BAIT

FLT3

CD135, FLK-2, FLK2, STK1, RP11-153M24.3
fms-related tyrosine kinase 3
Homo sapiens
PREY

GSK3A

glycogen synthase kinase 3 alpha
GO Process (33)
GO Function (4)
GO Component (2)

Gene Ontology Biological Process

Gene Ontology Cellular Component

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 Genome-Wide CRISPR Screen Identifies Genes Critical for Resistance to FLT3 Inhibitor AC220.

Hou P, Wu C, Wang Y, Qi R, Bhavanasi D, Zuo Z, Dos Santos C, Chen S, Chen Y, Zheng H, Wang H, Perl A, Guo D, Huang J

Acute myeloid leukemia (AML) is a malignant hematopoietic disease and the most common type of acute leukemia in adults. The mechanisms underlying drug resistance in AML are poorly understood. Activating mutations in FMS-like tyrosine kinase 3 (FLT3) are the most common molecular abnormality in AML. Quizartinib (AC220) is a potent and selective second-generation inhibitor of FLT3. It is in clinical ... [more]

Cancer Res. Dec. 15, 2016; 77(16);4402-4413 [Pubmed: 28625976]

Throughput

  • Low Throughput

Ontology Terms

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

Additional Notes

  • CRISPR GI screen
  • Cell Line: MV4-11 cells
  • Experimental Setup:Drug Exposure, 3 nM AC220
  • GIST: A-phenotypic positive genetic interaction
  • Library: GECKO
  • Significance Threshold: Only screen hits were published

Curated By

  • BioGRID