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anti-Rat (Rattus) ATR Antibodies:
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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
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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.
DNA alkylation damage leads to ATR (show ANTXR1 Antibodies)-Chk1 (show CHEK1 Antibodies) activation in cancer cells and ATR (show ANTXR1 Antibodies)-Chk1 (show CHEK1 Antibodies) 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 (show ANTXR1 Antibodies) and ATM (show ATM Antibodies) and the expression of ATR (show ANTXR1 Antibodies) and ATM (show ATM Antibodies) protein in NPC (show NPC1 Antibodies) 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 (show PRKG1 Antibodies)-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 (show ANTXR1 Antibodies) and Chk1 (show CHEK1 Antibodies) kinase activities are important for viral replication. The findings suggest that HSV-1 activates ATR (show ANTXR1 Antibodies) and Chk1 (show CHEK1 Antibodies) 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 (show TLK1 Antibodies) inhibitor, THD, or overexpression of NEK1 (show NEK1 Antibodies)-T141A mutant impaired ATR (show ANTXR1 Antibodies) and Chk1 (show CHEK1 Antibodies) activation, indicating the existence of a TLK1 (show TLK1 Antibodies)>NEK1 (show NEK1 Antibodies)>ATR (show ANTXR1 Antibodies)>Chk1 (show CHEK1 Antibodies) pathway. Indeed, overexpression of the NEK1 (show NEK1 Antibodies)-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 (show ANTXR1 Antibodies) is a promising strategy to enhance the antitumor activity of GEM (show GEM Antibodies) for treating pancreatic cancer
Suggest that activation of ATR (show ANTXR1 Antibodies)/CHK1 (show CHEK1 Antibodies) signaling pathway is key for Epstein Barr virus-induced B-cell transformation.
ATM (show ATM Antibodies) and Ataxia Telangiectasia and RAD3-related kinase have been identified as components of the DNA damage response (DDR (show DDR1 Antibodies)) pathways as mediators of resistance to IGF-1R (show IGF1R Antibodies) kinase inhibition in breast cancer cells
ATR plays a fundamental nuclear role in maintaining host genome integrity. RNAi-mediated inhibition of canonical ATR signaling suppresses genome replication.
The authors show, in live cells, that Ddx19 (show DDX19B Antibodies) transiently relocalizes from the nucleopore to the nucleus upon DNA damage, in an ATR/Chk1 (show CHEK1 Antibodies)-dependent manner, and that Ddx19 (show DDX19B Antibodies) 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 Antibodies) associates with Chk1 (show CHEK1 Antibodies); a serine residue (S86) in the Chk1 (show CHEK1 Antibodies)-binding motif of APE2 (show APEX2 Antibodies) is essential for Chk1 (show CHEK1 Antibodies) phosphorylation, indicating a Claspin (show CLSPN Antibodies)-like but distinct role for APE2 (show APEX2 Antibodies) in ATR-Chk1 (show CHEK1 Antibodies) signaling.
MRN (MRE11 (show MRE11A Antibodies)-RAD50 (show RAD50 Antibodies)-NBS1 (show NLRP2 Antibodies)) complex has role in ATR activation via TOPBP1 (show TOPBP1 Antibodies) recruitment.
ATM (show ATM Antibodies) activity is required for an early step in resection, leading to ATR activation, CtIP (show RBBP8 Antibodies)-T818 phosphorylation, and accumulation of CtIP (show RBBP8 Antibodies) on chromatin.
ATM (show ATM Antibodies) and ATR prevent accumulation of chromosomal abnormalities by promoting Mre11 (show MRE11A Antibodies)/Rad50 (show RAD50 Antibodies)/Nbs1 (show NLRP2 Antibodies) 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 Antibodies) and ATR phosphorylate the functionally critical replication protein Mcm2 (show MCM2 Antibodies) during both DNA damage and replication checkpoint responses in Xenopus egg extracts
ATRIP (show ATRIP Antibodies) must associate with ATR in order for ATR to carry out the phosphorylation of Chk1 (show CHEK1 Antibodies) effectively
PP2A counteracts ATM and ATR in a DNA damage checkpoint in Xenopus egg extracts
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 (show ATM Antibodies) inhibition represent potential therapeutic strategies for the treatment of AML (show RUNX1 Antibodies), especially MLL (show MLL Antibodies)-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 (show TRAF1 Antibodies)/NF-kappaB (show NFKB1 Antibodies)-regulated apoptosis and the p53 (show TP53 Antibodies)/PCNA (show PCNA Antibodies)- and ATM (show ATM Antibodies)/ATR-Chk1 (show CHEK1 Antibodies)/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.
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 (show GPT2 Antibodies) 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 Antibodies)) polymerases (Poleta, Polzeta) and DNA-damage-activated protein kinases (ATR, ATM (show ATM Antibodies))
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.
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