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BRENDA support

Literature summary for 3.4.24.B18 extracted from

  • Kondadi, A.K.; Wang, S.; Montagner, S.; Kladt, N.; Korwitz, A.; Martinelli, P.; Herholz, D.; Baker, M.J.; Schauss, A.C.; Langer, T.; Rugarli, E.I.
    Loss of the m-AAA protease subunit AFG3L2 causes mitochondrial transport defects and tau hyperphosphorylation (2014), EMBO J., 33, 1011-1026.
    View publication on PubMedView publication on EuropePMC

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion inner mitochondrial membrane Mus musculus 5739
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Organism

Organism UniProt Comment Textmining
Mus musculus
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-
-

Source Tissue

Source Tissue Comment Organism Textmining
cerebral cortical neuron
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Mus musculus
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Synonyms

Synonyms Comment Organism
AFG3L2 subunit Mus musculus

General Information

General Information Comment Organism
malfunction mutations in subunit AFG3L2 are associated with spinocerebellar ataxia SCA28. Depletion of subunit AFG3L2 leads to a specific defect of anterograde transport of mitochondria in cortical neurons. Deletion of subunit AFG3L2 in adult cortical neurons causes tau hyperphosphorylation and activation of protein kinase A and ERK1/2 kinases Mus musculus
physiological function subunit AFG3L2 is required cell-autonomously for survival of adult neurons Mus musculus