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