Gonzalez Walter G, Ramos Victoria, Diaz Maurizio, Garabedian Alyssa, Molano-Arevalo Juan Camilo, Fernandez-Lima Francisco, Miksovska Jaroslava
Department of Chemistry and Biochemistry, Florida International University , Miami, Florida 33199, United States.
School for Advanced Studies Homestead , Homestead, Florida 33030, United States.
Biochemistry. 2016 Mar 29;55(12):1873-86. doi: 10.1021/acs.biochem.6b00067. Epub 2016 Mar 7.
DREAM (also known as K(+) channel interacting protein 3 and calsenilin) is a calcium binding protein and an active modulator of KV4 channels in neuronal cells as well as a novel Ca(2+)-regulated transcriptional modulator. DREAM has also been associated with the regulation of Alzheimer's disease through the prevention of presenilin-2 fragmentation. Many interactions of DREAM with its binding partners (Kv4, calmodulin, DNA, and drugs) have been shown to be dependent on calcium. Therefore, understanding the structural changes induced by binding of metals to DREAM is essential for elucidating the mechanism of signal transduction and biological activity of this protein. Here, we show that the fluorescence emission and excitation spectra of the calcium luminescent analogue, Tb(3+), are enhanced upon binding to the EF-hands of DREAM due to a mechanism of energy transfer between Trp and Tb(3+). We also observe that unlike Tb(3+)-bound calmodulin, the luminescence lifetime of terbium bound to DREAM decays as a complex multiexponential (τaverage ∼ 1.8 ms) that is sensitive to perturbation of the protein structure and drug (NS5806) binding. Using isothermal calorimetry, we have determined that Tb(3+) binds to at least three sites with high affinity (Kd = 1.8 μM in the presence of Ca(2+)) and displaces bound Ca(2+) through an entropically driven mechanism (ΔH ∼ 12 kcal mol(-1), and TΔS ∼ 22 kcal mol(-1)). Furthermore, the hydrophobic probe 1,8-ANS shows that Tb(3+), like Ca(2+), triggers the exposure of a hydrophobic surface on DREAM, which modulates ligand binding. Analogous to Ca(2+) binding, Tb(3+) binding also induces the dimerization of DREAM. Secondary structural analyses using far-UV circular dichroism and trapped ion mobility spectrometry-mass spectrometry reveal that replacement of Ca(2+) with Tb(3+) preserves the folding state with minimal changes to the overall structure of DREAM. These findings pave the way for further investigation of the metal binding properties of DREAM using lanthanides as well as the study of DREAM-protein complexes by lanthanide resonance energy transfer or nuclear magnetic resonance.
DREAM(也称为钾离子通道相互作用蛋白3和钙调蛋白)是一种钙结合蛋白,是神经元细胞中KV4通道的活性调节剂,也是一种新型的钙调节转录调节剂。DREAM还通过预防早老素2片段化与阿尔茨海默病的调节相关。已表明DREAM与其结合伙伴(Kv4、钙调蛋白、DNA和药物)之间的许多相互作用都依赖于钙。因此,了解金属与DREAM结合所诱导的结构变化对于阐明该蛋白的信号转导机制和生物学活性至关重要。在此,我们表明,由于色氨酸与Tb(3+)之间的能量转移机制,钙发光类似物Tb(3+)与DREAM的EF手结合后,其荧光发射和激发光谱增强。我们还观察到,与结合Tb(3+)的钙调蛋白不同,与DREAM结合的铽的发光寿命以复杂的多指数形式衰减(平均τ约为1.8毫秒),该衰减对蛋白质结构的扰动和药物(NS5806)结合敏感。使用等温滴定量热法,我们确定Tb(3+)以高亲和力结合到至少三个位点(在存在Ca(2+)的情况下Kd = 1.8 μM),并通过熵驱动机制取代结合的Ca(2+)(ΔH约为12 kcal mol(-1),TΔS约为22 kcal mol(-1))。此外,疏水探针1,8-ANS表明,Tb(3+)与Ca(2+)一样,会触发DREAM上疏水表面的暴露,从而调节配体结合。与Ca(2+)结合类似,Tb(3+)结合也会诱导DREAM二聚化。使用远紫外圆二色性和捕获离子淌度质谱进行的二级结构分析表明,用Tb(3+)取代Ca(2+)可保持折叠状态,对DREAM的整体结构影响最小。这些发现为使用镧系元素进一步研究DREAM的金属结合特性以及通过镧系元素共振能量转移或核磁共振研究DREAM-蛋白质复合物铺平了道路。