BAIT

C16ORF72

PRO0149
chromosome 16 open reading frame 72
GO Process (0)
GO Function (0)
GO Component (0)
Homo sapiens
PREY

PSD

EFA6, EFA6A, PSD1, TYL, RP11-18I14.2
pleckstrin and Sec7 domain containing
GO Process (4)
GO Function (3)
GO Component (2)
Homo sapiens

Positive Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a less severe fitness defect than expected under a given condition. This term is reserved for high or low throughput studies with scores.

Publication

A novel p53 regulator, C16ORF72/TAPR1, buffers against telomerase inhibition.

Benslimane Y, Sanchez-Osuna M, Coulombe-Huntington J, Bertomeu T, Henry D, Huard C, Bonneil E, Thibault P, Tyers M, Harrington L

Telomere erosion in cells with insufficient levels of the telomerase reverse transcriptase (TERT), contributes to age-associated tissue dysfunction and senescence, and p53 plays a crucial role in this response. We undertook a genome-wide CRISPR screen to identify gene deletions that sensitized p53-positive human cells to telomerase inhibition. We uncovered a previously unannotated gene, C16ORF72, which we term Telomere Attrition and ... [more]

Aging Cell Apr. 01, 2021; 20(4);e13331 [Pubmed: 33660365]

Throughput

  • High Throughput

Ontology Terms

  • phenotype: growth abnormality (HP:0001507) [viability (PATO:0000169)]

Additional Notes

  • CRISPR GI screen
  • Cell Line: NALM-6
  • Experimental Setup: Timecourse
  • GIST: A-phenotypic positive genetic interaction
  • Library: TKOv3
  • Significance Threshold: >3.55

Curated By

  • BioGRID