The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

CACNA1I  -  calcium channel, voltage-dependent, T type...

Homo sapiens

Synonyms: Ca(v)3.3, Cav3.3, KIAA1120, Voltage-dependent T-type calcium channel subunit alpha-1I, Voltage-gated calcium channel subunit alpha Cav3.3, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of CACNA1I

  • This study investigated whether the T-type calcium channel gene CACNA1I causes susceptibility in the Chinese Han population to childhood absence epilepsy, a form of idiopathic generalized seizure disorder [1].
 

High impact information on CACNA1I

  • 3. Immunostaining studies revealed co-localization of CatSper1 and Ca(v)3.3 on the principal piece of human sperm tail [2].
  • Intriguingly, scaling of recovery rates was dramatically reduced in Ca(v)3.2 and Ca(v)3.3, but not Ca(v)3.1 subunits, when mock action potentials were superimposed on conditioning depolarizations [3].
  • 3. Similar voltage-dependent gating and kinetics were found for truncated versions of human Ca(v)3.3, which lack either 118 or 288 of the 490 amino acids that compose the carboxyl terminus [4].
  • Positive immunoreactivity to the Ca(v)3.1, Ca(v)3.2 and Ca(v)3.3 subunits of the T-type Ca(2+) channel was observed throughout the soma, dendrite and knob [5].
  • However, the discrimination by Nif of either various endogenous T-channel subtypes, evident from functional studies, or cloned Ca(v)3.1, Ca(v)3.2 and Ca(v)3.3 T-channel alpha 1 subunits have not been determined [6].
 

Biological context of CACNA1I

  • The human CACNA1I gene contains two regions of alternative splicing: variable inclusion of exon 9 and an alternative acceptor site within exon 33, which leads to deletion of 13 amino acids (Delta33) [7].
  • For this investigation, we searched for mutations in the 35 exons and exon-intron boundaries of the CACNA1I gene in 50 Han Chinese patients with childhood absence epilepsy [1].
  • In conclusion, contrasting anesthetic sensitivities of Ca(v)3.3 and nRT T-type Ca(2+) channels strongly suggest that different molecular structures of Ca(2+) channels give rise to slowly inactivating T-type Ca(2+) currents [8].
 

Anatomical context of CACNA1I

  • Here, we investigated the effects of Nif on currents induced by Ca(v)3.1, Ca(v)3.2 and Ca(v)3.3 expression in Xenopus oocytes or HEK-293 cells (I(alpha 1G), I(alpha 1H) and I(alpha 1I), respectively) and two kinetically distinct, "fast" and "slow", LVA currents in thalamic neurons (I(LVA,f) and I(LVA,s)) [6].
  • Some common features in the voltage- and state-dependence of Nif action on endogenous and recombinant currents together with previous data on T-channel alpha 1 subunits mRNA expression patterns in the thalamus point to Ca(v)3.1 and Ca(v)3.3 as the major contributors to thalamic I(LVA,f) and I(LVA,s), respectively [6].
 

Associations of CACNA1I with chemical compounds

 

Other interactions of CACNA1I

  • The structure of CACNA1I, the gene encoding alpha1I, a human brain T Ca2+ channel alpha1 subunit, was determined by comparison of polymerase chain reaction-amplified brain cDNA and genomic sequences [10].
  • Three T-channel genes were identified: CACNA1G, encoding Ca(v)3.1; CACNA1H, encoding Ca(v)3.2; and CACNA1I, encoding Ca(v)3 [11].

References

  1. CACNA1I Is Not Associated With Childhood Absence Epilepsy in the Chinese Han Population. Wang, J., Zhang, Y., Liang, J., Pan, H., Wu, H., Xu, K., Liu, X., Jiang, Y., Shen, Y., Wu, X. Pediatr. Neurol. (2006) [Pubmed]
  2. Association of Catsper1 or -2 with Ca(v)3.3 leads to suppression of T-type calcium channel activity. Zhang, D., Chen, J., Saraf, A., Cassar, S., Han, P., Rogers, J.C., Brioni, J.D., Sullivan, J.P., Gopalakrishnan, M. J. Biol. Chem. (2006) [Pubmed]
  3. T-type Ca2+ channels encode prior neuronal activity as modulated recovery rates. Uebachs, M., Schaub, C., Perez-Reyes, E., Beck, H. J. Physiol. (Lond.) (2006) [Pubmed]
  4. Cloning and expression of the human T-type channel Ca(v)3.3: insights into prepulse facilitation. Gomora, J.C., Murbartián, J., Arias, J.M., Lee, J.H., Perez-Reyes, E. Biophys. J. (2002) [Pubmed]
  5. T-type Ca(2+) channels mediate propagation of odor-induced Ca(2+) transients in rat olfactory receptor neurons. Gautam, S.H., Otsuguro, K.I., Ito, S., Saito, T., Habara, Y. Neuroscience (2007) [Pubmed]
  6. Contrasting the effects of nifedipine on subtypes of endogenous and recombinant T-type Ca2+ channels. Shcheglovitov, A., Zhelay, T., Vitko, Y., Osipenko, V., Perez-Reyes, E., Kostyuk, P., Shuba, Y. Biochem. Pharmacol. (2005) [Pubmed]
  7. Functional impact of alternative splicing of human T-type Cav3.3 calcium channels. Murbartián, J., Arias, J.M., Perez-Reyes, E. J. Neurophysiol. (2004) [Pubmed]
  8. Contrasting anesthetic sensitivities of T-type Ca2+ channels of reticular thalamic neurons and recombinant Ca(v)3.3 channels. Joksovic, P.M., Brimelow, B.C., Murbartián, J., Perez-Reyes, E., Todorovic, S.M. Br. J. Pharmacol. (2005) [Pubmed]
  9. Pharmacology of recombinant low-voltage activated calcium channels. Lacinová, L. Current drug targets. CNS and neurological disorders. (2004) [Pubmed]
  10. Structure and alternative splicing of the gene encoding alpha1I, a human brain T calcium channel alpha1 subunit. Mittman, S., Guo, J., Emerick, M.C., Agnew, W.S. Neurosci. Lett. (1999) [Pubmed]
  11. Molecular biology of T-type calcium channels. Perez-Reyes, E., Lory, P. CNS & neurological disorders drug targets (2006) [Pubmed]
 
WikiGenes - Universities