ATR and ATRIP: Partners in Checkpoint Signaling

By D. Cortez, Saritha Guntuku, Jun-Wei Qin, S. Elledge. Science, 2001

1,075 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/3b3b7e1b7c141260e9c4ad56c89495a7b590db23

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In Molecular Biology

1. J. Bartek
2. Stephen P. Jackson
3. J. Lukas
4. Yosef Shiloh
5. C. Lukas
6. S. Polo
7. L. Zou
8. Alexandre Maréchal

In Oncology

1. J. Bartek
2. Stephen P. Jackson
3. J. Lukas
4. Yosef Shiloh
5. P. Jeggo
6. L. Zou
7. Alexandre Maréchal
8. S. Polo

Citations in the corpus

• An expanded Ragulator is a GEF for the Rag GTPases that signal amino acid levels to mTORC1 (2012, neutral): “As the components of obligate heterodimers often behave (Cortez et al., 2001; Sancak et al., 2008), loss of either HBXIP or C7orf59 reduced the expression of its partner, but not of p14 (Figure 2A).”
• RNF8 ubiquitylates histones at DNA double-strand breaks and promotes assembly of repair proteins. (2007, neutral): “Finally, the assembly of ATR, a protein that specifically interacts with single-stranded DNA generated by DSB resection ( Cortez et al., 2001; Bekker-Jensen et al., 2006), was significantly delayed compared to both early and late chromatin assembly waves (Figure 3B), suggesting that the chromatin r”
• ATR: An Essential Regulator of Genome Integrity (2008, neutral): “However, ATR is essential for the viability of replicating human and mouse cells, whereas ATM is no”
• ATM and related protein kinases: safeguarding genome integrity (2003, background): “and is not compatible with cellular viability in cultur”
• Toward maintaining the genome: DNA damage and replication checkpoints. (2002, background): “Whether ATRIP possesses detectable DNA binding activity or is required for protein kinase activity of ATR is not yet known, although ATR and ATRIP colocalize to intranuclear foci after DNA damage or inhibition of replication (38).”
• DNA damage sensing by the ATM and ATR kinases. (2013, background): “In contrast to ATM, ATR is essential for the survival of proliferating cells and its deletion leads to early embryonic lethality in mouse and cell lethality in human cells (Brown and Baltimore 2000, 2003; de Klein et al. 2000; Cortez et al. 2001).”
• Functional uncoupling of MCM helicase and DNA polymerase activities activates the ATR-dependent checkpoint. (2005, background): “ATR, and its associated protein ATRIP, respond to a broad spectrum of genotoxic agents that includes ultraviolet light (UV), topoisomerase inhibitors, alkylating agents, and cis-platinum, as well as chemicals that disrupt replication, such as aphidicolin and hydroxyurea (HU) (Zhou and Elledge 2000; ”
• Cell-cycle checkpoints and cancer (2004, background): “ATR exists in a complex with the ATR-interacting protein (ATRIP), both before and after exposure to stresses such as ultraviolet irradiatio”
• ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks (2006, background): “, whereas ATR is recruited by ATR-interacting protein ( ATRIP ) to RPA-coated single-stranded DNA (ssDNA) that accumulates at stalled DNA replication forks or is generated by processing of the initial DNA damag”
• mTOR interacts with raptor to form a nutrient-sensitive complex that signals to the cell growth machinery. (2002, neutral): “(Cortez et al., 2001).”