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Gene Review

Sept5  -  septin 5

Rattus norvegicus

Synonyms: 5-Sep, CDCrel-1, CDCrel-1A, Cell division control-related protein 1, Peanut-like protein 1, ...
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Disease relevance of Sept5


High impact information on Sept5

  • Transfection of HIT-T15 cells with wild-type CDCrel-1 inhibited secretion, whereas GTPase dominant-negative mutants enhanced secretion [3].
  • These results show that CDCrel-1 overexpression exerts dopamine-dependent neurotoxicity and suggest that inhibition of dopamine secretion by CDCrel-1 may contribute to the development of AR-JP [1].
  • Here we show that recombinant adeno-associated virus-mediated CDCrel-1 gene transfer to the substantia nigra of rats results in a rapid onset (6-10 days) of nigral and striatal CDCrel-1 expression that is followed by a progressive loss of nigral dopaminergic neurons and a decline of the striatal dopamine levels [1].
  • Furthermore, CDCrel-1 inhibits the release of dopamine from stably-transfected PC12 cells, and pharmacological inhibition of tyrosine hydroxylase and dopamine synthesis in rats prevents CDCrel-1-induced nigral neurodegeneration [1].
  • Altered levels of the septin CDCrel-1 in isolation-reared rats may contribute to changes in neuronal connectivity and neurotransmission, and suggest a potential role for CDCrel-1 in schizophrenia related to chromosome 22q11 deletion syndrome [4].

Biological context of Sept5

  • Furthermore, Sept5 appears to inhibit exocytosis, possibly by regulating vesicle targeting and/or fusion events [5].
  • Alternative polyadenylation site selections resulted in various transcripts for CDCrel-1A including the fusion forms with another gene, platelet glycoprotein Ibbeta (GPIbbeta) [6].
  • CDCrel-1 modulates dopamine neurotransmission, binds to the SNARE protein syntaxin and maps onto a region of chromosome 22q11 deleted in velo-cardio-facial and DiGeorge syndromes, which are associated with increased prevalence of schizophrenia [4].

Anatomical context of Sept5

  • We have previously shown that Sept5 is predominantly expressed in the brain, where it associates with vesicles and membranes through its interaction with the SNARE domain of syntaxin 1A [5].
  • Reciprocal expression of infant- and adult-preferring transcripts of CDCrel-1 septin gene in the rat neocortex [6].
  • CDCrel-1 immunoreactivity was significantly lower in the striatum and marginally higher in the hippocampus of isolation-reared compared with socially reared animals [4].

Associations of Sept5 with chemical compounds

  • These results suggest that Parkin may be involved in the haloperidol-induced synaptic plasticity, since Parkin regulates the turnover of the synaptic protein, CDCrel-1 [7].

Other interactions of Sept5

  • Seven proteins showed significant changes in hydrocephalic H-Tx rats compared with Sprague-Dawley and normal H-Tx rats, including HMG-1, CDCrel-1A, mitochondrial ATP synthase, ERp29, NADP+-ICDH, CCT beta and gamma [2].


  1. Dopamine-dependent neurodegeneration in rats induced by viral vector-mediated overexpression of the parkin target protein, CDCrel-1. Dong, Z., Ferger, B., Paterna, J.C., Vogel, D., Furler, S., Osinde, M., Feldon, J., Büeler, H. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  2. Analysis of cerebellum proteomics in the hydrocephalic H-Tx rat. Li, X., Miyajima, M., Mineki, R., Taka, H., Murayama, K., Arai, H. Neuroreport (2005) [Pubmed]
  3. The septin CDCrel-1 binds syntaxin and inhibits exocytosis. Beites, C.L., Xie, H., Bowser, R., Trimble, W.S. Nat. Neurosci. (1999) [Pubmed]
  4. Abnormalities of presynaptic protein CDCrel-1 in striatum of rats reared in social isolation: relevance to neural connectivity in schizophrenia. Barr, A.M., Young, C.E., Sawada, K., Trimble, W.S., Phillips, A.G., Honer, W.G. Eur. J. Neurosci. (2004) [Pubmed]
  5. The septin Sept5/CDCrel-1 competes with alpha-SNAP for binding to the SNARE complex. Beites, C.L., Campbell, K.A., Trimble, W.S. Biochem. J. (2005) [Pubmed]
  6. Reciprocal expression of infant- and adult-preferring transcripts of CDCrel-1 septin gene in the rat neocortex. Toda, S., Kajii, Y., Sato, M., Nishikawa, T. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  7. Acute and chronic haloperidol treatments increase parkin mRNA levels in the rat brain. Nakahara, T., Gotoh, L., Motomura, K., Kawanami, N., Ohta, E., Hirano, M., Uchimura, H. Neurosci. Lett. (2001) [Pubmed]
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