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@ARTICLE{Skegro:57375,
author = {Skegro, D. and Pulvermuller, A. and Krafft, B. and Granzin,
J. and Hofmann, K. P. and Büldt, G. and Schlesinger, R.},
title = {{N}-terminal and {C}-terminal {D}omains of {A}rrestin
{B}oth {C}ontribute in {B}inding to {R}hodopsin (dagger)},
journal = {Photochemistry and photobiology},
volume = {83},
issn = {0031-8655},
address = {Malden, Mass.},
publisher = {Wiley-Blackwell},
reportid = {PreJuSER-57375},
pages = {385 - 393},
year = {2007},
note = {Record converted from VDB: 12.11.2012},
abstract = {Visual arrestin terminates the signal amplification cascade
in photoreceptor cells by blocking the interaction of light
activated phosphorylated rhodopsin with the G-protein
transducin. Although crystal structures of arrestin and
rhodopsin are available, it is still unknown how the complex
of the two proteins is formed. To investigate the
interaction sites of arrestin with rhodopsin various surface
regions of recombinant arrestin were sterically blocked by
different numbers of fluorophores (Alexa 633). The binding
was recorded by time-resolved light scattering. To
accomplish site-specific shielding of protein regions, in a
first step all three wild-type cysteines were replaced by
alanines. Nevertheless, regarding the magnitude and
specificity of rhodopsin binding, the protein is still fully
active. In a second step, new cysteines were introduced at
selected sites to allow covalent binding of fluorophores.
Upon attachment of Alexa 633 to the recombinant cysteines we
observed that these bulky labels residing in the concave
area of either the N- or the C-terminal domain do not
perturb the activity of arrestin. By simultaneously
modifying both domains with one Alexa 633 the binding
capacity was reduced. The presence of two Alexa 633
molecules in each domain prevented binding of rhodopsin to
arrestin. This observation indicates that both concave sites
participate in binding.},
keywords = {Animals / Arrestin: chemistry / Arrestin: genetics /
Arrestin: metabolism / Base Sequence / Binding Sites /
Cattle / Cysteine: chemistry / DNA Primers: genetics /
Fluorescent Dyes / Models, Molecular / Mutagenesis,
Site-Directed / Photochemistry / Protein Binding / Protein
Structure, Tertiary / Recombinant Proteins: chemistry /
Recombinant Proteins: genetics / Recombinant Proteins:
metabolism / Rhodopsin: metabolism / Signal Transduction /
Arrestin (NLM Chemicals) / DNA Primers (NLM Chemicals) /
Fluorescent Dyes (NLM Chemicals) / Recombinant Proteins (NLM
Chemicals) / Cysteine (NLM Chemicals) / Rhodopsin (NLM
Chemicals) / J (WoSType)},
cin = {INB-2},
ddc = {570},
cid = {I:(DE-Juel1)VDB805},
pnm = {Funktion und Dysfunktion des Nervensystems},
pid = {G:(DE-Juel1)FUEK409},
shelfmark = {Biochemistry $\&$ Molecular Biology / Biophysics},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:17132044},
UT = {WOS:000245658000025},
doi = {10.1562/2006-08-25-RA-1014},
url = {https://juser.fz-juelich.de/record/57375},
}