Stoychev Stoyan H, Nathaniel Christos, Fanucchi Sylvia, Brock Melissa, Li Sheng, Asmus Kyle, Woods Virgil L, Dirr Heini W
Protein Structure-Function Research Unit, School of Molecular and Cell Biology, University of the Witwatersrand, Johannesburg 250, South Africa.
Biochemistry. 2009 Sep 8;48(35):8413-21. doi: 10.1021/bi9010607.
Chloride intracellular channel protein 1 (CLIC1) functions as an anion channel in plasma and nuclear membranes when its soluble monomeric form converts to an integral-membrane form. The transmembrane region of CLIC1 is located in its thioredoxin-like domain 1, but the mechanism whereby the protein converts to its membrane conformation has yet to be determined. Since channel formation in membranes is enhanced at low pH (5 to 5.5), a condition that is found at the surface of membranes, the structural dynamics of soluble CLIC1 was studied at pH 7 and at pH 5.5 in the absence of membranes by amide hydrogen-deuterium exchange mass spectrometry (DXMS). Rapid hydrogen exchange data indicate that CLIC1 displays a similar core structure at these pH values. Domain 1 is less stable than the all-helical domain 2, and, while the structure of domain 1 remains intact, its conformational flexibility is further increased in an acidic environment (pH 5.5). In the absence of membrane, an acidic environment appears to prime the solution structure of CLIC1 by destabilizing domain 1 in order to lower the activation energy barrier for its conversion to the membrane-insertion conformation. The significantly enhanced H/D-exchange rates at pH 5.5 displayed by two segments (peptides 11-31 and 68-82) could be due to the protonation of acidic residues in salt bridges. One of these segments (peptide 11-31) includes part of the transmembrane region which, in the solution structure, consists of helix alpha1. This helix is intrinsically stable and is most likely retained in the membrane conformation. Strand beta2, another element of the transmembrane region, displays a propensity to form a helical structure and has putative N- and C-capping motifs, suggesting that it too most likely forms a helix in a lipid bilayer.
氯离子细胞内通道蛋白1(CLIC1)在其可溶性单体形式转变为整合膜形式时,作为血浆膜和核膜中的阴离子通道发挥作用。CLIC1的跨膜区域位于其硫氧还蛋白样结构域1中,但该蛋白转变为膜构象的机制尚未确定。由于膜中通道的形成在低pH值(5至5.5)时增强,这种情况在膜表面存在,因此通过酰胺氢-氘交换质谱法(DXMS)在无膜条件下,于pH 7和pH 5.5研究了可溶性CLIC1的结构动力学。快速氢交换数据表明,CLIC1在这些pH值下呈现相似的核心结构。结构域1不如全螺旋结构域2稳定,并且虽然结构域1的结构保持完整,但其构象灵活性在酸性环境(pH 5.5)中进一步增加。在无膜的情况下,酸性环境似乎通过使结构域1不稳定来引发CLIC1的溶液结构,以降低其转变为膜插入构象的活化能垒。两个片段(肽段11 - 31和68 - 82)在pH 5.5时显著增强的H/D交换速率可能是由于盐桥中酸性残基的质子化。这些片段之一(肽段11 - 31)包括跨膜区域的一部分,在溶液结构中该区域由α1螺旋组成。该螺旋本质上是稳定的,并且很可能保留在膜构象中。跨膜区域的另一个元件β2链倾向于形成螺旋结构,并具有推定的N端和C端封端基序,这表明它在脂质双层中也很可能形成螺旋。