Primary structure and functional expression of the ω-conotoxin-sensitive N-type calcium channel from rabbit brain

Facilitation of rabbit α1B calcium channels: involvement of endogenous Gβγ subunits

“…The following cDNAs were used: rabbit á1B (accession number, D14157 ;Fujita et al 1993) Fong et al 1986) and bovine Gãµ (M37183; Gautam, Baetscher, Aebersold & Simon, 1989) were provided by Dr M. Simon (CalTech, Pasadena, CA, USA). The C_terminal minigene of âARK1 (BTARKB) was provided by Dr R. Lefkowitz (Duke University, Durham, NC, USA).…”

N-Type Calcium Channels in the Developing Rat Hippocampus: Subunit, Complex, and Regional Expression

“…To resolve N-V DCC expression in detail, we raised specific polyclonal antibodies against the ␣ 1B and ␤ 3 subunits previously shown to form the major N-V DCC complex in brain (Wagner et al, 1988;Dubel et al, 1992;Westenbroek et al, 1992;Williams et al, 1992b;Brust et al, 1993;Fujita et al, 1993;Stea et al, 1993;Witcher et al, 1993;Leveque et al, 1994;Scott et al, 1996). High-titer antisera from rabbits immunized with synthetic peptides deduced from the coding sequences of ␣ 1B and ␤ 3 were assayed by immunoprecipitation and immunoblotting (Fig.…”

“…In brain, VDCCs are large (Ͼ400 kDa) heteromers composed of an ␣ 1 , ␣ 2 /␦, and ␤ subunit (Wagner et al, 1988;Hell et al, 1993Hell et al, , 1994Witcher et al, 1993;Hofmann et al, 1994;Leveque et al, 1994). Expression of VDCC gene products in Xenopus oocytes (Mori et al, 1991;Williams et al, 1992a) or transfected cells (Williams et al, 1992b;Fujita et al, 1993;Stea et al, 1993) shows that ␣ 1 subunits contain the ion channel pore, whereas the auxiliary ␣ 2 /␦ and ␤ subunits modulate optimal cell surface expression and channel kinetics (Brust et al, 1993;Castellano et al, 1993;Stea et al, 1993;Isom et al, 1994;Olcese et al, 1994). In rat brain, the ␣ 1 subunits are encoded by at least five discrete classes (A-E) of cDNA.…”

“…This V DCC has important roles in neurotransmitter release (Robitaille et al, 1990;Cohen et al, 1991;Haydon et al, 1994;Wheeler et al, 1994;Dunlap et al, 1995;Scholz and Miller, 1995), dendritic f unction (Mills et al, 1994), and neuronal migration (Komura and Rakic, 1992). Via expression Williams et al, 1992b;Brust et al, 1993;Fujita et al, 1993;Stea et al, 1993) and biochemical studies (Wagner et al, 1988;Westenbroek et al, 1992;Witcher et al, 1993;Leveque et al, 1994;Scott et al, 1996), it seems that most N-V DCC s in adult brain are ␣ 1B , ␣ 2 /␦, and ␤ 3 heteromers, although subpopulations containing ␤ 1 or ␤ 4 rather than ␤ 3 subunits also may exist (Scott et al, 1996). Using site-directed antibodies and selective fluorescent and radioactive labels, we have found that our data support a significant role for N-V DCCs in the development of the nervous system.…”

Endogenous cardiac Ca2+ channels do not overcome the E‐C coupling defect in immortalized dysgenic muscle cells: evidence for a missing link

“…Two other skeletal muscle L-VGCC subunit mRNAs; two transcripts for ~2/~ and numerous fl subunit transcripts are expressed at a level similar to that observed in control cells. Further, this provides an explanation as to why expression of skeletal [8], cardiac [28] and brain [29] c~ cDNAs in primary cultures of mdg muscle cells always elicited Ca 2~ channel currents that were very close to the native behavior.…”