BAIT

ALS2

3222402C23Rik, 9430073A21Rik, Als2cr6, Alsin, mKIAA1563
amyotrophic lateral sclerosis 2 (juvenile)
GO Process (21)
GO Function (11)
GO Component (20)
Mus musculus
PREY

SOD1

B430204E11Rik, Cu/Zn-SOD, CuZnSOD, Ipo-1, Ipo1, SODC, Sod-1
superoxide dismutase 1, soluble
GO Process (50)
GO Function (9)
GO Component (22)

Gene Ontology Biological Process

Mus musculus

Phenotypic Enhancement

A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

Publication

Loss of ALS2/Alsin exacerbates motor dysfunction in a SOD1-expressing mouse ALS model by disturbing endolysosomal trafficking.

Hadano S, Otomo A, Kunita R, Suzuki-Utsunomiya K, Akatsuka A, Koike M, Aoki M, Uchiyama Y, Itoyama Y, Ikeda JE

ALS2/alsin is a guanine nucleotide exchange factor for the small GTPase Rab5 and involved in macropinocytosis-associated endosome fusion and trafficking, and neurite outgrowth. ALS2 deficiency accounts for a number of juvenile recessive motor neuron diseases (MNDs). Recently, it has been shown that ALS2 plays a role in neuroprotection against MND-associated pathological insults, such as toxicity induced by mutant Cu/Zn superoxide ... [more]

PLoS ONE Mar. 27, 2010; 5(3);e9805 [Pubmed: 20339559]

Throughput

  • Low Throughput

Additional Notes

  • figure 1c.
  • figure 2.Loss of ALS2 aggravates motor dysfunction in SOD1-H46R mice.

Curated By

  • BioGRID