NDLI: Altered Expression and Assembly of N-type Calcium Channel α1B and β Subunits in Epileptic lethargic(lh/lh) Mouse

Content Provider	Journal of Biological Chemistry (JBC)
Author	McEnery, Maureen W. Copeland, Terry D. Vance, Courtney L.
Abstract	Voltage-dependent calcium channels (VDCC) are multisubunit complexes whose expression and targeting require the assembly of the pore-forming α1 with auxiliary β and α2/δ subunits. The developmentally regulated expression and differential assembly of β isoforms with the α1B subunit to form N-type VDCC suggested a unique role for the β4 isoform in VDCC maturation (Vance, C. L., Begg, C. M., Lee, W.-L., Haase, H., Copeland, T. D., and McEnery, M. W. (1998) J.Biol. Chem. 273, 14495–14502). The focus of this study is the expression and assembly of α1B and β isoforms in the epileptic mouse, lethargic(lh/lh), a mutant anticipated to produce a truncated β4 subunit (Burgess, D. L., Jones, J. M., Meisler, M. H., and Noebels, J. L. (1997) Cell 88, 385–392). In this report, we demonstrate that neither full-length nor truncated β4 protein is expressed in lh/lh mice. The absence of β4 inlh/lh mice is associated with decreased expression of N-type VDCC in forebrain and cerebellum. The most surprising characteristic of the lh/lh mouse is increased expression of β1b protein. This result suggests a previously unidentified cellular mechanism wherein expression of the total pool of available β subunits is under tight metabolic regulation. As a consequence of increased β1b expression, the β1b is increased in its incorporation into α1B/β complexes relative to wild type. Thus, in striking similarity to the population of N-type VDCC present in immature rat brain, the population of N-type VDCC present in adultlh/lh mice is characterized by the absence of β4 with increased β1b expression and assembly into N-type VDCC. It is intriguing to speculate that the increased excitability and susceptibility to seizures observed in the lh/lhmouse arises from the inappropriate expression of an immature population of N-type VDCC throughout neuronal development.
Related Links	http://www.jbc.org/content/273/34/21435.abstract
Ending Page	21438
Starting Page	21435
Page Count	4
File Format	HTM / HTML PDF
ISSN	00219258
Journal	Journal of Biological Chemistry (JBC)
Issue Number	34
Volume Number	273
DOI	10.1074/jbc.273.34.21435
e-ISSN	1083351X
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	1998-08-21
Access Restriction	Open
Subject Keyword	Voltage-dependent calcium channel (VDCC) Ω-conotoxin-sensitive VDCC (N-type VDCC) 230-kDa subunit of the N-type VDCC (α1B) 160-kDa subunit of N-type VDCC (α2/δ) 53–85-kDa subunits of N-type VDCC (β1–β4) 125I-labeled Tyr-22-ω-conotoxin GVIA (125I-CTX) 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate (CHAPS) Polyacrylamide gel electrophoresis (PAGE) Postnatal day 2. (P2)
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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