Sun P, Lou L, Maurer R A
Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland, Oregon 97201, USA.
J Biol Chem. 1996 Feb 9;271(6):3066-73. doi: 10.1074/jbc.271.6.3066.
The ability of activating transcription factor-1 (ATF1) or the cAMP response element-binding protein (CREB) to enhance transcription can be stimulated by increases in intracellular Ca2+ concentrations. To identify protein kinases which may mediate the ability of Ca2+ to activate these transcription factors, we compared the ability of constitutively active forms of several Ca2+/calmodulin-dependent protein kinases (CaM kinases) to activate ATF1 or CREB. We find that constitutively active CaM kinase I and IV can activate both ATF1 and CREB. In addition, expression vectors for full-length CaM kinase I and IV were able to augment the ability of Ca2+ influx to activate ATF1 or CREB consistent with a role for these kinases in mediating transcriptional responses to Ca2+ signaling. In contrast, CaM kinase II was unable to activate either ATF1 or CREB. These findings provide a potential mechanism that may permit variation in the ability of ATF1 and CREB to respond to changes in intracellular Ca2+ concentrations depending on differences in the relative concentrations of specific CaM kinases.
细胞内钙离子浓度升高可刺激激活转录因子-1（ATF1）或环磷酸腺苷反应元件结合蛋白（CREB）增强转录的能力。为了鉴定可能介导钙离子激活这些转录因子能力的蛋白激酶，我们比较了几种组成型活性形式的钙/钙调蛋白依赖性蛋白激酶（CaM激酶）激活ATF1或CREB的能力。我们发现组成型活性CaM激酶I和IV均可激活ATF1和CREB。此外，全长CaM激酶I和IV的表达载体能够增强钙离子内流激活ATF1或CREB的能力，这与这些激酶在介导对钙离子信号的转录反应中的作用一致。相比之下，CaM激酶II无法激活ATF1或CREB。这些发现提供了一种潜在机制，该机制可能使ATF1和CREB响应细胞内钙离子浓度变化的能力因特定CaM激酶相对浓度的差异而有所不同。
