PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33869222-4 2021 Huntington"s disease (HD) is an incurable neurodegenerative disorder that is caused by polyglutamine expansion in the huntingtin (HTT) protein, characterized by the loss of gamma-aminobutyric acid (GABA)-ergic medium spiny neurons (MSNs) in the striatum. gamma-Aminobutyric Acid 173-196 huntingtin Homo sapiens 118-128 33980291-7 2021 In thalamus, we observed a 5-HT1A-by-5-HTT and group-by-5-HTT interaction in GABA concentrations, with the 5-HTT high expressing genotype differing between groups and 5-HT1A genotypes. gamma-Aminobutyric Acid 77-81 huntingtin Homo sapiens 58-61 33980291-7 2021 In thalamus, we observed a 5-HT1A-by-5-HTT and group-by-5-HTT interaction in GABA concentrations, with the 5-HTT high expressing genotype differing between groups and 5-HT1A genotypes. gamma-Aminobutyric Acid 77-81 huntingtin Homo sapiens 58-61 33869222-4 2021 Huntington"s disease (HD) is an incurable neurodegenerative disorder that is caused by polyglutamine expansion in the huntingtin (HTT) protein, characterized by the loss of gamma-aminobutyric acid (GABA)-ergic medium spiny neurons (MSNs) in the striatum. gamma-Aminobutyric Acid 173-196 huntingtin Homo sapiens 130-133 33869222-4 2021 Huntington"s disease (HD) is an incurable neurodegenerative disorder that is caused by polyglutamine expansion in the huntingtin (HTT) protein, characterized by the loss of gamma-aminobutyric acid (GABA)-ergic medium spiny neurons (MSNs) in the striatum. gamma-Aminobutyric Acid 198-202 huntingtin Homo sapiens 118-128 33869222-4 2021 Huntington"s disease (HD) is an incurable neurodegenerative disorder that is caused by polyglutamine expansion in the huntingtin (HTT) protein, characterized by the loss of gamma-aminobutyric acid (GABA)-ergic medium spiny neurons (MSNs) in the striatum. gamma-Aminobutyric Acid 198-202 huntingtin Homo sapiens 130-133 27080129-1 2016 BACKGROUND: Huntington"s disease (HD) is an incurable hereditary neurodegenerative disorder, which manifests itself as a loss of GABAergic medium spiny (GABA MS) neurons in the striatum and caused by an expansion of the CAG repeat in exon 1 of the huntingtin gene. gamma-Aminobutyric Acid 129-133 huntingtin Homo sapiens 248-258 33425919-5 2020 The dysregulation of Ca2+ homeostasis is postulated to be a cause of HD progression because the SOCE pathway is indirectly and abnormally activated by mutant huntingtin (HTT) in gamma-aminobutyric acid (GABA)ergic medium spiny neurons (MSNs) from the striatum in HD models before the first symptoms of the disease appear. gamma-Aminobutyric Acid 178-201 huntingtin Homo sapiens 158-168 33425919-5 2020 The dysregulation of Ca2+ homeostasis is postulated to be a cause of HD progression because the SOCE pathway is indirectly and abnormally activated by mutant huntingtin (HTT) in gamma-aminobutyric acid (GABA)ergic medium spiny neurons (MSNs) from the striatum in HD models before the first symptoms of the disease appear. gamma-Aminobutyric Acid 178-201 huntingtin Homo sapiens 170-173 33425919-5 2020 The dysregulation of Ca2+ homeostasis is postulated to be a cause of HD progression because the SOCE pathway is indirectly and abnormally activated by mutant huntingtin (HTT) in gamma-aminobutyric acid (GABA)ergic medium spiny neurons (MSNs) from the striatum in HD models before the first symptoms of the disease appear. gamma-Aminobutyric Acid 203-207 huntingtin Homo sapiens 158-168 33425919-5 2020 The dysregulation of Ca2+ homeostasis is postulated to be a cause of HD progression because the SOCE pathway is indirectly and abnormally activated by mutant huntingtin (HTT) in gamma-aminobutyric acid (GABA)ergic medium spiny neurons (MSNs) from the striatum in HD models before the first symptoms of the disease appear. gamma-Aminobutyric Acid 203-207 huntingtin Homo sapiens 170-173 22508027-11 2012 Upon differentiation, the Htt(7Q/7Q) and Htt(140Q/140Q) generated numerous Beta(III)-Tubulin- and GABA-positive neurons; however, after 15 days the cellular architecture of the differentiated Htt(140Q/140Q) cultures changed compared to Htt(7Q/7Q) cultures and included a marked increase of GFAP-positive cells. gamma-Aminobutyric Acid 98-102 huntingtin Homo sapiens 26-29 22508027-11 2012 Upon differentiation, the Htt(7Q/7Q) and Htt(140Q/140Q) generated numerous Beta(III)-Tubulin- and GABA-positive neurons; however, after 15 days the cellular architecture of the differentiated Htt(140Q/140Q) cultures changed compared to Htt(7Q/7Q) cultures and included a marked increase of GFAP-positive cells. gamma-Aminobutyric Acid 98-102 huntingtin Homo sapiens 41-44 22508027-11 2012 Upon differentiation, the Htt(7Q/7Q) and Htt(140Q/140Q) generated numerous Beta(III)-Tubulin- and GABA-positive neurons; however, after 15 days the cellular architecture of the differentiated Htt(140Q/140Q) cultures changed compared to Htt(7Q/7Q) cultures and included a marked increase of GFAP-positive cells. gamma-Aminobutyric Acid 98-102 huntingtin Homo sapiens 41-44 22508027-11 2012 Upon differentiation, the Htt(7Q/7Q) and Htt(140Q/140Q) generated numerous Beta(III)-Tubulin- and GABA-positive neurons; however, after 15 days the cellular architecture of the differentiated Htt(140Q/140Q) cultures changed compared to Htt(7Q/7Q) cultures and included a marked increase of GFAP-positive cells. gamma-Aminobutyric Acid 98-102 huntingtin Homo sapiens 41-44 20152113-1 2010 The density of GABA(A) receptors (GABA(A)Rs) at synapses regulates brain excitability, and altered inhibition may contribute to Huntington"s disease, which is caused by a polyglutamine repeat in the protein huntingtin. gamma-Aminobutyric Acid 15-19 huntingtin Homo sapiens 207-217 20152113-6 2010 When huntingtin is mutated, as in Huntington"s disease, GABA(A)R transport and inhibitory synaptic currents are reduced. gamma-Aminobutyric Acid 56-60 huntingtin Homo sapiens 5-15