dictate responses to DNA damage and oxidative stress. Human U2OS osteosarcoma cells were depleted for endogenous ATM using short hairpin RNA (shRNA) and induced to express various ATM alleles as indicated. (A) Cells were induced for ATM expression with doxycycline (10 ng/ml) and exposed to camptothecin (CPT) (10 μM) for 1 hour. ATM activity was examined using antibodies directed against phospho-Kap1 Ser824, and ATM levels were assessed with anti-ATM antibody. (B) U2OS cells were treated as in (A) except that expression was induced with doxycycline (1 μg/ml). ATM activity was assessed with antibodies directed against ATM, phospho-ATM Ser1981, Kap1, phospho-Kap1 Ser824, Chk2, and phospho-Chk2 Thr68 as indicated. (C) U2OS cells expressing shRNA against ATM (shATM) and either vector (CTRL) or various ATM alleles as in (B) were treated with 10 μM CPT for 1 hour, and the levels of phosphorylated Kap1 were determined, in comparison to total Kap1 protein, and normalized with the phosphorylated signal from WT ATM–expressing cells. NS, not significant. (D) U2OS cells were depleted of endogenous ATM and induced for recombinant ATM expression as in (B) but were exposed to IR (10 Gy) followed by 1-hour recovery. Phosphorylation was assessed as in (B). (E) U2OS cells were treated as in (B) but exposed to 100 μM H2O2 or arsenite for 1 hour in the presence of doxycycline (1 μg/ml). Phosphorylation was assessed as in (B). (F) U2OS cells expressing various ATM alleles as in (B) were treated with 100 μM H2O2 for 1 hour in serum-free medium, and the amount of phosphorylated Chk2 was quantitated in comparison to total Chk2 protein and normalized with the phosphorylated signal from WT ATM–expressing cells. Data are means ± SD of three independent experiments. *P < 0.05 and **P < 0.005. Ji-Hoon Lee et al., Sci. Signal. 2018;11:eaan5598 Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works