BAIT

ETAA1

ETAA16
Ewing tumor-associated antigen 1
Fanconi Anemia Project
GO Process (0)
GO Function (0)
GO Component (0)
Homo sapiens
PREY

LRRC57

leucine rich repeat containing 57
GO Process (0)
GO Function (0)
GO Component (1)

Gene Ontology Cellular Component

Homo sapiens

Synthetic Lethality

A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.

Publication

Regulation of ETAA1-mediated ATR activation couples DNA replication fidelity and genome stability.

Achuthankutty D, Thakur RS, Haahr P, Hoffmann S, Drainas AP, Bizard AH, Weischenfeldt J, Hickson ID, Mailand N

The ATR kinase is a master regulator of the cellular response to DNA replication stress. Activation of ATR relies on dual pathways involving the TopBP1 and ETAA1 proteins, both of which harbor ATR-activating domains (AADs). However, the exact contribution of the recently discovered ETAA1 pathway to ATR signaling in different contexts remains poorly understood. Here, using an unbiased CRISPR-Cas9-based genome-scale ... [more]

J. Cell Biol. Dec. 02, 2019; 218(12);3943-3953 [Pubmed: 31615875]

Throughput

  • High Throughput

Additional Notes

  • CRISPR GI screen
  • Cell Line: HELA
  • Experimental Setup: Negative Selection
  • GIST: A-phenotypic negative genetic interaction
  • Library: Geckov2
  • Significance Threshold: p<0.01

Curated By

  • BioGRID