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Polyclonal ATR Primary Antibody for IHC (p) - ABIN4948298
Zhou, Lu, Wulf, Lu: Phosphorylation-dependent prolyl isomerization: a novel signaling regulatory mechanism. in Cellular and molecular life sciences : CMLS 2001
Show all 3 Pubmed References
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.
Here, the authors show that ARP8, a subunit of the INO80 chromatin remodeling complex, is phosphorylated after etoposide treatment. The etoposide-induced phosphorylation of ARP8 is regulated by ATM and ATR, and attenuates its interaction with INO80.
ATR inhibition may be beneficial for cancer patients with reduced levels of RNASEH2.
iPSC model revealed a novel effect of the ATR mutation in mitotic processes of NPCs and NPC-specific missplicing, accompanied by the recovery of neuronal defects using a splicing rectifier.
The ATR-Chk1 and ATM-Chk2 signalings in male breast cancer (MBC).
ATR signalling adversely impact survival in PTEN-deficient breast cancers. ATR inhibition is synthetically lethal in PTEN-deficient triple-negative breast cancer (TNBC) cells
Studies indicate mechanism for translocation of Tuberous Sclerosis Complex (TSC complex) protein to lysosomes in response to DNA damage, which depends on ATM and Rad3-related protein (ATR)/checkpoint kinase 1 (Chk1)-mediated rhoB GTP-binding protein (RhoB) phosphorylation and sumoylation.
ATR inhibition synergizes with WEE1 inhibition in TNBC.
Identification of novel ATR mutations in oropharyngeal squamous cell carcinoma patients who do not have Seckel syndrome and are HPV negative suggesting that functional loss of ATR may be an important step in the aetiology of oropharyngeal cancer.
ATR couples DNA replication with mitosis and preserves genome integrity by enforcing an S/G2 checkpoint.
Findings indicate that nuclear phosphoinositide lipids (PPIs) metabolism mediates an early damage response to specifically recruit ataxia telangiectasia and Rad3-related protein (ATR).
Inhibition of FPR1 and/or NADPH oxidase functions prevents VEGFR2 transactivation and the triggering of the downstream signalling cascades.
the sequence of administration of an ATR kinase inhibitor and a DNA damaging agent impacts the DNA damage induced by the combination. experiments identify competing ATR and Cdc7 kinase-dependent mechanisms at replication origins in human cells.
The observations suggest a novel role of ATR kinase in mediating its own signal attenuation via PPM1D recruitment to chromatin as an essential mechanism for restarting the stalled forks, cell cycle re-entry and cellular recovery from replication stress.
DNA alkylation damage leads to ATR-Chk1 activation in cancer cells and ATR-Chk1 activation mitigates replication stress caused by mismatch repair-dependent processing of DNA damage.
The ATR kinase inhibitor VX-970 (NSC 780162) is in clinical development in combination with primary cytotoxic agents.
The mRNA levels of ATR and ATM and the expression of ATR and ATM protein in NPC tissues were significantly higher than those in adjacent normal tissues. The colony formation assay showed that the colony-forming rate decreased, showing radiation dose-dependent and CGK-733 concentration-dependent manners.
a mitosis-specific and R loop-driven ATR pathway acts at centromeres to promote faithful chromosome segregation, revealing functions of R loops and ATR in suppressing chromosome instability.
both ATR and Chk1 kinase activities are important for viral replication. The findings suggest that HSV-1 activates ATR and Chk1 during early stages of infection and utilizes the enzymes to promote its own replication. The observation may be exploitable for antiviral approaches.
Following DNA damage, addition of the TLK1 inhibitor, THD, or overexpression of NEK1-T141A mutant impaired ATR and Chk1 activation, indicating the existence of a TLK1>NEK1>ATR>Chk1 pathway. Indeed, overexpression of the NEK1-T141A mutant resulted in an altered cell cycle response after exposure of cells to oxidative stress, including bypass of G1 arrest and implementation of an intra S-phase checkpoint.
These findings suggest that inhibition of ATR is a promising strategy to enhance the antitumor activity of GEM for treating pancreatic cancer
The authors show, in live cells, that Ddx19 transiently relocalizes from the nucleopore to the nucleus upon DNA damage, in an ATR/Chk1-dependent manner, and that Ddx19 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 associates with Chk1; a serine residue (S86) in the Chk1-binding motif of APE2 is essential for Chk1 phosphorylation, indicating a Claspin-like but distinct role for APE2 in ATR-Chk1 signaling.
MRN (MRE11-RAD50-NBS1) complex has role in ATR activation via TOPBP1 recruitment.
ATM activity is required for an early step in resection, leading to ATR activation, CtIP-T818 phosphorylation, and accumulation of CtIP on chromatin.
ATM and ATR prevent accumulation of chromosomal abnormalities by promoting Mre11/Rad50/Nbs1 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 and ATR phosphorylate the functionally critical replication protein Mcm2 during both DNA damage and replication checkpoint responses in Xenopus egg extracts
ATRIP must associate with ATR in order for ATR to carry out the phosphorylation of Chk1 effectively
PP2A counteracts ATM and ATR in a DNA damage checkpoint in Xenopus egg extracts
Data show that recombinant TopBP1 induces a large increase in the kinase activity of both Xenopus and human ATR-ATRIP.
Cut5 plays a crucial role in the initial amplification step of the ATR-Chk1 signaling pathway at the stalled replication fork.
Data show that ATM (ataxia-telangiectasia mutated) regulates Xenopus TopBP1 by phosphorylating serine 1131 and thereby strongly enhancing association of TopBP1 with ATR(ATM and Rad3-related).
interaction of the 9-1-1 complex (Rad9-Hus1-Rad1) with the BRCT I-II region of TopBP1 is necessary for binding of ATR-ATRIP to the ATR-activating domain of TopBP1 and the ensuing activation of ATR
ATM and ATR control mitotic events in vertebrate cells by targeting CEP63 and centrosome dependent spindle assembly.
The Fanconi anemia protein FANCM is controlled by FANCD2 and the ATR/ATM pathways.
An absence of 53BP1 leads to defective ATR-Chk1-p53 signaling.
nearly identical POT1b subunit of shelterin has been shown to be much less proficient than POT1a in repression of ATR
The results reveal mechanistic differences between ATR inhibition and ATR loss, with implications for ATR signaling and cancer therapy.
Date indicate tthat ataxia telangiectasia and rad3 related protein (ATR) as a critical regulator of meiosis.
Data show that ataxia telangiectasia and rad3 related protein (ATR) plays multiple roles in mammalian meiotic recombination.
These data suggest that ATM and ATR are part of the cellular "infrastructure" that maintains the excitatory/inhibitory balance of the nervous system.
ATR mutant tumors exhibit both the accumulation of multiple mutations and the altered expression of inflammatory genes, resulting in decreased T cell recruitment and increased recruitment of macrophages known to spur tumor invasion.
Results from our analysis showed that Pak1 overexpression, knockdown and Pak1 knockout cell line models showed that Pak1 confers protection to keratinocytes from UV-B-induced apoptosis and DNA damage via ATR
Collectively, these data indicated that ATR or ATM inhibition represent potential therapeutic strategies for the treatment of AML, especially MLL-driven leukemias.
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/NF-kappaB-regulated apoptosis and the p53/PCNA- and ATM/ATR-Chk1/2-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 has a prominent role in the ATR-Chk1 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 and ATR kinases by TRF2 and TPP1-bound POT1a/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
Observations suggest that ATR mediates a mechanical response to membrane stress that could be caused by chromatin dynamics and is important for genome integrity.
Mutant ATR and ATM seeds are highly resistant to aging, establishing ATM and ATR as determinants of seed viability.
ATR function together with SOG1 and ALT2 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) polymerases (Poleta, Polzeta) and DNA-damage-activated protein kinases (ATR, ATM)
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]
ATM and ATR act redundantly to inhibit sustained interactions between non-homologous chromatids.
Aluminum-dependent root-growth inhibition primarily arises from DNA damage coupled with AtATR-controlled blockage of cell-cycle progression and terminal differentiation because of loss of the root-quiescent center.
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