Product Name: ATR (2175-2189)
Product Number: PE-01ATC85
Size: 200 µg      Price:38.00
1 mg      $US77.00
Peptide Name: ATR (2175-2189)

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: CAMWMMTAVSKSSYPM

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1823.2 Da

Peptide Purity Percent after Synthesis and Purification: >50

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Scientific Background: ATR is a protein-serine/threonine kinase of the Atypical group and PIKK family. It functions as a DNA damage sensor, and plays a pivotal role in the regulation of the cell cycle. ATR appears to be a tumour suppressor protein; cancer-related mutations in human tumours point to a loss of function of the protein kinase. Active ATR normally acts to inhibit tumour cell proliferation. ATR levels are up-regulated 1.6-fold in human tumours compared to most other protein kinases. Loss-of-function mutations in ATR, which abolish its DNA damage detection ability, have been linked to hemangiomas. Somatic mutations in the ATR gene are rarely observed in human cancer specimens, with the possible exception of sporadic stomach and endometrial cancers that display microsatellite instability. In animal studies, mice heterozygous for a loss-of-function mutation in the ATR gene exhibit similar survival times as wild-type mice, but have an increased occurence of tumour formation. Caffeine is an inhibitor of ATR. Interestingly, caffeine exposure is known to sensitize tumours to ionizing radiation and other toxic agents, which is associated with the disruption of cell-cycle checkpoints. It works in a complex with ATRIP. ATR responds to DNA damage and replication stresses and activates proteins that mediate DNA repair. It's other roles involve checkpoint signalling by interacting with CHK1, fragile site stabilty and regulation of centrosome duplication. Upon cellular exposure to genotoxic stresses, such as ionizing radiation (IR), ultraviolent light (UV), or DNA replication stalling, ATR phosphorylates BRCA1, CHEK1, MCM2, RAD17, RPA2, SMC1, and p53/TP53, which collectively function to promote cell cycle arrest, DNA repair, recombination, and potentially apoptosis.