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Findings reveal a novel role for ATR in cilia signaling distinct from its canonical function during replication and strengthen emerging links between cilia function and development.
REV3/ATR knockdown enhances the cytotoxicity of cisplatin in non-small cell lung cells.
ATR (show ANTXR1 ELISA Kits) promotes homologous recombination after CDK (show CDK4 ELISA Kits)-driven DNA end resection.
Authors examine how the replication stress response that is controlled by the kinase ataxia telangiectasia and Rad3-related (ATR) senses and resolves threats to DNA integrity so that the DNA remains available to read in all of our cells. They discuss the multiple data that have revealed an elegant yet increasingly complex mechanism of ATR activation. [Review]
results reveal a previously unknown role for transcription factor IIH in ATR kinase activation in non-replicating, non-cycling cells
Our data reveal that BETi can potentiate the cell stress and death caused by ATR inhibitors. This suggests that ATRi can be used in combination therapies of lymphomas without the use of genotoxic drugs
Ultraviolet rays-induced ATR (show ANTXR1 ELISA Kits) and ATM (show ATM ELISA Kits) recruitment and activation differ in G1 and S phases due to the existence of distinct types of DNA lesions, which promote assembly of different proteins involved in the process of DNA repair and checkpoint activation.
Small molecule ATR (show ANTXR1 ELISA Kits) and Chk1 (show CHEK1 ELISA Kits) inhibitors potently sensitize lymphoma cells to UVA radiation and induce a prominent apoptotic response
ATR (show ANTXR1 ELISA Kits) inhibition potentiated Chk1 (show CHEK1 ELISA Kits) inhibitor induced replication stress and cytotoxicity via the abrogation of ATR (show ANTXR1 ELISA Kits)-dependent feedback activation of Chk1 (show CHEK1 ELISA Kits) induced by Chk1 (show CHEK1 ELISA Kits) inhibitor generated replication stress in tumor cell lines.
Our data suggests that total cellular b-catenin levels decrease in the presence of secreted frizzled-related protein 1 (show SFRP1 ELISA Kits) and Wnt inhibitory factor 1 (show WIF1 ELISA Kits), and a significant increase in cell death after tyrosine kinase (show TXK ELISA Kits) inhibitor treatment is observed. On the contrary, when secreted frizzled-related protein 1 (show SFRP1 ELISA Kits) is suppressed, total b-catenin levels increase in the cell and the cells become resistant to tyrosine kinase (show TXK ELISA Kits) inhibitors.
HPV31 regulates RRM2 (show RRM2 ELISA Kits) levels through expression of E7 and activation of the ATR (show ANTXR1 ELISA Kits)-Chk1 (show CHEK1 ELISA Kits)-E2F1 (show E2F1 ELISA Kits) DNA damage response, which is essential to combat replication stress upon entry into S-phase.
The authors show, in live cells, that Ddx19 (show DDX19B ELISA Kits) transiently relocalizes from the nucleopore to the nucleus upon DNA damage, in an ATR/Chk1 (show CHEK1 ELISA Kits)-dependent manner, and that Ddx19 (show DDX19B ELISA Kits) nuclear relocalization is required to clear R-loops (DNA:RNA hybrids).
ATR-Chk1 DDR pathway appears to be dispensable for the preferential association of REV1 to MMC-damaged chromatin.
APE2 (show APEX2 ELISA Kits) associates with Chk1 (show CHEK1 ELISA Kits); a serine residue (S86) in the Chk1 (show CHEK1 ELISA Kits)-binding motif of APE2 (show APEX2 ELISA Kits) is essential for Chk1 (show CHEK1 ELISA Kits) phosphorylation, indicating a Claspin (show CLSPN ELISA Kits)-like but distinct role for APE2 (show APEX2 ELISA Kits) in ATR-Chk1 (show CHEK1 ELISA Kits) signaling.
MRN (MRE11 (show MRE11A ELISA Kits)-RAD50 (show RAD50 ELISA Kits)-NBS1 (show NLRP2 ELISA Kits)) complex has role in ATR activation via TOPBP1 (show TOPBP1 ELISA Kits) recruitment.
ATM (show ATM ELISA Kits) activity is required for an early step in resection, leading to ATR activation, CtIP (show RBBP8 ELISA Kits)-T818 phosphorylation, and accumulation of CtIP (show RBBP8 ELISA Kits) on chromatin.
ATM (show ATM ELISA Kits) and ATR prevent accumulation of chromosomal abnormalities by promoting Mre11 (show MRE11A ELISA Kits)/Rad50 (show RAD50 ELISA Kits)/Nbs1 (show NLRP2 ELISA Kits) dependent recovery of collapsed replication forks.
Human CDC6 physically interacts with ATR, a crucial checkpoint kinase, in a manner that is stimulated by phosphorylation by Cdk and the CDC6-ATR interaction is conserved in Xenopus.
ATM (show ATM ELISA Kits) and ATR phosphorylate the functionally critical replication protein Mcm2 (show MCM2 ELISA Kits) during both DNA damage and replication checkpoint responses in Xenopus egg extracts
ATRIP (show ATRIP ELISA Kits) must associate with ATR in order for ATR to carry out the phosphorylation of Chk1 (show CHEK1 ELISA Kits) effectively
PP2A counteracts ATM and ATR in a DNA damage checkpoint in Xenopus egg extracts
DNA damage induces a kinetochore-based ATM/ATR-independent spindle assembly checkpoint arrest.
work reveals that simulated microgravity promotes the apoptotic response through a combined modulation of the Uev1A/TICAM/TRAF (show TRAF1 ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits)-regulated apoptosis and the p53 (show TP53 ELISA Kits)/PCNA (show PCNA ELISA Kits)- and ATM (show ATM ELISA Kits)/ATR-Chk1 (show CHEK1 ELISA Kits)/2-controlled DNA-damage response pathways.
Atr deletion in cerebellar granule neuron progenitors (CGNPs) induced proliferation-associated DNA damage, p53 activation, apoptosis and cerebellar hypoplasia in mice. Genetic deletion of Atr blocked tumorigenesis in medulloblastoma-prone SmoM2 mice.
ATR controls DNA damage-induced G2 checkpoint control and apoptosis in proliferating neurons.
CDC25A-deficient embryonic stem cells resist high doses of ATR inhibitors, which we show is due to their failure to prematurely enter mitosis in response to the drugs.
These results therefore suggest that whereas DNA polymerase stalling at DNA lesions activates ATR to protect cell viability and prevent apoptosis, the stalling of RNA polymerases instead activates ATR to induce an apoptotic form of cell death in non-cycling cells.
RAD9 (show RAD9A ELISA Kits) has a prominent role in the ATR-Chk1 (show CHEK1 ELISA Kits) pathway that is necessary for successful formation of the damage-sensing complex and DNA damage checkpoint signaling.
telomeres are protected from hyper-resection through the repression of the ATM (show ATM ELISA Kits) and ATR kinases by TRF2 (show TERF2 ELISA Kits) and TPP1 (show TPP1 ELISA Kits)-bound POT1a (show POT1 ELISA Kits)/b, respectively.
DNA double-strand breaks by Cr(VI) are targeted to euchromatin and cause ATR-dependent phosphorylation of histone H2AX and its ubiquitination.
ATR suppresses endogenous DNA damage and allows completion of homologous recombination repair
ATR function together with SOG1 and ALT2 (show GPT2 ELISA Kits) to halt root growth and promote terminal differentiation in response to chronic Aluminum exposure.
Data suggest that an RNA G-quadruplex of the G(3)L(1-7) class resides in the 5prime-untranslated region of ATR mRNA and appears to function in down-regulation of mRNA translation.
ATR and MKP1 play distinct roles in response to UV-B stress.MKP1-regulated and ATR-mediated DNA damage pathways operate independently of each other.
findings indicate that ATR and CST (CTC1/STN1/TEN1) act synergistically to maintain genome integrity and telomere length homeostasis
TANMEI/ALT2 works in conjunction with ATR to detect Al-dependent DNA damage and actively halt root growth to allow for repair of this damage.
Short telomeres in tert mutant plants activate both ATM and ATR. Absence of telomerase elicits and ATM and ATR-dependent DNA damage response at telomeres.
cooperation among DNA translesion synthesis (TLS (show FUS ELISA Kits)) polymerases (Poleta, Polzeta) and DNA-damage-activated protein kinases (ATR, ATM (show ATM ELISA Kits))
Data show that the ATM-SOG1 and ATR-SOG1 pathways both transmit DSB-derived signals and that either one suffices for endocycle induction.
The MRN complex is essential for activation of the ATM and ATR kinases in response to irradiation.
Both ATM and ATR contribute to the induction of a CYCB1;1:GUS fusion by IR, but only ATR is required for the persistence of this response. [ATR]
The protein encoded by this gene belongs the PI3/PI4-kinase family, and is most closely related to ATM, a protein kinase encoded by the gene mutated in ataxia telangiectasia. This protein and ATM share similarity with Schizosaccharomyces pombe rad3, a cell cycle checkpoint gene required for cell cycle arrest and DNA damage repair in response to DNA damage. This kinase has been shown to phosphorylate checkpoint kinase CHK1, checkpoint proteins RAD17, and RAD9, as well as tumor suppressor protein BRCA1. Mutations of this gene are associated with Seckel syndrome. An alternatively spliced transcript variant of this gene has been reported, however, its full length nature is not known. Transcript variants utilizing alternative polyA sites exist.
ataxia telangiectasia and Rad3 related
, ataxia telangiectasia and Rad3 related protein
, serine/threonine-protein kinase ATR-like
, FRAP-related protein 1
, FRAP-related protein-1
, MEC1, mitosis entry checkpoint 1, homolog
, Rad3 related protein
, ataxia telangiectasia and Rad3-related protein
, protein kinase ATR
, serine/threonine-protein kinase ATR
, checkpoint kinase
, protein kinase
, serine/threonine-protein kinase atr