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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.
Nucleotide biosynthesis in ATR-inhibited acute lymphoblastic leukemia (ALL) cells reveals substantial remaining de novo and salvage activities, and could not eliminate the disease in vivo.
AZD7762 demonstrates synergy with regard to inhibition of AR-CDC6 (zeige CDC6 ELISA Kits)-ATR (zeige ANTXR1 ELISA Kits)-Chk1 (zeige CHEK1 ELISA Kits) signaling.
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.
Rif1 (zeige INSL6 ELISA Kits) can mediate MCM dephosphorylation at replication forks and that the stability of dephosphorylated replisomes strongly depends on Chk1 (zeige CHEK1 ELISA Kits) activity.
the sequence ultraviolet-pyrimidine dimers-nucleotide excision repair pathway-ATR-RNAPII-Alternative splicing (AS) as a pathway linking DNA damage repair to the control of both RNAPII phosphorylation and AS regulation.
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 (zeige ANTXR1 ELISA Kits) or ATM (zeige ATM ELISA Kits) inhibition represent potential therapeutic strategies for the treatment of AML (zeige RUNX1 ELISA Kits), especially MLL (zeige MLL ELISA Kits)-driven leukemias.
PM2.5 exposure strongly induced the activation of the ATR (ATR (zeige ANTXR1 ELISA Kits) serine/threonine kinase (zeige TLK2 ELISA Kits))-CHEK1/CHK1 (checkpoint kinase 1 (zeige CHEK1 ELISA Kits)) axis, which subsequently triggered TP53 (zeige TP53 ELISA Kits)-dependent autophagy and VEGFA (zeige VEGFA ELISA Kits) production in Beas-2B cells.
REV3/ATR knockdown enhances the cytotoxicity of cisplatin in non-small cell lung cells.
ATR (zeige ANTXR1 ELISA Kits) promotes homologous recombination after CDK (zeige CDK4 ELISA Kits)-driven DNA end resection.
The authors show, in live cells, that Ddx19 (zeige DDX19B ELISA Kits) transiently relocalizes from the nucleopore to the nucleus upon DNA damage, in an ATR/Chk1 (zeige CHEK1 ELISA Kits)-dependent manner, and that Ddx19 (zeige 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 (zeige APEX2 ELISA Kits) associates with Chk1 (zeige CHEK1 ELISA Kits); a serine residue (S86) in the Chk1 (zeige CHEK1 ELISA Kits)-binding motif of APE2 (zeige APEX2 ELISA Kits) is essential for Chk1 (zeige CHEK1 ELISA Kits) phosphorylation, indicating a Claspin (zeige CLSPN ELISA Kits)-like but distinct role for APE2 (zeige APEX2 ELISA Kits) in ATR-Chk1 (zeige CHEK1 ELISA Kits) signaling.
MRN (MRE11 (zeige MRE11A ELISA Kits)-RAD50 (zeige RAD50 ELISA Kits)-NBS1 (zeige NLRP2 ELISA Kits)) complex has role in ATR activation via TOPBP1 (zeige TOPBP1 ELISA Kits) recruitment.
ATM (zeige ATM ELISA Kits) activity is required for an early step in resection, leading to ATR activation, CtIP (zeige RBBP8 ELISA Kits)-T818 phosphorylation, and accumulation of CtIP (zeige RBBP8 ELISA Kits) on chromatin.
ATM (zeige ATM ELISA Kits) and ATR prevent accumulation of chromosomal abnormalities by promoting Mre11 (zeige MRE11A ELISA Kits)/Rad50 (zeige RAD50 ELISA Kits)/Nbs1 (zeige 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 (zeige ATM ELISA Kits) and ATR phosphorylate the functionally critical replication protein Mcm2 (zeige MCM2 ELISA Kits) during both DNA damage and replication checkpoint responses in Xenopus egg extracts
ATRIP (zeige ATRIP ELISA Kits) must associate with ATR in order for ATR to carry out the phosphorylation of Chk1 (zeige CHEK1 ELISA Kits) effectively
PP2A counteracts ATM and ATR in a DNA damage checkpoint in Xenopus egg extracts
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 (zeige ATM ELISA Kits) inhibition represent potential therapeutic strategies for the treatment of AML (zeige RUNX1 ELISA Kits), especially MLL (zeige MLL ELISA Kits)-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 (zeige TRAF1 ELISA Kits)/NF-kappaB (zeige NFKB1 ELISA Kits)-regulated apoptosis and the p53 (zeige TP53 ELISA Kits)/PCNA (zeige PCNA ELISA Kits)- and ATM (zeige ATM ELISA Kits)/ATR-Chk1 (zeige 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 (zeige RAD9A ELISA Kits) has a prominent role in the ATR-Chk1 (zeige CHEK1 ELISA Kits) pathway that is necessary for successful formation of the damage-sensing complex and DNA damage checkpoint signaling.
ATR function together with SOG1 and ALT2 (zeige 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 (zeige FUS ELISA Kits)) polymerases (Poleta, Polzeta) and DNA-damage-activated protein kinases (ATR, ATM (zeige 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