000			03007na a2200289 4500
003			H12O
005			20210625062809.0
008			130622s2011 xxx||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_aGarcía-Consuegra Galiana, Inés _91867 _eInstituto de Investigación i+12
100			_aHoenicka, Janet _91868 _ePsiquiatría
100			_9656 _aJiménez Arriero, Miguel Ángel _ePsiquiatría
100			_9653 _aPalomo Álvarez, Tomás _d(1989-2010) _ePsiquiatría
100			_aPonce Alfaro, Guillermo _9727 _ePsiquiatría
245	0	3	_aThe ANKK1 protein associated with addictions has nuclear and cytoplasmic localization and shows a differential response of Ala239Thr to apomorphine _h[artículo]
260			_bNeurotoxicity Research, _c2011.
300			_a20(1):32-39.
500			_aFormato Vancouver: Garrido E, Palomo T, Ponce G, García Consuegra I, Jiménez Arriero MA, Hoenicka J. The ANKK1 protein associated with addictions has nuclear and cytoplasmic localization and shows a differential response of Ala239Thr to apomorphine. Neurotox Res. 2011;20(1):32-9.
501			_aPMID: 20845092
504			_aContiene 26 referencias
520			_aThe TaqIA single-nucleotide polymorphism (SNP), which is the most widely studied genetic polymorphism in addictions, is located at the gene that encodes the RIP kinase ANKK1 near the gene for dopamine receptor D2. The TaqIA SNP is in strong linkage disequilibrium with the SNP rs7118900, which changes the alanine at position 239 to threonine in the ANKK1 protein (Ala239/A2; Thr239/A1). In silico analysis has predicted that this polymorphic substitution creates an additional phosphorylation site in the kinase domain of ANKK1. To investigate the contribution of ANKK1 to the pathophysiology of TaqIA-associated phenotypes, we analyzed transfected HEK293T cells with the human ANKK1-kinase(Ala239) and ANKK1-kinase(Thr239) variants tagged with GFP. We observed that the ANKK1-kinase is located in both the nucleus and the cytoplasm, suggesting that there is nucleocytoplasmic shuttling of this putative signal transducer. In addition, we found that the Ala239Thr ANKK1-kinase polymorphism exhibited strong expression differences in both the nucleus and the cytoplasm at basal level and when stimulated with the dopamine agonist apomorphine. Specifically, the ANKK1-kinase(Thr239) variant showed the highest level of basal protein expression, while ANKK1-kinase(Ala239) was 0.64-fold lower. After treatment with apomorphine, ANKK1-kinase(Ala239) showed a 2.4-fold increment in protein levels, whereas a 0.67-fold reduction was observed in ANKK1-kinase(Thr239). Thus, here we provide the first evidence of functional ANKK1 differences that are marked by TaqIA and could be associated with vulnerability to addiction.
710			_9150 _aServicio de Psiquiatría
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/9/pc9371.pdf _ySolicitar documento
942			_n0 _2ddc _cART
999			_c9371 _d9371