Ueda T, Ichikawa Y, Kusaka I
Department of Microbiology, Saitama Medical School, Japan.
FEBS Lett. 1988 Jul 18;234(2):272-4. doi: 10.1016/0014-5793(88)80096-6.
GTP and IP3 induced Ca2+ release from an internal store in permeabilized murine thymocytes loaded with Ca2+ by ATP. Ca2+ release was dependent on the concentration of GTP: half-maximal release with 0.5 microM and maximal release with 10 microM. The GTP effect was completely abolished by 100 microM GTP gamma S, GMPPNP and UTP. None of the other nucleotides used except ITP induced Ca2+ release. When GTP was added after the effect of IP3 had virtually subsided, and vice versa, further Ca2+ release occurred, which led to the conclusion that the mechanism of GTP-mediated Ca2+ release may be different from that of IP3-mediated release.
GTP和IP3可诱导通过ATP加载了Ca2+的通透化小鼠胸腺细胞从内部储存库释放Ca2+。Ca2+释放取决于GTP的浓度:0.5微摩尔时达到半数最大释放,10微摩尔时达到最大释放。100微摩尔的GTPγS、GMPPNP和UTP可完全消除GTP的作用。除ITP外,所使用的其他核苷酸均未诱导Ca2+释放。当IP3的作用几乎消退后加入GTP,反之亦然,都会发生进一步的Ca2+释放,由此得出结论,GTP介导的Ca2+释放机制可能与IP3介导的释放机制不同。