PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25979114-4 2015 Here we illustrate this concept using the example of spinal and bulbar muscular atrophy, a neurodegenerative disease caused by polyglutamine expansion in the androgen receptor. polyglutamine 127-140 androgen receptor Homo sapiens 158-175 25979114-5 2015 Emerging evidence suggests that two key post-translational modifications of polyglutamine-expanded androgen receptor, namely serine phosphorylation by protein kinase B/Akt and arginine methylation by protein arginine methyltransferases, occur at the same consensus site, are mutually exclusive, and have opposing effects on neurotoxicity. polyglutamine 76-89 androgen receptor Homo sapiens 99-116 28031874-3 2015 Here, we review the role the folding of the AR plays in the pathogenesis of spinal-bulbar muscular atrophy (SBMA), a neuromuscular degenerative disease arising from expansion of the polyglutamine repeat. polyglutamine 182-195 androgen receptor Homo sapiens 44-46 29124176-1 2015 Expansion of a polyglutamine-encoding trinucleotide CAG repeat in the androgen receptor (AR) to more than 37 repeats is responsible for the X-linked neuromuscular disease spinal and bulbar muscular atrophy (SBMA). polyglutamine 15-28 androgen receptor Homo sapiens 70-87 29124176-1 2015 Expansion of a polyglutamine-encoding trinucleotide CAG repeat in the androgen receptor (AR) to more than 37 repeats is responsible for the X-linked neuromuscular disease spinal and bulbar muscular atrophy (SBMA). polyglutamine 15-28 androgen receptor Homo sapiens 89-91 29124176-1 2015 Expansion of a polyglutamine-encoding trinucleotide CAG repeat in the androgen receptor (AR) to more than 37 repeats is responsible for the X-linked neuromuscular disease spinal and bulbar muscular atrophy (SBMA). polyglutamine 15-28 androgen receptor Homo sapiens 207-211 29124176-7 2015 The possible mechanism behind these polyglutamine-induced alterations in AR function is discussed. polyglutamine 36-49 androgen receptor Homo sapiens 73-75 25663674-1 2015 Spinal and bulbar muscular atrophy (SBMA) is characterized by progressive muscle weakness linked to a polyglutamine expansion in the androgen receptor (AR). polyglutamine 102-115 androgen receptor Homo sapiens 36-40 26246877-1 2015 BACKGROUND: The androgen receptor (AR) gene contains a polymorphic trinucleotide repeat that encodes a polyglutamine tract in its N-terminal transactivation domain (N- TAD). polyglutamine 103-116 androgen receptor Homo sapiens 16-33 26246877-1 2015 BACKGROUND: The androgen receptor (AR) gene contains a polymorphic trinucleotide repeat that encodes a polyglutamine tract in its N-terminal transactivation domain (N- TAD). polyglutamine 103-116 androgen receptor Homo sapiens 35-37 25663674-1 2015 Spinal and bulbar muscular atrophy (SBMA) is characterized by progressive muscle weakness linked to a polyglutamine expansion in the androgen receptor (AR). polyglutamine 102-115 androgen receptor Homo sapiens 133-150 25663674-1 2015 Spinal and bulbar muscular atrophy (SBMA) is characterized by progressive muscle weakness linked to a polyglutamine expansion in the androgen receptor (AR). polyglutamine 102-115 androgen receptor Homo sapiens 152-154 25449082-2 2014 METHODS: Polyglutamine expansion (PQE) induced by a duplication of CAG trinucleotide tandem-repeat in exon 1 of the AR gene was detected with PCR and T-clone sequencing. polyglutamine 9-22 androgen receptor Homo sapiens 116-118 25263716-2 2015 AIB1 gene (amplified in breast cancer-1), an androgen receptor (AR) coactivator, expresses a polyglutamine (poly-Q) sequence within the carboxyl-terminal coding region. polyglutamine 93-106 androgen receptor Homo sapiens 45-62 25263716-2 2015 AIB1 gene (amplified in breast cancer-1), an androgen receptor (AR) coactivator, expresses a polyglutamine (poly-Q) sequence within the carboxyl-terminal coding region. polyglutamine 93-106 androgen receptor Homo sapiens 64-66 25263716-2 2015 AIB1 gene (amplified in breast cancer-1), an androgen receptor (AR) coactivator, expresses a polyglutamine (poly-Q) sequence within the carboxyl-terminal coding region. polyglutamine 108-114 androgen receptor Homo sapiens 45-62 25263716-2 2015 AIB1 gene (amplified in breast cancer-1), an androgen receptor (AR) coactivator, expresses a polyglutamine (poly-Q) sequence within the carboxyl-terminal coding region. polyglutamine 108-114 androgen receptor Homo sapiens 64-66 26428534-2 2015 This review focuses on the relation between BSMA and the effect of the expanded polyglutamine (poly-Q) androgen receptor (AR) on mitochondrial functions. polyglutamine 80-93 androgen receptor Homo sapiens 103-120 26428534-2 2015 This review focuses on the relation between BSMA and the effect of the expanded polyglutamine (poly-Q) androgen receptor (AR) on mitochondrial functions. polyglutamine 80-93 androgen receptor Homo sapiens 122-124 26428534-2 2015 This review focuses on the relation between BSMA and the effect of the expanded polyglutamine (poly-Q) androgen receptor (AR) on mitochondrial functions. polyglutamine 95-101 androgen receptor Homo sapiens 103-120 26428534-2 2015 This review focuses on the relation between BSMA and the effect of the expanded polyglutamine (poly-Q) androgen receptor (AR) on mitochondrial functions. polyglutamine 95-101 androgen receptor Homo sapiens 122-124 25108912-0 2014 Polyglutamine-expanded androgen receptor interferes with TFEB to elicit autophagy defects in SBMA. polyglutamine 0-13 androgen receptor Homo sapiens 93-97 25398798-2 2014 In humans, ethnic groups with higher prevalence of PCA have higher serum androgens concentrations and shorter polyglutamine (CAG) repeat lengths in the androgen receptor (AR) gene. polyglutamine 110-123 androgen receptor Homo sapiens 152-169 25398798-2 2014 In humans, ethnic groups with higher prevalence of PCA have higher serum androgens concentrations and shorter polyglutamine (CAG) repeat lengths in the androgen receptor (AR) gene. polyglutamine 110-123 androgen receptor Homo sapiens 171-173 24925468-1 2014 Spinal and bulbar muscular atrophy (SBMA, Kennedy"s disease) is a motor neuron disease caused by polyglutamine repeat expansion in the androgen receptor. polyglutamine 97-110 androgen receptor Homo sapiens 135-152 25108912-3 2014 Here we consider X-linked spinal and bulbar muscular atrophy (SBMA), a repeat disorder caused by polyglutamine-expanded androgen receptor (polyQ-AR). polyglutamine 97-110 androgen receptor Homo sapiens 62-66 25157508-1 2014 Polyglutamine expansion in the androgen receptor, causing X-linked spinal and bulbar muscular atrophy, impairs its function as a transcriptional coactivator regulating an extensive network of proteins involved in protein clearance. polyglutamine 0-13 androgen receptor Homo sapiens 31-48 24742193-1 2014 Spinal and bulbar muscular atrophy (SBMA) is a late-onset, progressive neurodegenerative disease linked to a polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 109-122 androgen receptor Homo sapiens 36-40 24742193-1 2014 Spinal and bulbar muscular atrophy (SBMA) is a late-onset, progressive neurodegenerative disease linked to a polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 124-129 androgen receptor Homo sapiens 36-40 24742458-2 2014 SBMA is caused by CAG-polyglutamine (polyQ) repeat expansions in the androgen receptor (AR) gene. polyglutamine 22-35 androgen receptor Homo sapiens 0-4 24742458-2 2014 SBMA is caused by CAG-polyglutamine (polyQ) repeat expansions in the androgen receptor (AR) gene. polyglutamine 37-42 androgen receptor Homo sapiens 0-4 25309920-1 2014 The history of polyglutamine diseases dates back approximately 20 years to the discovery of a polyglutamine repeat in the androgen receptor of SBMA followed by the identification of similar expansion mutations in Huntington"s disease, SCA1, DRPLA, and the other spinocerebellar ataxias. polyglutamine 15-28 androgen receptor Homo sapiens 122-139 25309920-1 2014 The history of polyglutamine diseases dates back approximately 20 years to the discovery of a polyglutamine repeat in the androgen receptor of SBMA followed by the identification of similar expansion mutations in Huntington"s disease, SCA1, DRPLA, and the other spinocerebellar ataxias. polyglutamine 15-28 androgen receptor Homo sapiens 143-147 23420040-2 2013 SBMA is caused by expansion of a polyglutamine (polyQ) tract in the gene coding for the androgen receptor (AR). polyglutamine 48-53 androgen receptor Homo sapiens 0-4 23644820-1 2013 Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromuscular disease caused by expansion of a polyglutamine (polyQ) tract in the androgen receptor (AR). polyglutamine 105-118 androgen receptor Homo sapiens 36-40 23644820-1 2013 Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromuscular disease caused by expansion of a polyglutamine (polyQ) tract in the androgen receptor (AR). polyglutamine 105-118 androgen receptor Homo sapiens 140-157 23644820-1 2013 Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromuscular disease caused by expansion of a polyglutamine (polyQ) tract in the androgen receptor (AR). polyglutamine 105-118 androgen receptor Homo sapiens 159-161 23644820-1 2013 Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromuscular disease caused by expansion of a polyglutamine (polyQ) tract in the androgen receptor (AR). polyglutamine 120-125 androgen receptor Homo sapiens 36-40 23644820-1 2013 Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromuscular disease caused by expansion of a polyglutamine (polyQ) tract in the androgen receptor (AR). polyglutamine 120-125 androgen receptor Homo sapiens 140-157 23644820-1 2013 Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromuscular disease caused by expansion of a polyglutamine (polyQ) tract in the androgen receptor (AR). polyglutamine 120-125 androgen receptor Homo sapiens 159-161 25182772-6 2014 However, there have been disagreements regarding the shape of these oligomers, as most studies have been carried out with peptide fragments of the androgen receptor containing different lengths of polyglutamine stretch. polyglutamine 197-210 androgen receptor Homo sapiens 147-164 25182772-7 2014 We have isolated the wild-type AR with a polyglutamine stretch of 22 (ARQ22) and a mutant receptor with a stretch of 65 (ARQ65) using a baculovirus system and have analyzed the oligomeric structures formed by these receptors with atomic force microscopy. polyglutamine 41-54 androgen receptor Homo sapiens 31-33 23656576-1 2014 Spinal and bulbar muscular atrophy, or Kennedy"s disease, is an X-linked motor neuron disease caused by polyglutamine repeat expansion in the androgen receptor. polyglutamine 104-117 androgen receptor Homo sapiens 142-159 23810450-1 2013 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron disease caused by an abnormal expansion of a tandem CAG repeat in exon 1 of the androgen receptor (AR) gene that results in an abnormally long polyglutamine tract (polyQ) in the AR protein. polyglutamine 211-224 androgen receptor Homo sapiens 36-40 23810450-1 2013 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron disease caused by an abnormal expansion of a tandem CAG repeat in exon 1 of the androgen receptor (AR) gene that results in an abnormally long polyglutamine tract (polyQ) in the AR protein. polyglutamine 211-224 androgen receptor Homo sapiens 148-165 23810450-1 2013 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron disease caused by an abnormal expansion of a tandem CAG repeat in exon 1 of the androgen receptor (AR) gene that results in an abnormally long polyglutamine tract (polyQ) in the AR protein. polyglutamine 232-237 androgen receptor Homo sapiens 36-40 23810450-1 2013 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron disease caused by an abnormal expansion of a tandem CAG repeat in exon 1 of the androgen receptor (AR) gene that results in an abnormally long polyglutamine tract (polyQ) in the AR protein. polyglutamine 232-237 androgen receptor Homo sapiens 148-165 23420040-2 2013 SBMA is caused by expansion of a polyglutamine (polyQ) tract in the gene coding for the androgen receptor (AR). polyglutamine 33-46 androgen receptor Homo sapiens 0-4 23420040-2 2013 SBMA is caused by expansion of a polyglutamine (polyQ) tract in the gene coding for the androgen receptor (AR). polyglutamine 33-46 androgen receptor Homo sapiens 88-105 23420040-2 2013 SBMA is caused by expansion of a polyglutamine (polyQ) tract in the gene coding for the androgen receptor (AR). polyglutamine 33-46 androgen receptor Homo sapiens 107-109 23420040-2 2013 SBMA is caused by expansion of a polyglutamine (polyQ) tract in the gene coding for the androgen receptor (AR). polyglutamine 48-53 androgen receptor Homo sapiens 88-105 23420040-2 2013 SBMA is caused by expansion of a polyglutamine (polyQ) tract in the gene coding for the androgen receptor (AR). polyglutamine 48-53 androgen receptor Homo sapiens 107-109 22609045-3 2012 The cause of SBMA is the expansion of a trinucleotide CAG repeat encoding a polyglutamine tract within the first exon of the androgen receptor (AR) gene. polyglutamine 76-89 androgen receptor Homo sapiens 13-17 23467468-0 2013 Androgen receptor polyglutamine repeat number: models of selection and disease susceptibility. polyglutamine 18-31 androgen receptor Homo sapiens 0-17 23467468-1 2013 Variation in polyglutamine repeat number in the androgen receptor (AR CAGn) is negatively correlated with the transcription of androgen-responsive genes and is associated with susceptibility to an extensive list of human disease. polyglutamine 13-26 androgen receptor Homo sapiens 48-65 23719921-0 2013 Cell biological approaches to investigate polyglutamine-expanded AR metabolism. polyglutamine 42-55 androgen receptor Homo sapiens 65-67 23719921-1 2013 Spinal and bulbar muscular atrophy (SBMA) is a late-onset neurodegenerative disease caused by a polyglutamine expansion in the androgen receptor (AR). polyglutamine 96-109 androgen receptor Homo sapiens 36-40 23719921-1 2013 Spinal and bulbar muscular atrophy (SBMA) is a late-onset neurodegenerative disease caused by a polyglutamine expansion in the androgen receptor (AR). polyglutamine 96-109 androgen receptor Homo sapiens 127-144 23719921-1 2013 Spinal and bulbar muscular atrophy (SBMA) is a late-onset neurodegenerative disease caused by a polyglutamine expansion in the androgen receptor (AR). polyglutamine 96-109 androgen receptor Homo sapiens 146-148 23719921-3 2013 Mutation of discreet functional domains of the AR and sites of posttranslational modification enable the detailed analysis of the role of AR function and metabolism in toxicity and aggregation of polyglutamine-expanded AR. polyglutamine 196-209 androgen receptor Homo sapiens 47-49 23719921-3 2013 Mutation of discreet functional domains of the AR and sites of posttranslational modification enable the detailed analysis of the role of AR function and metabolism in toxicity and aggregation of polyglutamine-expanded AR. polyglutamine 196-209 androgen receptor Homo sapiens 138-140 23719921-3 2013 Mutation of discreet functional domains of the AR and sites of posttranslational modification enable the detailed analysis of the role of AR function and metabolism in toxicity and aggregation of polyglutamine-expanded AR. polyglutamine 196-209 androgen receptor Homo sapiens 138-140 22609045-3 2012 The cause of SBMA is the expansion of a trinucleotide CAG repeat encoding a polyglutamine tract within the first exon of the androgen receptor (AR) gene. polyglutamine 76-89 androgen receptor Homo sapiens 125-142 22609045-3 2012 The cause of SBMA is the expansion of a trinucleotide CAG repeat encoding a polyglutamine tract within the first exon of the androgen receptor (AR) gene. polyglutamine 76-89 androgen receptor Homo sapiens 144-146 22609045-5 2012 The ligand-dependent nuclear accumulation of the polyglutamine-expanded AR protein is central to the gender-specific pathogenesis of SBMA, although additional steps, e.g., DNA binding, inter-domain interactions, and post-translational modification of AR, modify toxicity. polyglutamine 49-62 androgen receptor Homo sapiens 72-74 22609045-5 2012 The ligand-dependent nuclear accumulation of the polyglutamine-expanded AR protein is central to the gender-specific pathogenesis of SBMA, although additional steps, e.g., DNA binding, inter-domain interactions, and post-translational modification of AR, modify toxicity. polyglutamine 49-62 androgen receptor Homo sapiens 133-137 22609045-5 2012 The ligand-dependent nuclear accumulation of the polyglutamine-expanded AR protein is central to the gender-specific pathogenesis of SBMA, although additional steps, e.g., DNA binding, inter-domain interactions, and post-translational modification of AR, modify toxicity. polyglutamine 49-62 androgen receptor Homo sapiens 251-253 22609045-6 2012 The interactions with co-regulators are another requisite for the toxic properties of the polyglutamine-expanded AR. polyglutamine 90-103 androgen receptor Homo sapiens 113-115 22609045-7 2012 It is also shown that the polyglutamine-expanded AR induces diverse molecular events, such as transcriptional dysregulation, axonal transport disruption, and mitochondrial dysfunction, which play causative roles in the neurodegeneration in SBMA. polyglutamine 26-39 androgen receptor Homo sapiens 49-51 22609045-7 2012 It is also shown that the polyglutamine-expanded AR induces diverse molecular events, such as transcriptional dysregulation, axonal transport disruption, and mitochondrial dysfunction, which play causative roles in the neurodegeneration in SBMA. polyglutamine 26-39 androgen receptor Homo sapiens 240-244 22158719-2 2012 The disease is caused by the expansion of a trinucleotide CAG repeat encoding a polyglutamine tract within the first exon of the androgen receptor (AR) gene. polyglutamine 80-93 androgen receptor Homo sapiens 129-146 22796525-5 2012 Interestingly, CCT chaperonin shows higher binding affinity to polyglutamine expanded androgen receptor than that of the wild-type. polyglutamine 63-76 androgen receptor Homo sapiens 86-103 22660636-1 2012 Spinal and bulbar muscular atrophy (SBMA) is an inherited neurodegenerative disorder caused by the expansion of the polyglutamine (polyQ) tract of the androgen receptor (AR-polyQ). polyglutamine 116-129 androgen receptor Homo sapiens 36-40 22660636-1 2012 Spinal and bulbar muscular atrophy (SBMA) is an inherited neurodegenerative disorder caused by the expansion of the polyglutamine (polyQ) tract of the androgen receptor (AR-polyQ). polyglutamine 116-129 androgen receptor Homo sapiens 151-168 22660636-1 2012 Spinal and bulbar muscular atrophy (SBMA) is an inherited neurodegenerative disorder caused by the expansion of the polyglutamine (polyQ) tract of the androgen receptor (AR-polyQ). polyglutamine 131-136 androgen receptor Homo sapiens 36-40 22660636-1 2012 Spinal and bulbar muscular atrophy (SBMA) is an inherited neurodegenerative disorder caused by the expansion of the polyglutamine (polyQ) tract of the androgen receptor (AR-polyQ). polyglutamine 131-136 androgen receptor Homo sapiens 151-168 23024039-0 2012 Role of androgen receptor polyQ chain elongation in Kennedy"s disease and use of natural osmolytes as potential therapeutic targets. polyglutamine 26-31 androgen receptor Homo sapiens 8-25 23024039-2 2012 Expansion of polyQ chain length in the androgen receptor (AR) causes spinal and bulbar muscular atrophy (SBMA) or Kennedy"s disease. polyglutamine 13-18 androgen receptor Homo sapiens 39-56 23024039-2 2012 Expansion of polyQ chain length in the androgen receptor (AR) causes spinal and bulbar muscular atrophy (SBMA) or Kennedy"s disease. polyglutamine 13-18 androgen receptor Homo sapiens 58-60 23024039-2 2012 Expansion of polyQ chain length in the androgen receptor (AR) causes spinal and bulbar muscular atrophy (SBMA) or Kennedy"s disease. polyglutamine 13-18 androgen receptor Homo sapiens 105-109 23024039-9 2012 In this review, we discuss the role of polyQ chain length extension in the pathophysiology of SBMA and the use of osmolytes as potential therapeutic tool. polyglutamine 39-44 androgen receptor Homo sapiens 94-98 21940984-1 2012 Androgen receptor (AR) CAG(n) (polyglutamine) and GGN(n) (polyglycine) repeat polymorphisms determine part of the androgenic effect and may influence adiposity. polyglutamine 31-44 androgen receptor Homo sapiens 0-17 22158719-2 2012 The disease is caused by the expansion of a trinucleotide CAG repeat encoding a polyglutamine tract within the first exon of the androgen receptor (AR) gene. polyglutamine 80-93 androgen receptor Homo sapiens 148-150 20846673-2 2010 Poly-Q-expanded AR accumulates in nuclei, undergoes fragmentation and initiates degeneration and loss of motor neurons and dorsal root ganglia. polyglutamine 0-6 androgen receptor Homo sapiens 16-18 23196565-1 2012 Spinal and bulbar muscular atrophy (SBMA), or Kennedy"s disease, is an adult-onset lower motor neuron disease caused by the expansion of a trinucleotide CAG repeat encoding a polyglutamine tract within the first exon of the androgen receptor (AR) gene. polyglutamine 175-188 androgen receptor Homo sapiens 36-40 23196565-1 2012 Spinal and bulbar muscular atrophy (SBMA), or Kennedy"s disease, is an adult-onset lower motor neuron disease caused by the expansion of a trinucleotide CAG repeat encoding a polyglutamine tract within the first exon of the androgen receptor (AR) gene. polyglutamine 175-188 androgen receptor Homo sapiens 224-241 23196565-1 2012 Spinal and bulbar muscular atrophy (SBMA), or Kennedy"s disease, is an adult-onset lower motor neuron disease caused by the expansion of a trinucleotide CAG repeat encoding a polyglutamine tract within the first exon of the androgen receptor (AR) gene. polyglutamine 175-188 androgen receptor Homo sapiens 243-245 23196565-2 2012 The testosterone-dependent nuclear accumulation of polyglutamine-expanded AR protein is central to the pathogenesis. polyglutamine 51-64 androgen receptor Homo sapiens 74-76 22131404-2 2011 The androgen receptor (AR) is substantially modified, in response to hormone binding, by phosphorylation, sumoylation, and acetylation; these modifications might thus contribute to DHT-dependent polyglutamine (polyQ)-expanded AR proteotoxicity in spinal and bulbar muscular atrophy (SBMA). polyglutamine 195-208 androgen receptor Homo sapiens 23-25 22131404-2 2011 The androgen receptor (AR) is substantially modified, in response to hormone binding, by phosphorylation, sumoylation, and acetylation; these modifications might thus contribute to DHT-dependent polyglutamine (polyQ)-expanded AR proteotoxicity in spinal and bulbar muscular atrophy (SBMA). polyglutamine 195-208 androgen receptor Homo sapiens 283-287 22131404-2 2011 The androgen receptor (AR) is substantially modified, in response to hormone binding, by phosphorylation, sumoylation, and acetylation; these modifications might thus contribute to DHT-dependent polyglutamine (polyQ)-expanded AR proteotoxicity in spinal and bulbar muscular atrophy (SBMA). polyglutamine 210-215 androgen receptor Homo sapiens 4-21 22131404-2 2011 The androgen receptor (AR) is substantially modified, in response to hormone binding, by phosphorylation, sumoylation, and acetylation; these modifications might thus contribute to DHT-dependent polyglutamine (polyQ)-expanded AR proteotoxicity in spinal and bulbar muscular atrophy (SBMA). polyglutamine 210-215 androgen receptor Homo sapiens 23-25 22131404-2 2011 The androgen receptor (AR) is substantially modified, in response to hormone binding, by phosphorylation, sumoylation, and acetylation; these modifications might thus contribute to DHT-dependent polyglutamine (polyQ)-expanded AR proteotoxicity in spinal and bulbar muscular atrophy (SBMA). polyglutamine 210-215 androgen receptor Homo sapiens 283-287 22131404-4 2011 Our studies reveal that SIRT1 also offers protection against polyQ-expanded AR by deacetylating the AR at lysines 630/632/633. polyglutamine 61-66 androgen receptor Homo sapiens 76-78 22131404-4 2011 Our studies reveal that SIRT1 also offers protection against polyQ-expanded AR by deacetylating the AR at lysines 630/632/633. polyglutamine 61-66 androgen receptor Homo sapiens 100-102 22131404-5 2011 This finding suggested that nuclear AR acetylation plays a role in the aberrant metabolism and toxicity of polyQ-expanded AR. polyglutamine 107-112 androgen receptor Homo sapiens 36-38 22131404-5 2011 This finding suggested that nuclear AR acetylation plays a role in the aberrant metabolism and toxicity of polyQ-expanded AR. polyglutamine 107-112 androgen receptor Homo sapiens 122-124 22131404-6 2011 Subsequent studies revealed that the polyQ-expanded AR is hyperacetylated and that pharmacologic reduction of acetylation reduces mutant AR aggregation. polyglutamine 37-42 androgen receptor Homo sapiens 52-54 22131404-7 2011 Moreover, genetic mutation to inhibit polyQ-expanded AR acetylation of lysines 630/632/633 substantially decreased its aggregation and completely abrogated its toxicity in cell lines and motor neurons. polyglutamine 38-43 androgen receptor Homo sapiens 53-55 22131404-8 2011 Our studies also reveal one means by which the AR acetylation state likely modifies polyQ-expanded AR metabolism and toxicity, through its effect on DHT-dependent AR stabilization. polyglutamine 84-89 androgen receptor Homo sapiens 47-49 22131404-8 2011 Our studies also reveal one means by which the AR acetylation state likely modifies polyQ-expanded AR metabolism and toxicity, through its effect on DHT-dependent AR stabilization. polyglutamine 84-89 androgen receptor Homo sapiens 99-101 22131404-8 2011 Our studies also reveal one means by which the AR acetylation state likely modifies polyQ-expanded AR metabolism and toxicity, through its effect on DHT-dependent AR stabilization. polyglutamine 84-89 androgen receptor Homo sapiens 99-101 22131404-9 2011 Overall, our findings reveal a neuroprotective function of SIRT1 that operates through its deacetylation of polyQ-expanded AR and highlight the potential of both SIRT1 and AR acetylation as powerful therapeutic targets in SBMA. polyglutamine 108-113 androgen receptor Homo sapiens 123-125 21712734-12 2011 CONCLUSIONS: Shorter polyglutamine stretch in the androgen receptor correlates with more severe CAD and worse predisposing factors in postmenopausal women undergoing coronary angiography. polyglutamine 21-34 androgen receptor Homo sapiens 50-67 21664238-0 2011 Corepressor effect on androgen receptor activity varies with the length of the CAG encoded polyglutamine repeat and is dependent on receptor/corepressor ratio in prostate cancer cells. polyglutamine 91-104 androgen receptor Homo sapiens 22-39 21664238-8 2011 These data suggest that the extent to which the CAG encoded polyglutamine repeat influences AR activity represents a balance between corepressor and coactivator occupancy of the same ligand-dependent and independent AR interaction surfaces. polyglutamine 60-73 androgen receptor Homo sapiens 92-94 21664238-8 2011 These data suggest that the extent to which the CAG encoded polyglutamine repeat influences AR activity represents a balance between corepressor and coactivator occupancy of the same ligand-dependent and independent AR interaction surfaces. polyglutamine 60-73 androgen receptor Homo sapiens 216-218 21284948-5 2011 The polyQ chain length impacts AR"s ability to interact with critical coregulators, which in turn modulates its transcriptional efficacy. polyglutamine 4-9 androgen receptor Homo sapiens 31-33 21284948-7 2011 In this review article, we discuss multiple aspects of the role of polyQ chain length in the actions of the AR, their importance in prostate cancer development and progression, and SBMA with an aim to understand the underlying mechanisms involved in these diseases, which can be targeted for future therapeutic approaches. polyglutamine 67-72 androgen receptor Homo sapiens 108-110 21216197-1 2011 BACKGROUND: Spinal and bulbar muscular atrophy (SBMA) is caused by polyglutamine expansion in the androgen receptor, which results in ligand-dependent toxicity. polyglutamine 67-80 androgen receptor Homo sapiens 48-52 21216197-1 2011 BACKGROUND: Spinal and bulbar muscular atrophy (SBMA) is caused by polyglutamine expansion in the androgen receptor, which results in ligand-dependent toxicity. polyglutamine 67-80 androgen receptor Homo sapiens 98-115 20826791-1 2010 Polyglutamine expansion within the androgen receptor (AR) causes spinal and bulbar muscular atrophy (SBMA) and is associated with misfolded and aggregated species of the mutant AR. polyglutamine 0-13 androgen receptor Homo sapiens 35-52 20826791-1 2010 Polyglutamine expansion within the androgen receptor (AR) causes spinal and bulbar muscular atrophy (SBMA) and is associated with misfolded and aggregated species of the mutant AR. polyglutamine 0-13 androgen receptor Homo sapiens 54-56 20826791-1 2010 Polyglutamine expansion within the androgen receptor (AR) causes spinal and bulbar muscular atrophy (SBMA) and is associated with misfolded and aggregated species of the mutant AR. polyglutamine 0-13 androgen receptor Homo sapiens 101-105 20826791-1 2010 Polyglutamine expansion within the androgen receptor (AR) causes spinal and bulbar muscular atrophy (SBMA) and is associated with misfolded and aggregated species of the mutant AR. polyglutamine 0-13 androgen receptor Homo sapiens 177-179 22720173-1 2012 Spinal and bulbar muscular atrophy (SBMA) is the first member identified among polyglutamine diseases characterized by slowly progressive muscle weakness and atrophy of the bulbar, facial, and limb muscles pathologically associated with motor neuron loss in the spinal cord and brainstem. polyglutamine 79-92 androgen receptor Homo sapiens 36-40 22131404-2 2011 The androgen receptor (AR) is substantially modified, in response to hormone binding, by phosphorylation, sumoylation, and acetylation; these modifications might thus contribute to DHT-dependent polyglutamine (polyQ)-expanded AR proteotoxicity in spinal and bulbar muscular atrophy (SBMA). polyglutamine 195-208 androgen receptor Homo sapiens 4-21 21745497-2 2011 Expansion of polyglutamine in the androgen receptor is responsible for spinal and bulbar muscular atrophy (SBMA), a neuromuscular disorder characterized by the loss of lower motor neurons in the brainstem and spinal cord. polyglutamine 13-26 androgen receptor Homo sapiens 34-51 21745497-2 2011 Expansion of polyglutamine in the androgen receptor is responsible for spinal and bulbar muscular atrophy (SBMA), a neuromuscular disorder characterized by the loss of lower motor neurons in the brainstem and spinal cord. polyglutamine 13-26 androgen receptor Homo sapiens 107-111 19617210-1 2011 The exon-1 of the androgen receptor (AR) gene contains two repeat length polymorphisms which modify either the amount of AR protein inside the cell (GGN(n), polyglycine) or its transcriptional activity (CAG(n), polyglutamine). polyglutamine 211-224 androgen receptor Homo sapiens 18-35 19617210-1 2011 The exon-1 of the androgen receptor (AR) gene contains two repeat length polymorphisms which modify either the amount of AR protein inside the cell (GGN(n), polyglycine) or its transcriptional activity (CAG(n), polyglutamine). polyglutamine 211-224 androgen receptor Homo sapiens 37-39 21949845-0 2011 ZMIZ1 preferably enhances the transcriptional activity of androgen receptor with short polyglutamine tract. polyglutamine 87-100 androgen receptor Homo sapiens 58-75 21949845-1 2011 The androgen receptor (AR) is a ligand-induced transcription factor and contains the polyglutamine (polyQ) tracts within its N-terminal transactivation domain. polyglutamine 85-98 androgen receptor Homo sapiens 4-21 21949845-1 2011 The androgen receptor (AR) is a ligand-induced transcription factor and contains the polyglutamine (polyQ) tracts within its N-terminal transactivation domain. polyglutamine 85-98 androgen receptor Homo sapiens 23-25 21949845-1 2011 The androgen receptor (AR) is a ligand-induced transcription factor and contains the polyglutamine (polyQ) tracts within its N-terminal transactivation domain. polyglutamine 100-105 androgen receptor Homo sapiens 4-21 21949845-1 2011 The androgen receptor (AR) is a ligand-induced transcription factor and contains the polyglutamine (polyQ) tracts within its N-terminal transactivation domain. polyglutamine 100-105 androgen receptor Homo sapiens 23-25 21949845-2 2011 The length of polyQ tracts has been suggested to alter AR transcriptional activity in prostate cancer along with other endocrine and neurologic disorders. polyglutamine 14-19 androgen receptor Homo sapiens 55-57 20691641-1 2010 BACKGROUND: Spinal and bulbar muscular atrophy is a hereditary motor neuron disease caused by the expansion of a polyglutamine tract in the androgen receptor. polyglutamine 113-126 androgen receptor Homo sapiens 140-157 20410122-7 2010 Furthermore, overexpression of TbetaRII dampens polyglutamine-induced cytotoxicity in a neuroblastoma cell line expressing the pathogenic AR. polyglutamine 48-61 androgen receptor Homo sapiens 138-140 20410122-8 2010 The present study thus indicates that disruption of TGF-beta due to the transcriptional dysregulation of TbetaRII is associated with polyglutamine-induced motor neuron damage in SBMA. polyglutamine 133-146 androgen receptor Homo sapiens 178-182 19497852-0 2009 Small ubiquitin-like modifier (SUMO) modification of the androgen receptor attenuates polyglutamine-mediated aggregation. polyglutamine 86-99 androgen receptor Homo sapiens 57-74 20140226-4 2010 Sequences that flank the polyglutamine tract of AR and Htt might influence protein aggregation and toxicity through protein-protein interactions, but this has not been studied in detail. polyglutamine 25-38 androgen receptor Homo sapiens 48-50 19770590-2 2009 We have recently reported that lack of access of nuclear polyglutamine-expanded androgen receptor (AR) to the autophagic degradation pathway is a critical point in pathogenesis. polyglutamine 57-70 androgen receptor Homo sapiens 80-97 19770590-2 2009 We have recently reported that lack of access of nuclear polyglutamine-expanded androgen receptor (AR) to the autophagic degradation pathway is a critical point in pathogenesis. polyglutamine 57-70 androgen receptor Homo sapiens 99-101 19770590-3 2009 When mutant AR is contained within the cytoplasm, it can be degraded by autophagy, resulting in amelioration of its toxic effects, as has been observed in other polyglutamine expansion diseases involving cytoplasmic mutant proteins. polyglutamine 161-174 androgen receptor Homo sapiens 12-14 18289734-3 2009 Here, we demonstrate that specific sequences outside the polyQ stretch of the human androgen receptor contribute to polyQ pathology. polyglutamine 57-62 androgen receptor Homo sapiens 84-101 18289734-3 2009 Here, we demonstrate that specific sequences outside the polyQ stretch of the human androgen receptor contribute to polyQ pathology. polyglutamine 116-121 androgen receptor Homo sapiens 84-101 18289734-6 2009 In contrast, the same double mutation in an androgen receptor with an extended polyQ stretch was less toxic. polyglutamine 79-84 androgen receptor Homo sapiens 44-61 20030248-1 2009 Spinal and bulbar muscular atrophy (SBMA) is a polyglutamine-mediated lower motor neuron disease characterized by slowly progressive muscle weakness and atrophy. polyglutamine 47-60 androgen receptor Homo sapiens 36-40 19833203-3 2010 In a reporter gene assay using two-tandem repeats of an androgen response element, deletion of glutamine tracts significantly increased AR transactivation in the following order: wild-type<a single deletion of polyQ or Q5<double deletion of polyQ and Q6<double deletion of polyQ and Q5<triple deletion. polyglutamine 213-218 androgen receptor Homo sapiens 136-138 19833203-3 2010 In a reporter gene assay using two-tandem repeats of an androgen response element, deletion of glutamine tracts significantly increased AR transactivation in the following order: wild-type<a single deletion of polyQ or Q5<double deletion of polyQ and Q6<double deletion of polyQ and Q5<triple deletion. polyglutamine 247-252 androgen receptor Homo sapiens 136-138 19833203-4 2010 Deletion of polyQ alone or combined deletion of polyQ and Q5 from an AR mutant lacking the ligand-binding domain, which is constitutively active due to activation function-1, increased AR transactivation. polyglutamine 12-17 androgen receptor Homo sapiens 185-187 19833203-4 2010 Deletion of polyQ alone or combined deletion of polyQ and Q5 from an AR mutant lacking the ligand-binding domain, which is constitutively active due to activation function-1, increased AR transactivation. polyglutamine 48-53 androgen receptor Homo sapiens 185-187 19833203-6 2010 Q5, like polyQ, was found to be involved in the interaction between the NH(2)- and COOH-terminal regions of AR (N-C interaction). polyglutamine 9-14 androgen receptor Homo sapiens 108-110 19833203-7 2010 These results indicate that the inhibitory effects of polyQ and Q5 on AR transactivation are the due, at least in part, to their negative regulation of N-C interaction. polyglutamine 54-59 androgen receptor Homo sapiens 70-72 19497852-2 2009 The resulting expanded polyglutamine tract in the N-terminal region of the receptor renders AR prone to ligand-dependent misfolding and formation of oligomers and aggregates that are linked to neuronal toxicity. polyglutamine 23-36 androgen receptor Homo sapiens 92-94 19497852-6 2009 Consistent with this view, we find that gratuitous enhancement of overall SUMOylation significantly reduced the formation of polyglutamine-expanded AR aggregates without affecting the levels of the receptor. polyglutamine 125-138 androgen receptor Homo sapiens 148-150 19497852-10 2009 Our findings therefore reveal a novel function of SUMOylation and suggest that approaches that enhance AR SUMOylation may be of clinical use in polyglutamine expansion diseases. polyglutamine 144-157 androgen receptor Homo sapiens 103-105 19168451-2 2009 The AR gene has a repetitive DNA sequence in exon 1 that encodes a polyglutamine tract. polyglutamine 67-80 androgen receptor Homo sapiens 4-6 19486304-1 2009 Spinal and bulbar muscular atrophy (SBMA) is an hereditary, adult-onset, lower motor neuron disease caused by an aberrant elongation of a trinucleotide CAG repeat, which encodes the polyglutamine tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 182-195 androgen receptor Homo sapiens 36-40 19486304-1 2009 Spinal and bulbar muscular atrophy (SBMA) is an hereditary, adult-onset, lower motor neuron disease caused by an aberrant elongation of a trinucleotide CAG repeat, which encodes the polyglutamine tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 182-195 androgen receptor Homo sapiens 228-245 19486304-1 2009 Spinal and bulbar muscular atrophy (SBMA) is an hereditary, adult-onset, lower motor neuron disease caused by an aberrant elongation of a trinucleotide CAG repeat, which encodes the polyglutamine tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 182-195 androgen receptor Homo sapiens 247-249 19231085-0 2009 Polymorphism of the long polyglutamine tract in the human androgen receptor influences craving of men in alcohol withdrawal. polyglutamine 25-38 androgen receptor Homo sapiens 58-75 19383805-1 2009 OBJECTIVE: The human androgen receptor (AR) contains a polyglutamine and a polyglycine stretch which are highly polymorphic and are coded respectively by a CAG and GGN repeat in exon 1 of the AR gene. polyglutamine 55-68 androgen receptor Homo sapiens 21-38 19383805-1 2009 OBJECTIVE: The human androgen receptor (AR) contains a polyglutamine and a polyglycine stretch which are highly polymorphic and are coded respectively by a CAG and GGN repeat in exon 1 of the AR gene. polyglutamine 55-68 androgen receptor Homo sapiens 40-42 19383805-1 2009 OBJECTIVE: The human androgen receptor (AR) contains a polyglutamine and a polyglycine stretch which are highly polymorphic and are coded respectively by a CAG and GGN repeat in exon 1 of the AR gene. polyglutamine 55-68 androgen receptor Homo sapiens 192-194 19261388-5 2009 In the present study, we hypothesized that common variation in two functional polymorphisms in the androgen receptor gene, the polyglutamine (CAG) and/or polyglycine (GGN) repeats, would influence memory function in healthy subjects. polyglutamine 127-140 androgen receptor Homo sapiens 99-116 19399234-1 2009 Spinal and bulbar muscular atrophy (SBMA) is a hereditary motor neuron disease caused by the expansion of a polyglutamine tract in the androgen receptor (AR). polyglutamine 108-121 androgen receptor Homo sapiens 36-40 19237573-0 2009 Aberrant E2F activation by polyglutamine expansion of androgen receptor in SBMA neurotoxicity. polyglutamine 27-40 androgen receptor Homo sapiens 54-71 19237573-0 2009 Aberrant E2F activation by polyglutamine expansion of androgen receptor in SBMA neurotoxicity. polyglutamine 27-40 androgen receptor Homo sapiens 75-79 19237573-1 2009 Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative disorder caused by a polyglutamine repeat (polyQ) expansion within the human androgen receptor (AR). polyglutamine 108-113 androgen receptor Homo sapiens 36-40 19237573-1 2009 Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative disorder caused by a polyglutamine repeat (polyQ) expansion within the human androgen receptor (AR). polyglutamine 108-113 androgen receptor Homo sapiens 142-159 19237573-1 2009 Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative disorder caused by a polyglutamine repeat (polyQ) expansion within the human androgen receptor (AR). polyglutamine 108-113 androgen receptor Homo sapiens 161-163 19237573-6 2009 Androgen-dependent association of Rbf or Rb with AR was remarkably potentiated by aberrant polyQ expansion. polyglutamine 91-96 androgen receptor Homo sapiens 49-51 19237573-10 2009 We conclude that abnormal expansion of polyQ may potentiate innate androgen-dependent association of AR with Rb. polyglutamine 39-44 androgen receptor Homo sapiens 101-103 19399234-1 2009 Spinal and bulbar muscular atrophy (SBMA) is a hereditary motor neuron disease caused by the expansion of a polyglutamine tract in the androgen receptor (AR). polyglutamine 108-121 androgen receptor Homo sapiens 135-152 19399234-1 2009 Spinal and bulbar muscular atrophy (SBMA) is a hereditary motor neuron disease caused by the expansion of a polyglutamine tract in the androgen receptor (AR). polyglutamine 108-121 androgen receptor Homo sapiens 154-156 19100835-3 2009 A peculiar AR mutation, the CAG-repeat expansion encoding the AR-polyglutamine (polyQ) tract, generates a neurotoxic gain-of-function(s) in this mutant AR (ARpolyQ). polyglutamine 65-78 androgen receptor Homo sapiens 11-13 19100835-3 2009 A peculiar AR mutation, the CAG-repeat expansion encoding the AR-polyglutamine (polyQ) tract, generates a neurotoxic gain-of-function(s) in this mutant AR (ARpolyQ). polyglutamine 65-78 androgen receptor Homo sapiens 62-64 19100835-3 2009 A peculiar AR mutation, the CAG-repeat expansion encoding the AR-polyglutamine (polyQ) tract, generates a neurotoxic gain-of-function(s) in this mutant AR (ARpolyQ). polyglutamine 65-78 androgen receptor Homo sapiens 62-64 19100835-3 2009 A peculiar AR mutation, the CAG-repeat expansion encoding the AR-polyglutamine (polyQ) tract, generates a neurotoxic gain-of-function(s) in this mutant AR (ARpolyQ). polyglutamine 80-85 androgen receptor Homo sapiens 11-13 19100835-3 2009 A peculiar AR mutation, the CAG-repeat expansion encoding the AR-polyglutamine (polyQ) tract, generates a neurotoxic gain-of-function(s) in this mutant AR (ARpolyQ). polyglutamine 80-85 androgen receptor Homo sapiens 62-64 19100835-3 2009 A peculiar AR mutation, the CAG-repeat expansion encoding the AR-polyglutamine (polyQ) tract, generates a neurotoxic gain-of-function(s) in this mutant AR (ARpolyQ). polyglutamine 80-85 androgen receptor Homo sapiens 62-64 19228953-1 2009 Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromuscular disorder caused by a polyglutamine (polyQ) repeat expansion in the androgen receptor (AR). polyglutamine 93-106 androgen receptor Homo sapiens 36-40 19228953-1 2009 Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromuscular disorder caused by a polyglutamine (polyQ) repeat expansion in the androgen receptor (AR). polyglutamine 108-113 androgen receptor Homo sapiens 36-40 19228953-9 2009 As apoptotic mediators are candidates for toxic fragment generation and other cellular processes linked to neuron dysfunction, delineation of the apoptotic activation pathway induced by polyQ-expanded AR may shed light on the pathogenic cascade in SBMA and other motor neuron diseases. polyglutamine 186-191 androgen receptor Homo sapiens 248-252 18776683-1 2008 Abnormal polyglutamine (polyQ) expansion in the N-terminal domain of the human androgen receptor (hAR) is known to cause spinobulbar muscular atrophy (SBMA), a hereditary human neurodegenerative disorder. polyglutamine 24-29 androgen receptor Homo sapiens 79-96 18775514-1 2008 Kennedy disease (KD, or spinal and bulbar muscular atrophy) is caused by a CAG/polyglutamine expansion in the androgen receptor (AR) gene. polyglutamine 79-92 androgen receptor Homo sapiens 110-127 18775514-1 2008 Kennedy disease (KD, or spinal and bulbar muscular atrophy) is caused by a CAG/polyglutamine expansion in the androgen receptor (AR) gene. polyglutamine 79-92 androgen receptor Homo sapiens 129-131 18762554-0 2008 Consequences of poly-glutamine repeat length for the conformation and folding of the androgen receptor amino-terminal domain. polyglutamine 16-30 androgen receptor Homo sapiens 85-102 18762554-2 2008 The amino-terminal domain of the androgen receptor (AR-NTD) has a poly-Q repeat between 9 and 36 residues, which when it expands above 40 residues results in spinal bulbar muscular atrophy. polyglutamine 66-72 androgen receptor Homo sapiens 33-50 18824496-1 2009 Spinal and bulbar muscular atrophy (SBMA) is a motor neuron disease caused by polyglutamine expansion mutation in the androgen receptor (AR). polyglutamine 78-91 androgen receptor Homo sapiens 36-40 18824496-1 2009 Spinal and bulbar muscular atrophy (SBMA) is a motor neuron disease caused by polyglutamine expansion mutation in the androgen receptor (AR). polyglutamine 78-91 androgen receptor Homo sapiens 118-135 18824496-1 2009 Spinal and bulbar muscular atrophy (SBMA) is a motor neuron disease caused by polyglutamine expansion mutation in the androgen receptor (AR). polyglutamine 78-91 androgen receptor Homo sapiens 137-139 18840639-14 2009 Weaker transcriptional activity of the AR with longer CAG-encoded polyglutamine repeats appears to be totally or nearly totally compensated for by higher T levels. polyglutamine 66-79 androgen receptor Homo sapiens 39-41 19095061-1 2009 The exon 1 of the human androgen receptor (AR) gene contains two length polymorphisms of CAG (polyglutamine) and GGN (polyglycine). polyglutamine 94-107 androgen receptor Homo sapiens 24-41 19095061-1 2009 The exon 1 of the human androgen receptor (AR) gene contains two length polymorphisms of CAG (polyglutamine) and GGN (polyglycine). polyglutamine 94-107 androgen receptor Homo sapiens 43-45 18776683-1 2008 Abnormal polyglutamine (polyQ) expansion in the N-terminal domain of the human androgen receptor (hAR) is known to cause spinobulbar muscular atrophy (SBMA), a hereditary human neurodegenerative disorder. polyglutamine 24-29 androgen receptor Homo sapiens 151-155 18573880-4 2008 The overexpression of profilin reduces the aggregation of polyglutamine-expanded Htt and androgen receptor (AR) peptides. polyglutamine 58-71 androgen receptor Homo sapiens 108-110 18586675-1 2008 Huntington disease derives from a critically expanded polyglutamine tract in the huntingtin (Htt) protein; a similar polyglutamine expansion in the androgen receptor (AR) causes spinobulbar muscular atrophy. polyglutamine 117-130 androgen receptor Homo sapiens 148-165 18586675-1 2008 Huntington disease derives from a critically expanded polyglutamine tract in the huntingtin (Htt) protein; a similar polyglutamine expansion in the androgen receptor (AR) causes spinobulbar muscular atrophy. polyglutamine 117-130 androgen receptor Homo sapiens 167-169 18321505-1 2008 Kennedy Disease/Spinal Bulbar Muscular Atrophy (KD/SBMA) is a progressive neurodegenerative disease caused by genetic polyglutamine expansion of the androgen receptor. polyglutamine 118-131 androgen receptor Homo sapiens 51-55 18625411-1 2008 Polyglutamine repeat expansion in the androgen receptor is responsible for the motor neuron degeneration in X-linked spinal and bulbar muscular atrophy (SBMA; Kennedy"s disease). polyglutamine 0-13 androgen receptor Homo sapiens 38-55 18625411-1 2008 Polyglutamine repeat expansion in the androgen receptor is responsible for the motor neuron degeneration in X-linked spinal and bulbar muscular atrophy (SBMA; Kennedy"s disease). polyglutamine 0-13 androgen receptor Homo sapiens 153-157 18625411-2 2008 This mutation, like the other polyglutamine repeat expansions, has proven to be toxic itself by a gain-of-function effect; however, a growing body of evidence indicates that loss of androgen receptor normal function simultaneously contributes to SBMA disease pathology, and, conversely, that normal androgen receptor signaling mediates important trophic effects upon motor neurons. polyglutamine 30-43 androgen receptor Homo sapiens 182-199 18321505-1 2008 Kennedy Disease/Spinal Bulbar Muscular Atrophy (KD/SBMA) is a progressive neurodegenerative disease caused by genetic polyglutamine expansion of the androgen receptor. polyglutamine 118-131 androgen receptor Homo sapiens 149-166 17868456-1 2007 BACKGROUND: Huntington"s disease, spinal and bulbar muscular atrophy, and spinocerebellar ataxia 17 (SCA17) are caused by expansions in the polyglutamine (polyQ) repeats in Huntingtin protein (Htt), androgen receptor protein (AR), and TATA-binding protein (TBP), respectively. polyglutamine 140-153 androgen receptor Homo sapiens 199-216 17945479-3 2008 Surprisingly, the polymorphism involving the CAG triplet repeat expansion of the AR gene, coding for a polyglutamine (PolyGln) tract in the N-terminal transactivation domain of the AR protein, has been involved either in endocrine or neurological disorders. polyglutamine 103-116 androgen receptor Homo sapiens 81-83 17945479-3 2008 Surprisingly, the polymorphism involving the CAG triplet repeat expansion of the AR gene, coding for a polyglutamine (PolyGln) tract in the N-terminal transactivation domain of the AR protein, has been involved either in endocrine or neurological disorders. polyglutamine 103-116 androgen receptor Homo sapiens 181-183 17945479-3 2008 Surprisingly, the polymorphism involving the CAG triplet repeat expansion of the AR gene, coding for a polyglutamine (PolyGln) tract in the N-terminal transactivation domain of the AR protein, has been involved either in endocrine or neurological disorders. polyglutamine 118-125 androgen receptor Homo sapiens 81-83 17945479-3 2008 Surprisingly, the polymorphism involving the CAG triplet repeat expansion of the AR gene, coding for a polyglutamine (PolyGln) tract in the N-terminal transactivation domain of the AR protein, has been involved either in endocrine or neurological disorders. polyglutamine 118-125 androgen receptor Homo sapiens 181-183 17945479-5 2008 ; the molecular mechanisms of these alterations are thought to involve a modulation of AR transcriptional competence, which inversely correlates with the PolyGln length. polyglutamine 154-161 androgen receptor Homo sapiens 87-89 17854832-2 2008 Nuclear accumulation of mutant AR with expanded polyglutamines in motor neurons is a major pathogenic mechanism. polyglutamine 48-62 androgen receptor Homo sapiens 31-33 18263633-1 2008 Association of long polyglutamine tracts in exon 1 of the androgen receptor gene with idiopathic male infertility. polyglutamine 20-33 androgen receptor Homo sapiens 58-75 17728127-1 2007 The exon 1 of the human androgen receptor gene (AR) contains both CAG (polyglutamine) and GGN (polyglycine) repeat length polymorphisms. polyglutamine 71-84 androgen receptor Homo sapiens 24-41 17868456-1 2007 BACKGROUND: Huntington"s disease, spinal and bulbar muscular atrophy, and spinocerebellar ataxia 17 (SCA17) are caused by expansions in the polyglutamine (polyQ) repeats in Huntingtin protein (Htt), androgen receptor protein (AR), and TATA-binding protein (TBP), respectively. polyglutamine 155-160 androgen receptor Homo sapiens 199-216 17881894-6 2007 A novel method of AR modulation has been demonstrated in spinal and bulbar muscular atrophy, a disease defined by a polyglutamine repeat expansion which leads to gain-of-function changes in AR and neuromuscular pathology. polyglutamine 116-129 androgen receptor Homo sapiens 18-20 17881894-6 2007 A novel method of AR modulation has been demonstrated in spinal and bulbar muscular atrophy, a disease defined by a polyglutamine repeat expansion which leads to gain-of-function changes in AR and neuromuscular pathology. polyglutamine 116-129 androgen receptor Homo sapiens 190-192 17470458-1 2007 Spinal and bulbar muscular atrophy (SBMA) is a progressive neurodegenerative disease caused by an expansion of the polyglutamine tract in the androgen receptor (AR). polyglutamine 115-128 androgen receptor Homo sapiens 36-40 17596176-13 2007 CONCLUSIONS: Men with KD have a reduced risk of AGA, likely to be due to a functional alteration in the AR caused by the polyglutamine expansion. polyglutamine 121-134 androgen receptor Homo sapiens 104-106 17470458-1 2007 Spinal and bulbar muscular atrophy (SBMA) is a progressive neurodegenerative disease caused by an expansion of the polyglutamine tract in the androgen receptor (AR). polyglutamine 115-128 androgen receptor Homo sapiens 142-159 17470458-1 2007 Spinal and bulbar muscular atrophy (SBMA) is a progressive neurodegenerative disease caused by an expansion of the polyglutamine tract in the androgen receptor (AR). polyglutamine 115-128 androgen receptor Homo sapiens 161-163 17470458-6 2007 Furthermore, in motor neuron-derived MN-1 cells toxicity associated with polyglutamine-expanded AR is rescued by co-expression with Akt. polyglutamine 73-86 androgen receptor Homo sapiens 96-98 17122035-9 2006 These observations indicate that polyglutamine-dependent transcriptional dysregulation of dynactin 1 plays a crucial role in the reversible neuronal dysfunction in the early stage of SBMA. polyglutamine 33-46 androgen receptor Homo sapiens 183-187 17322500-1 2007 OBJECTIVE: The androgen receptor (AR) gene contains a CAG repeat polymorphism coding for a polyglutamine chain, the length of which is inversely correlated with AR transcriptional activity. polyglutamine 91-104 androgen receptor Homo sapiens 15-32 17322500-1 2007 OBJECTIVE: The androgen receptor (AR) gene contains a CAG repeat polymorphism coding for a polyglutamine chain, the length of which is inversely correlated with AR transcriptional activity. polyglutamine 91-104 androgen receptor Homo sapiens 34-36 17322500-1 2007 OBJECTIVE: The androgen receptor (AR) gene contains a CAG repeat polymorphism coding for a polyglutamine chain, the length of which is inversely correlated with AR transcriptional activity. polyglutamine 91-104 androgen receptor Homo sapiens 161-163 17447523-7 2007 SBMA is a hereditary neurodegenerative disease caused by expansion of a trinucleotide CAG repeat, which encodes the polyglutamine tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 116-129 androgen receptor Homo sapiens 0-4 17447523-7 2007 SBMA is a hereditary neurodegenerative disease caused by expansion of a trinucleotide CAG repeat, which encodes the polyglutamine tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 116-129 androgen receptor Homo sapiens 162-179 17447523-7 2007 SBMA is a hereditary neurodegenerative disease caused by expansion of a trinucleotide CAG repeat, which encodes the polyglutamine tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 116-129 androgen receptor Homo sapiens 181-183 17447523-8 2007 Animal models carrying human mutant AR gene recapitulate polyglutamine-mediated motor neuron degeneration, providing insights into the pathogenesis of SBMA. polyglutamine 57-70 androgen receptor Homo sapiens 36-38 17055185-2 2007 It is suggested here that the X-linked androgen receptor gene (AR) has a major modifying effect on speed of neuronal transmission and thus on g. The AR is polymorphic in its N-terminal transactivation domain which encodes a polyglutamine tract (CAGn) with a parametric mean of n=21 CAG repeats and normal variation between n=11 and n=30 repeats . polyglutamine 224-237 androgen receptor Homo sapiens 39-56 17185503-5 2006 In spinal and bulbar muscular atrophy (SBMA), the pathogenic gene product is polyglutamine (polyQ)-expanded androgen receptor (AR), which belongs to the Hsp90 client protein family and is known to be degraded by 17-AAG. polyglutamine 77-90 androgen receptor Homo sapiens 39-43 17185503-5 2006 In spinal and bulbar muscular atrophy (SBMA), the pathogenic gene product is polyglutamine (polyQ)-expanded androgen receptor (AR), which belongs to the Hsp90 client protein family and is known to be degraded by 17-AAG. polyglutamine 77-90 androgen receptor Homo sapiens 108-125 17185503-5 2006 In spinal and bulbar muscular atrophy (SBMA), the pathogenic gene product is polyglutamine (polyQ)-expanded androgen receptor (AR), which belongs to the Hsp90 client protein family and is known to be degraded by 17-AAG. polyglutamine 77-90 androgen receptor Homo sapiens 127-129 17185503-5 2006 In spinal and bulbar muscular atrophy (SBMA), the pathogenic gene product is polyglutamine (polyQ)-expanded androgen receptor (AR), which belongs to the Hsp90 client protein family and is known to be degraded by 17-AAG. polyglutamine 92-97 androgen receptor Homo sapiens 39-43 17185503-5 2006 In spinal and bulbar muscular atrophy (SBMA), the pathogenic gene product is polyglutamine (polyQ)-expanded androgen receptor (AR), which belongs to the Hsp90 client protein family and is known to be degraded by 17-AAG. polyglutamine 92-97 androgen receptor Homo sapiens 108-125 17185503-5 2006 In spinal and bulbar muscular atrophy (SBMA), the pathogenic gene product is polyglutamine (polyQ)-expanded androgen receptor (AR), which belongs to the Hsp90 client protein family and is known to be degraded by 17-AAG. polyglutamine 92-97 androgen receptor Homo sapiens 127-129 17185503-6 2006 We have recently demonstrated that administration of an anticancer agent 17-AAG significantly ameliorated polyQ-mediated motor neuron degeneration by reducing the total amount of mutant AR. polyglutamine 106-111 androgen receptor Homo sapiens 186-188 16804045-3 2006 Both patients had a short polyglycine (polyG) repeat of 10 residues and a relatively long polyglutamine (polyQ) repeat of 28 and 30 residues within the transactivation domain of the AR. polyglutamine 90-103 androgen receptor Homo sapiens 182-184 16804045-3 2006 Both patients had a short polyglycine (polyG) repeat of 10 residues and a relatively long polyglutamine (polyQ) repeat of 28 and 30 residues within the transactivation domain of the AR. polyglutamine 105-110 androgen receptor Homo sapiens 182-184 16813680-8 2006 However, in patients with bilateral undescended testis, a less functional androgen receptor through a longer polyglutamine chain may have a role in its pathogenesis. polyglutamine 109-122 androgen receptor Homo sapiens 74-91 16513111-2 2006 The cause of SBMA is expansion of a trinucleotide CAG repeat, which encodes the polyglutamine tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 80-93 androgen receptor Homo sapiens 13-17 16513111-2 2006 The cause of SBMA is expansion of a trinucleotide CAG repeat, which encodes the polyglutamine tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 80-93 androgen receptor Homo sapiens 126-143 16513111-2 2006 The cause of SBMA is expansion of a trinucleotide CAG repeat, which encodes the polyglutamine tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 80-93 androgen receptor Homo sapiens 145-147 16513111-5 2006 Animal models carrying human mutant AR gene recapitulate polyglutamine-mediated motor neuron degeneration, providing clues to the pathogenesis of SBMA. polyglutamine 57-70 androgen receptor Homo sapiens 36-38 16513111-5 2006 Animal models carrying human mutant AR gene recapitulate polyglutamine-mediated motor neuron degeneration, providing clues to the pathogenesis of SBMA. polyglutamine 57-70 androgen receptor Homo sapiens 146-150 16751763-1 2006 Expansion of the polyglutamine (polyQ) stretch in the androgen receptor (AR) protein leads to spinal and bulbar muscular atrophy (SBMA), a neurodegenerative disease characterized by lower motor neuron degeneration. polyglutamine 17-30 androgen receptor Homo sapiens 54-71 16751763-1 2006 Expansion of the polyglutamine (polyQ) stretch in the androgen receptor (AR) protein leads to spinal and bulbar muscular atrophy (SBMA), a neurodegenerative disease characterized by lower motor neuron degeneration. polyglutamine 17-30 androgen receptor Homo sapiens 73-75 16751763-1 2006 Expansion of the polyglutamine (polyQ) stretch in the androgen receptor (AR) protein leads to spinal and bulbar muscular atrophy (SBMA), a neurodegenerative disease characterized by lower motor neuron degeneration. polyglutamine 17-30 androgen receptor Homo sapiens 130-134 16751763-1 2006 Expansion of the polyglutamine (polyQ) stretch in the androgen receptor (AR) protein leads to spinal and bulbar muscular atrophy (SBMA), a neurodegenerative disease characterized by lower motor neuron degeneration. polyglutamine 32-37 androgen receptor Homo sapiens 54-71 16751763-1 2006 Expansion of the polyglutamine (polyQ) stretch in the androgen receptor (AR) protein leads to spinal and bulbar muscular atrophy (SBMA), a neurodegenerative disease characterized by lower motor neuron degeneration. polyglutamine 32-37 androgen receptor Homo sapiens 73-75 16751763-1 2006 Expansion of the polyglutamine (polyQ) stretch in the androgen receptor (AR) protein leads to spinal and bulbar muscular atrophy (SBMA), a neurodegenerative disease characterized by lower motor neuron degeneration. polyglutamine 32-37 androgen receptor Homo sapiens 130-134 16425262-2 2006 We evaluate how the number of polyglutamine (CAG) repeats of the AR gene influence colorectal cancer in conjunction with vitamin D, sunshine exposure and VDR. polyglutamine 30-43 androgen receptor Homo sapiens 65-67 16782802-2 2006 In the present study, subcellular association between HAP1 and androgen receptor (AR) with a long polyglutamine tract (polyQ) derived from spinal-and-bulbar-muscular-atrophy (SBMA) was examined using HEp-2 cells cotransfected with HAP1 and/or normal ARQ25, SBMA-mutant ARQ65 or deletion-mutant AR cDNAs. polyglutamine 98-111 androgen receptor Homo sapiens 63-80 16782802-2 2006 In the present study, subcellular association between HAP1 and androgen receptor (AR) with a long polyglutamine tract (polyQ) derived from spinal-and-bulbar-muscular-atrophy (SBMA) was examined using HEp-2 cells cotransfected with HAP1 and/or normal ARQ25, SBMA-mutant ARQ65 or deletion-mutant AR cDNAs. polyglutamine 98-111 androgen receptor Homo sapiens 82-84 16782802-2 2006 In the present study, subcellular association between HAP1 and androgen receptor (AR) with a long polyglutamine tract (polyQ) derived from spinal-and-bulbar-muscular-atrophy (SBMA) was examined using HEp-2 cells cotransfected with HAP1 and/or normal ARQ25, SBMA-mutant ARQ65 or deletion-mutant AR cDNAs. polyglutamine 98-111 androgen receptor Homo sapiens 139-180 16782802-2 2006 In the present study, subcellular association between HAP1 and androgen receptor (AR) with a long polyglutamine tract (polyQ) derived from spinal-and-bulbar-muscular-atrophy (SBMA) was examined using HEp-2 cells cotransfected with HAP1 and/or normal ARQ25, SBMA-mutant ARQ65 or deletion-mutant AR cDNAs. polyglutamine 98-111 androgen receptor Homo sapiens 175-179 16782802-2 2006 In the present study, subcellular association between HAP1 and androgen receptor (AR) with a long polyglutamine tract (polyQ) derived from spinal-and-bulbar-muscular-atrophy (SBMA) was examined using HEp-2 cells cotransfected with HAP1 and/or normal ARQ25, SBMA-mutant ARQ65 or deletion-mutant AR cDNAs. polyglutamine 119-124 androgen receptor Homo sapiens 63-80 16782802-2 2006 In the present study, subcellular association between HAP1 and androgen receptor (AR) with a long polyglutamine tract (polyQ) derived from spinal-and-bulbar-muscular-atrophy (SBMA) was examined using HEp-2 cells cotransfected with HAP1 and/or normal ARQ25, SBMA-mutant ARQ65 or deletion-mutant AR cDNAs. polyglutamine 119-124 androgen receptor Homo sapiens 82-84 16782802-2 2006 In the present study, subcellular association between HAP1 and androgen receptor (AR) with a long polyglutamine tract (polyQ) derived from spinal-and-bulbar-muscular-atrophy (SBMA) was examined using HEp-2 cells cotransfected with HAP1 and/or normal ARQ25, SBMA-mutant ARQ65 or deletion-mutant AR cDNAs. polyglutamine 119-124 androgen receptor Homo sapiens 139-180 16782802-2 2006 In the present study, subcellular association between HAP1 and androgen receptor (AR) with a long polyglutamine tract (polyQ) derived from spinal-and-bulbar-muscular-atrophy (SBMA) was examined using HEp-2 cells cotransfected with HAP1 and/or normal ARQ25, SBMA-mutant ARQ65 or deletion-mutant AR cDNAs. polyglutamine 119-124 androgen receptor Homo sapiens 175-179 16161040-3 2006 A polymorphic CAG repeat in exon 1 of the AR gene encodes a polyglutamine tract that is inversely correlated with the transcriptional activity of this gene. polyglutamine 60-73 androgen receptor Homo sapiens 42-44 15659427-1 2005 Spinal and bulbar muscular atrophy (SBMA) is an inherited adult onset motor neuron disease caused by the expansion of a polyglutamine (polyQ) tract within the androgen receptor (AR), affecting only males. polyglutamine 120-133 androgen receptor Homo sapiens 36-40 16079302-0 2005 Human expanded polyglutamine androgen receptor mutants in neurodegeneration as a novel ligand target. polyglutamine 15-28 androgen receptor Homo sapiens 29-46 16079302-2 2005 SBMA is caused by mutation of the expanded polyglutamine (polyQ) stretches in the AR gene. polyglutamine 43-56 androgen receptor Homo sapiens 0-4 16079302-2 2005 SBMA is caused by mutation of the expanded polyglutamine (polyQ) stretches in the AR gene. polyglutamine 43-56 androgen receptor Homo sapiens 82-84 16079302-2 2005 SBMA is caused by mutation of the expanded polyglutamine (polyQ) stretches in the AR gene. polyglutamine 58-63 androgen receptor Homo sapiens 0-4 16079302-2 2005 SBMA is caused by mutation of the expanded polyglutamine (polyQ) stretches in the AR gene. polyglutamine 58-63 androgen receptor Homo sapiens 82-84 15956082-2 2005 Previous studies have proposed that genetic factors including mosaicism, parental origin of the supernumerary X-chromosome, skewed X inactivation, and androgen receptor (AR) polyglutamine repeat length may contribute to phenotypic variability in KS. polyglutamine 174-187 androgen receptor Homo sapiens 151-168 15956082-2 2005 Previous studies have proposed that genetic factors including mosaicism, parental origin of the supernumerary X-chromosome, skewed X inactivation, and androgen receptor (AR) polyglutamine repeat length may contribute to phenotypic variability in KS. polyglutamine 174-187 androgen receptor Homo sapiens 170-172 16365010-1 2005 PURPOSE: The androgen receptor (AR) harbors a polymorphic CAG repeat sequence in exon 1, coding for a polyglutamine tract whose length inversely correlates with AR transactivation function. polyglutamine 102-115 androgen receptor Homo sapiens 13-30 16365010-1 2005 PURPOSE: The androgen receptor (AR) harbors a polymorphic CAG repeat sequence in exon 1, coding for a polyglutamine tract whose length inversely correlates with AR transactivation function. polyglutamine 102-115 androgen receptor Homo sapiens 32-34 16365010-1 2005 PURPOSE: The androgen receptor (AR) harbors a polymorphic CAG repeat sequence in exon 1, coding for a polyglutamine tract whose length inversely correlates with AR transactivation function. polyglutamine 102-115 androgen receptor Homo sapiens 161-163 15659427-1 2005 Spinal and bulbar muscular atrophy (SBMA) is an inherited adult onset motor neuron disease caused by the expansion of a polyglutamine (polyQ) tract within the androgen receptor (AR), affecting only males. polyglutamine 120-133 androgen receptor Homo sapiens 159-176 15659427-1 2005 Spinal and bulbar muscular atrophy (SBMA) is an inherited adult onset motor neuron disease caused by the expansion of a polyglutamine (polyQ) tract within the androgen receptor (AR), affecting only males. polyglutamine 120-133 androgen receptor Homo sapiens 178-180 15659427-1 2005 Spinal and bulbar muscular atrophy (SBMA) is an inherited adult onset motor neuron disease caused by the expansion of a polyglutamine (polyQ) tract within the androgen receptor (AR), affecting only males. polyglutamine 135-140 androgen receptor Homo sapiens 36-40 15659427-1 2005 Spinal and bulbar muscular atrophy (SBMA) is an inherited adult onset motor neuron disease caused by the expansion of a polyglutamine (polyQ) tract within the androgen receptor (AR), affecting only males. polyglutamine 135-140 androgen receptor Homo sapiens 159-176 15659427-1 2005 Spinal and bulbar muscular atrophy (SBMA) is an inherited adult onset motor neuron disease caused by the expansion of a polyglutamine (polyQ) tract within the androgen receptor (AR), affecting only males. polyglutamine 135-140 androgen receptor Homo sapiens 178-180 15757859-2 2005 The androgen receptor has two polymorphic sites in exon 1, with different numbers of CAG and GGC repeats, resulting in variable lengths of polyglutamine and polyglycine stretches. polyglutamine 139-152 androgen receptor Homo sapiens 4-21 15198988-1 2004 The androgen receptor (AR) gene contains a polymorphic trinucleotide repeat region, (CAG)(n), in its N-terminal transactivation domain (NTD) that encodes a polyglutamine (polyQ) tract in the receptor protein. polyglutamine 156-169 androgen receptor Homo sapiens 4-21 15954500-2 2005 In the past decade, the link between the CAG polyglutamine tract, situated on exon one of the AR gene, and reduced spermatogenesis has become a controversial one. polyglutamine 45-58 androgen receptor Homo sapiens 94-96 16433248-1 2005 Individuals whose androgen receptors have short polyglutamine tracts (resulting from CAG repeats) may have greater receptor signaling activity of the androgen receptor. polyglutamine 48-61 androgen receptor Homo sapiens 18-35 15897156-2 2005 The underlying cause of this ligand-dependent neurodegenerative disease is expansion of the CAG trinucleotide repeat in the androgen receptor (AR) gene which leads to lengthening of the polyglutamine tract in the AR protein. polyglutamine 186-199 androgen receptor Homo sapiens 124-141 15897156-2 2005 The underlying cause of this ligand-dependent neurodegenerative disease is expansion of the CAG trinucleotide repeat in the androgen receptor (AR) gene which leads to lengthening of the polyglutamine tract in the AR protein. polyglutamine 186-199 androgen receptor Homo sapiens 143-145 15897156-2 2005 The underlying cause of this ligand-dependent neurodegenerative disease is expansion of the CAG trinucleotide repeat in the androgen receptor (AR) gene which leads to lengthening of the polyglutamine tract in the AR protein. polyglutamine 186-199 androgen receptor Homo sapiens 213-215 15897156-3 2005 Recently, the effects of the polyglutamine-expanded AR have been explored in a number of cellular and animal models. polyglutamine 29-42 androgen receptor Homo sapiens 52-54 15897156-9 2005 Although the question of why only a distinct subset of neurons is affected by polyglutamine expansion of the AR remains unsolved, future research will provide further insights into the mechanisms contributing to disease progression in SBMA. polyglutamine 78-91 androgen receptor Homo sapiens 109-111 15198988-1 2004 The androgen receptor (AR) gene contains a polymorphic trinucleotide repeat region, (CAG)(n), in its N-terminal transactivation domain (NTD) that encodes a polyglutamine (polyQ) tract in the receptor protein. polyglutamine 156-169 androgen receptor Homo sapiens 23-25 15198988-1 2004 The androgen receptor (AR) gene contains a polymorphic trinucleotide repeat region, (CAG)(n), in its N-terminal transactivation domain (NTD) that encodes a polyglutamine (polyQ) tract in the receptor protein. polyglutamine 171-176 androgen receptor Homo sapiens 4-21 15198988-1 2004 The androgen receptor (AR) gene contains a polymorphic trinucleotide repeat region, (CAG)(n), in its N-terminal transactivation domain (NTD) that encodes a polyglutamine (polyQ) tract in the receptor protein. polyglutamine 171-176 androgen receptor Homo sapiens 23-25 15044606-1 2004 The androgen receptor (AR) has two polymorphic sites in exon 1, characterized by different numbers of CAG and GGC repeats resulting in variable lengths of polyglutamine and polyglycine stretches. polyglutamine 155-168 androgen receptor Homo sapiens 4-21 15044606-1 2004 The androgen receptor (AR) has two polymorphic sites in exon 1, characterized by different numbers of CAG and GGC repeats resulting in variable lengths of polyglutamine and polyglycine stretches. polyglutamine 155-168 androgen receptor Homo sapiens 23-25 15152038-2 2004 We have developed a transgenic model of the polyglutamine disease spinal and bulbar muscular atrophy (SBMA), an adult-onset, slowly progressive motor neuron disease caused by polyglutamine expansion in the androgen receptor (AR). polyglutamine 44-57 androgen receptor Homo sapiens 102-106 15151675-4 2004 The causative protein in Kennedy"s disease, with a polyglutamine expansion residing in the first N-terminal domain, is the androgen receptor. polyglutamine 51-64 androgen receptor Homo sapiens 123-140 14652007-0 2003 The polyglycine and polyglutamine repeats in the androgen receptor gene in Japanese and Caucasian populations. polyglutamine 20-33 androgen receptor Homo sapiens 49-66 14966121-2 2004 Shortening of the polymorphic N-terminal polyglutamine (poly(Q)) tract of the AR gene leads to transcriptional hyperactivity and has been correlated with an increased risk of prostate cancer. polyglutamine 41-54 androgen receptor Homo sapiens 78-80 15003278-0 2004 Degradation properties of polyglutamine-expanded human androgen receptor in transfected cells. polyglutamine 26-39 androgen receptor Homo sapiens 55-72 15003278-1 2004 Spinal and bulbar muscular atrophy is an inherited motor neuronopathy caused by the expansion of a polyglutamine sequence in the androgen receptor. polyglutamine 99-112 androgen receptor Homo sapiens 129-146 15003278-6 2004 These results suggest that the presence of an expanded polyglutamine sequence does not influence degradation rates directly and that differential regulation of steady-state levels of the androgen receptor in neurons would require neuron-specific, polyglutamine-dependent, factors. polyglutamine 247-260 androgen receptor Homo sapiens 187-204 14709594-1 2004 Spinobulbar muscular atrophy is a neurodegenerative disorder caused by expansion of a CAG triplet repeat sequence encoding a polyglutamine tract in the androgen receptor. polyglutamine 125-138 androgen receptor Homo sapiens 152-169 14743468-1 2004 BACKGROUND: The amino-terminal transcriptional activation domain of the androgen receptor (AR) gene contains two polymorphic trinucleotide repeat segments that encode polyglutamine (CAG)n and polyglycine (GGC)n tracts. polyglutamine 167-180 androgen receptor Homo sapiens 72-89 14743468-1 2004 BACKGROUND: The amino-terminal transcriptional activation domain of the androgen receptor (AR) gene contains two polymorphic trinucleotide repeat segments that encode polyglutamine (CAG)n and polyglycine (GGC)n tracts. polyglutamine 167-180 androgen receptor Homo sapiens 91-93 14698481-0 2004 The effect of polyglutamine expansion in the human androgen receptor on its ability to suppress beta-catenin-Tcf/Lef dependent transcription. polyglutamine 14-27 androgen receptor Homo sapiens 51-68 14698481-1 2004 Expansion of the polyglutamine repeat region of the androgen receptor (AR) results in Kennedy"s disease, a neurological disorder typified by degeneration of motor neurons in the brain stem and spinal cord. polyglutamine 17-30 androgen receptor Homo sapiens 52-69 14698481-1 2004 Expansion of the polyglutamine repeat region of the androgen receptor (AR) results in Kennedy"s disease, a neurological disorder typified by degeneration of motor neurons in the brain stem and spinal cord. polyglutamine 17-30 androgen receptor Homo sapiens 71-73 14698481-2 2004 As the AR has been shown to inhibit beta-catenin dependent (Wnt) signalling we asked if expansion of the polyglutamine repeats might affect this property of the protein. polyglutamine 105-118 androgen receptor Homo sapiens 7-9 14652007-1 2003 Human androgen receptor (AR) gene contains two polymorphic trinucleotide repeats of CAG and GGC, which code for polyglutamine and polyglycine tracts in the N-terminal domain in which the receptor activity resides. polyglutamine 112-125 androgen receptor Homo sapiens 6-23 14652007-1 2003 Human androgen receptor (AR) gene contains two polymorphic trinucleotide repeats of CAG and GGC, which code for polyglutamine and polyglycine tracts in the N-terminal domain in which the receptor activity resides. polyglutamine 112-125 androgen receptor Homo sapiens 25-27 15152501-1 2003 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a hereditary motor neuron disease that affects males, caused by the expansion of a polyglutamine (polyQ) tract in androgen receptor (AR). polyglutamine 162-175 androgen receptor Homo sapiens 36-40 14974917-2 2003 The length of the polyglutamine stretch of the transactivation domain (CAG repeat) of the androgen receptor (AR) inversely affects androgen activity. polyglutamine 18-31 androgen receptor Homo sapiens 90-107 14974917-2 2003 The length of the polyglutamine stretch of the transactivation domain (CAG repeat) of the androgen receptor (AR) inversely affects androgen activity. polyglutamine 18-31 androgen receptor Homo sapiens 109-111 15152501-1 2003 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a hereditary motor neuron disease that affects males, caused by the expansion of a polyglutamine (polyQ) tract in androgen receptor (AR). polyglutamine 162-175 androgen receptor Homo sapiens 193-210 15152501-1 2003 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a hereditary motor neuron disease that affects males, caused by the expansion of a polyglutamine (polyQ) tract in androgen receptor (AR). polyglutamine 162-175 androgen receptor Homo sapiens 212-214 15152501-1 2003 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a hereditary motor neuron disease that affects males, caused by the expansion of a polyglutamine (polyQ) tract in androgen receptor (AR). polyglutamine 177-182 androgen receptor Homo sapiens 36-40 15152501-1 2003 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a hereditary motor neuron disease that affects males, caused by the expansion of a polyglutamine (polyQ) tract in androgen receptor (AR). polyglutamine 177-182 androgen receptor Homo sapiens 193-210 15152501-1 2003 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a hereditary motor neuron disease that affects males, caused by the expansion of a polyglutamine (polyQ) tract in androgen receptor (AR). polyglutamine 177-182 androgen receptor Homo sapiens 212-214 15152501-3 2003 The transgenic mouse (Tg) model carrying a full-length human AR with expanded polyQ has significant gender-related motor impairment. polyglutamine 78-83 androgen receptor Homo sapiens 61-63 12824190-1 2003 Phosphorylation of the polyglutamine-expanded form of androgen receptor regulates its cleavage by caspase-3 and enhances cell death. polyglutamine 23-36 androgen receptor Homo sapiens 54-71 14691592-1 2003 BACKGROUND AND PURPOSE: The length of polymorphic CAG trinucleotide repeats in the polyglutamine region of the androgen receptor (AR) gene has been suggested to be inversely correlated with the transactivation function of the AR. polyglutamine 83-96 androgen receptor Homo sapiens 111-128 14691592-1 2003 BACKGROUND AND PURPOSE: The length of polymorphic CAG trinucleotide repeats in the polyglutamine region of the androgen receptor (AR) gene has been suggested to be inversely correlated with the transactivation function of the AR. polyglutamine 83-96 androgen receptor Homo sapiens 130-132 14691592-1 2003 BACKGROUND AND PURPOSE: The length of polymorphic CAG trinucleotide repeats in the polyglutamine region of the androgen receptor (AR) gene has been suggested to be inversely correlated with the transactivation function of the AR. polyglutamine 83-96 androgen receptor Homo sapiens 226-228 12824190-2 2003 X-linked spinal and bulbar muscular atrophy is a degenerative disease affecting motor neurons that is caused by polyglutamine (polyQ) expansion within the androgen receptor (AR). polyglutamine 112-125 androgen receptor Homo sapiens 155-172 12824190-2 2003 X-linked spinal and bulbar muscular atrophy is a degenerative disease affecting motor neurons that is caused by polyglutamine (polyQ) expansion within the androgen receptor (AR). polyglutamine 112-125 androgen receptor Homo sapiens 174-176 12824190-2 2003 X-linked spinal and bulbar muscular atrophy is a degenerative disease affecting motor neurons that is caused by polyglutamine (polyQ) expansion within the androgen receptor (AR). polyglutamine 127-132 androgen receptor Homo sapiens 155-172 12824190-2 2003 X-linked spinal and bulbar muscular atrophy is a degenerative disease affecting motor neurons that is caused by polyglutamine (polyQ) expansion within the androgen receptor (AR). polyglutamine 127-132 androgen receptor Homo sapiens 174-176 12824190-3 2003 The polyQ-expanded form of AR is cytotoxic to cells, and proteolytic cleavage enhances cell death. polyglutamine 4-9 androgen receptor Homo sapiens 27-29 12824190-6 2003 The polyQ expansion in AR activates three MAP kinase pathways, causing increasing levels of phosphorylation of p44/42, p38, and SAPK/JNK MAP kinase. polyglutamine 4-9 androgen receptor Homo sapiens 23-25 12824190-11 2003 We propose a mechanism by which phosphorylation at serine 514 of AR enhances the ability of caspase-3 to cleave AR and generate cytotoxic polyQ fragments. polyglutamine 138-143 androgen receptor Homo sapiens 65-67 12641825-3 2003 Subtle modulations of the transcriptional activity induced by the AR have also been observed and frequently assigned to a polyglutamine stretch of variable length within the N-terminal domain of the receptor. polyglutamine 122-135 androgen receptor Homo sapiens 66-68 12714591-2 2003 The N-terminal fragment of AR containing the expanded polyglutamine tract aggregates in cytoplasm and/or in nucleus and induces cell death. polyglutamine 54-67 androgen receptor Homo sapiens 27-29 12788064-0 2003 Implications of a polyglutamine tract in the function of the human androgen receptor. polyglutamine 18-31 androgen receptor Homo sapiens 67-84 12788064-2 2003 The AR gene contains a long polymorphic CAG repeat, coding for a polyglutamine tract. polyglutamine 65-78 androgen receptor Homo sapiens 4-6 12788064-3 2003 In the full size AR, the deletion of the polyglutamine tract results in an increase in the transactivation through canonical AREs. polyglutamine 41-54 androgen receptor Homo sapiens 17-19 11875046-1 2002 Spinal and bulbar muscular atrophy (SBMA) is one of a growing number of neurodegenerative diseases caused by a polyglutamine-encoding CAG trinucleotide repeat expansion, and is caused by an expansion within exon 1 of the androgen receptor (AR) gene. polyglutamine 111-124 androgen receptor Homo sapiens 36-40 12567414-3 2003 However, previous studies have suggested that the polyglutamine motif within exon 1 of the androgen receptor gene (AR) which expands in cases of spinobulbar muscular atrophy differs in that it is apparently mitotically stable. polyglutamine 50-63 androgen receptor Homo sapiens 91-108 12634316-1 2003 The androgen receptor gene has a polymorphic trinucleotide repeat that encodes a polyglutamine tract in its N-terminal transactivation domain. polyglutamine 81-94 androgen receptor Homo sapiens 4-21 12638777-6 2003 Independent of missense mutations, studies involving Singaporean, Australian, North American and Japanese subjects indicate that increases in length of a trinucleotide repeat (CAG) tract, encoding a polyglutamine stretch in the transactivation domain of the AR, are associated with increased risk of defective spermatogenesis and undermasculinization. polyglutamine 199-212 androgen receptor Homo sapiens 258-260 12478141-0 2003 Androgen receptor gene polyglutamine length is associated with testicular histology in infertile patients. polyglutamine 23-36 androgen receptor Homo sapiens 0-17 12478141-2 2003 The androgen receptor gene (AR) has a repetitive DNA sequence in exon 1 that encodes a polyglutamine tract. polyglutamine 87-100 androgen receptor Homo sapiens 4-21 12388541-1 2002 Spinal and bulbar muscular atrophy (SBMA, Kennedy"s disease) is one of a group of progressive neurodegenerative diseases resulting from a polyglutamine repeat expansion. polyglutamine 138-151 androgen receptor Homo sapiens 36-40 12189162-7 2002 Motor dysfunction was observed in both male and female animals, showing that in SBMA the polyglutamine repeat expansion causes a dominant gain-of-function mutation in the AR. polyglutamine 89-102 androgen receptor Homo sapiens 80-84 12372281-0 2002 Androgen-dependent neurodegeneration by polyglutamine-expanded human androgen receptor in Drosophila. polyglutamine 40-53 androgen receptor Homo sapiens 69-86 12372281-1 2002 Spinal and bulbar muscular atrophy (SBMA) is an X-linked, adult-onset, neurodegenerative disorder affecting only males and is caused by expanded polyglutamine (polyQ) stretches in the N-terminal A/B domain of human androgen receptor (hAR). polyglutamine 160-165 androgen receptor Homo sapiens 215-232 12161010-1 2002 The first exon of the human androgen receptor (AR) contains a translated CAG (poly-glutamine) repeat. polyglutamine 78-92 androgen receptor Homo sapiens 28-45 12161010-1 2002 The first exon of the human androgen receptor (AR) contains a translated CAG (poly-glutamine) repeat. polyglutamine 78-92 androgen receptor Homo sapiens 47-49 12648179-1 2003 BACKGROUND: The modulatory domain of the human androgen receptor gene contains a polymorphic CAG repeat coding for a polyglutamine tract. polyglutamine 117-130 androgen receptor Homo sapiens 47-64 12648179-2 2003 The length of the polyglutamine tract is inversely correlated with transcriptional activity of the androgen receptor. polyglutamine 18-31 androgen receptor Homo sapiens 99-116 12648179-3 2003 As androgens are crucial to spermatogenesis, decreased transcriptional activity of the androgen receptor associated with a long polyglutamine tract could lead to failure in spermatogenesis. polyglutamine 128-141 androgen receptor Homo sapiens 87-104 12534933-5 2003 Secondly, variations in the polymorphic poly glutamine segment within the N-terminal end of the androgen receptor have been ascribed to correlate with fertility aspects possibly because of modifications of transcriptional regulatory mechanisms. polyglutamine 40-54 androgen receptor Homo sapiens 96-113 14526186-4 2003 The molecular basis of SBMA is the expansion of a trinucleotide CAG repeat, which encodes the polyglutamine (polyQ) tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 94-107 androgen receptor Homo sapiens 23-27 14526186-4 2003 The molecular basis of SBMA is the expansion of a trinucleotide CAG repeat, which encodes the polyglutamine (polyQ) tract, in the first exon of the androgen receptor (AR) gene. polyglutamine 109-114 androgen receptor Homo sapiens 23-27 12165558-1 2002 Kennedy"s disease is a degenerative disease of motor neurons in which the causative mutation is expansion of a CAG/polyglutamine tract near the 5" end of the androgen receptor gene. polyglutamine 115-128 androgen receptor Homo sapiens 158-175 12165558-9 2002 Our findings suggest that polyglutamine expansion alters androgen receptor function by promoting its degradation and by modifying its activity as a transcription factor. polyglutamine 26-39 androgen receptor Homo sapiens 57-74 12200228-2 2002 A novel AR N-terminal-interacting protein (ARNIP) was isolated using the yeast two-hybrid system and its interaction with amino acids 11-172 of the normal or corresponding region of the polyglutamine-expanded human AR confirmed by glutathione S-transferase pulldown assays. polyglutamine 186-199 androgen receptor Homo sapiens 8-10 11875046-1 2002 Spinal and bulbar muscular atrophy (SBMA) is one of a growing number of neurodegenerative diseases caused by a polyglutamine-encoding CAG trinucleotide repeat expansion, and is caused by an expansion within exon 1 of the androgen receptor (AR) gene. polyglutamine 111-124 androgen receptor Homo sapiens 221-238 11016637-1 2000 The length of the polymorphic CAG trinucleotide repeat in the polyglutamine region of the androgen receptor (AR) gene is inversely correlated with the transactivation function of the AR. polyglutamine 62-75 androgen receptor Homo sapiens 90-107 11857028-1 2002 We have shown recently that a 15-mer phosphorothioate oligodeoxynucleotide (ODNas750/15) that hybridizes to the (CAG)n polyglutamine region of mRNA encoding human androgen receptor (AR) inhibits the expression of AR in LNCaP prostate cancer cells in vitro. polyglutamine 119-132 androgen receptor Homo sapiens 163-180 11857028-1 2002 We have shown recently that a 15-mer phosphorothioate oligodeoxynucleotide (ODNas750/15) that hybridizes to the (CAG)n polyglutamine region of mRNA encoding human androgen receptor (AR) inhibits the expression of AR in LNCaP prostate cancer cells in vitro. polyglutamine 119-132 androgen receptor Homo sapiens 182-184 11857028-1 2002 We have shown recently that a 15-mer phosphorothioate oligodeoxynucleotide (ODNas750/15) that hybridizes to the (CAG)n polyglutamine region of mRNA encoding human androgen receptor (AR) inhibits the expression of AR in LNCaP prostate cancer cells in vitro. polyglutamine 119-132 androgen receptor Homo sapiens 213-215 11766302-2 2001 Spinal and bulbar muscular atrophy (Kennedy"s disease) is an X-linked disease, resulting from expansion of the polyglutamine stretch in the N-terminal part of the androgen receptor. polyglutamine 111-124 androgen receptor Homo sapiens 163-180 11571732-4 2001 A polymorphic CAG repeat within exon 1 of the AR encodes for a polyglutamine tract, with length range of 8 to 33 repeats, which is inversely correlated with the transcriptional activity of the AR. polyglutamine 63-76 androgen receptor Homo sapiens 46-48 11571732-4 2001 A polymorphic CAG repeat within exon 1 of the AR encodes for a polyglutamine tract, with length range of 8 to 33 repeats, which is inversely correlated with the transcriptional activity of the AR. polyglutamine 63-76 androgen receptor Homo sapiens 193-195 11479228-0 2001 Short polyglutamine tracts in the androgen receptor are protective against breast cancer in the general population. polyglutamine 6-19 androgen receptor Homo sapiens 34-51 11479228-9 2001 Short polyglutamine repeats in the AR protein have been reported to be associated with an increase in the capacity of the receptor to activate transcription of reporter genes in vitro. polyglutamine 6-19 androgen receptor Homo sapiens 35-37 11479228-11 2001 This suggests that differences in the number of polyglutamines in the AR protein may influence individual risk of breast cancer, especially in postmenopausal women, and that this apparent protection could be the consequence of an increased response/sensitivity to androgens. polyglutamine 48-62 androgen receptor Homo sapiens 70-72 11443190-0 2001 Evidence that longer androgen receptor polyglutamine repeats are a causal factor for genital abnormalities. polyglutamine 39-52 androgen receptor Homo sapiens 21-38 11443190-1 2001 Moderate to severe undermasculinized genitalia was recently shown to be associated with longer polyglutamine repeats within the androgen receptor [AR(Gln)n]. polyglutamine 95-108 androgen receptor Homo sapiens 128-145 11331614-1 2001 We generated transgenic mice that expressed a highly expanded 239 polyglutamine (polyQ) repeat under the control of the human androgen receptor promoter. polyglutamine 66-79 androgen receptor Homo sapiens 126-143 11331614-1 2001 We generated transgenic mice that expressed a highly expanded 239 polyglutamine (polyQ) repeat under the control of the human androgen receptor promoter. polyglutamine 81-86 androgen receptor Homo sapiens 126-143 11400322-12 2001 As for the therapeutic strategies, the overexpression of Hsp70 and Hsp40 chaperones acted together to protect a cultured neuronal cell model of SBMA from inclusion formation and cell death by mutant AR with expanded polyglutamine tract. polyglutamine 216-229 androgen receptor Homo sapiens 144-148 11732276-2 2001 A degenerative process of the motor neurons is associated with an increase in the number of CAG repeats encoding a polyglutamine stretch within the androgen receptor. polyglutamine 115-128 androgen receptor Homo sapiens 148-165 12481545-10 2002 Although these findings provide insight into the toxic function of the expanded polyglutamine protein, additional investigations have led to the finding that intrinsic AR transactivational function is somewhat diminished in the presence of the expanded polyglutamine; this likely leads to the partial androgen insensitivity that characterizes patients with SBMA. polyglutamine 253-266 androgen receptor Homo sapiens 357-361 11719253-0 2001 Polyglutamine tract expansion of the androgen receptor in a motoneuronal model of spinal and bulbar muscular atrophy. polyglutamine 0-13 androgen receptor Homo sapiens 37-54 11719253-3 2001 The identification of polyQ expansion in SBMA led to the discovery of an entire class of neurodegenerative disorders. polyglutamine 22-27 androgen receptor Homo sapiens 41-45 11719263-1 2001 Spinobulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by the expansion of the polyglutamine (polyGln) tract in the human androgen receptor (hAR). polyglutamine 98-111 androgen receptor Homo sapiens 30-34 11719263-1 2001 Spinobulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by the expansion of the polyglutamine (polyGln) tract in the human androgen receptor (hAR). polyglutamine 98-111 androgen receptor Homo sapiens 141-158 11719263-1 2001 Spinobulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by the expansion of the polyglutamine (polyGln) tract in the human androgen receptor (hAR). polyglutamine 113-120 androgen receptor Homo sapiens 30-34 11719263-1 2001 Spinobulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by the expansion of the polyglutamine (polyGln) tract in the human androgen receptor (hAR). polyglutamine 113-120 androgen receptor Homo sapiens 141-158 15111251-9 2001 Surprisingly, addition of Mibolerone a synthetic androgen significantly decreased inclusion formation in both WT and polyGln-expanded AR-transfected cells. polyglutamine 117-124 androgen receptor Homo sapiens 134-136 11396657-6 2001 Studies involving Singaporean, Australian, North American and Japanese subjects have established that increases in length of a trinucleotide repeat (CAG) tract, encoding a polyglutamine stretch in the transactivation domain of the androgen receptor, are associated with increased risk of defective spermatogenesis and undermasculinization. polyglutamine 172-185 androgen receptor Homo sapiens 231-248 11335100-1 2001 Spinal bulbar muscular atrophy (SBMA) is one of a family of inherited neurodegenerative diseases caused by expansion of CAG encoding polyglutamine repeats; in SBMA the affected gene is the androgen receptor. polyglutamine 133-146 androgen receptor Homo sapiens 32-36 11335100-1 2001 Spinal bulbar muscular atrophy (SBMA) is one of a family of inherited neurodegenerative diseases caused by expansion of CAG encoding polyglutamine repeats; in SBMA the affected gene is the androgen receptor. polyglutamine 133-146 androgen receptor Homo sapiens 189-206 11155740-11 2000 Our data indicate that ARA24 could also interact with AR, and that this binding is decreased by an expanding poly-glutamine (Q) length within AR. polyglutamine 109-123 androgen receptor Homo sapiens 23-25 11155740-11 2000 Our data indicate that ARA24 could also interact with AR, and that this binding is decreased by an expanding poly-glutamine (Q) length within AR. polyglutamine 109-123 androgen receptor Homo sapiens 54-56 11155740-12 2000 The length of the poly-Q stretch in the AR N-terminal domain is inversely correlated with the transcriptional activity of AR. polyglutamine 18-24 androgen receptor Homo sapiens 40-42 11016637-1 2000 The length of the polymorphic CAG trinucleotide repeat in the polyglutamine region of the androgen receptor (AR) gene is inversely correlated with the transactivation function of the AR. polyglutamine 62-75 androgen receptor Homo sapiens 109-111 11016637-1 2000 The length of the polymorphic CAG trinucleotide repeat in the polyglutamine region of the androgen receptor (AR) gene is inversely correlated with the transactivation function of the AR. polyglutamine 62-75 androgen receptor Homo sapiens 183-185 11016637-12 2000 Because of the significance of AR in prostate cancer, investigation of factors that interact with the polyglutamine region of the AR gene to alter AR function and modulate prostate cancer risk is an important area for future research. polyglutamine 102-115 androgen receptor Homo sapiens 130-132 11016637-12 2000 Because of the significance of AR in prostate cancer, investigation of factors that interact with the polyglutamine region of the AR gene to alter AR function and modulate prostate cancer risk is an important area for future research. polyglutamine 102-115 androgen receptor Homo sapiens 130-132 10727996-10 1999 N-terminal polyglutamine tract expansion limits AR transactivation, causing a form of mild androgen insensitivity. polyglutamine 11-24 androgen receptor Homo sapiens 48-50 10917202-4 2000 Among the various AR antisense ODNs tested, a 15-base ODN targeting the CAG repeats encoding the poly-glutamine region of the AR (as750/15) was found to be most effective. polyglutamine 97-111 androgen receptor Homo sapiens 18-20 10917202-4 2000 Among the various AR antisense ODNs tested, a 15-base ODN targeting the CAG repeats encoding the poly-glutamine region of the AR (as750/15) was found to be most effective. polyglutamine 97-111 androgen receptor Homo sapiens 126-128 10749991-0 2000 Longer polyglutamine tracts in the androgen receptor are associated with moderate to severe undermasculinized genitalia in XY males. polyglutamine 7-20 androgen receptor Homo sapiens 35-52 10639135-1 2000 Spinobulbar muscular atrophy and Huntington"s disease are caused by polyglutamine expansion in the androgen receptor and huntingtin, respectively, and their pathogenesis has been associated with abnormal nuclear localization and aggregation of truncated forms of these proteins. polyglutamine 68-81 androgen receptor Homo sapiens 99-116 10643885-2 1999 The androgen receptor contains a polymorphic polyglutamine repeat and expansion of this repeat to beyond approximately 40 causes spinobulbar muscular atrophy (SBMA; also known as Kennedy"s disease), a genetic form of motor neurone disease. polyglutamine 45-58 androgen receptor Homo sapiens 4-21 10643885-2 1999 The androgen receptor contains a polymorphic polyglutamine repeat and expansion of this repeat to beyond approximately 40 causes spinobulbar muscular atrophy (SBMA; also known as Kennedy"s disease), a genetic form of motor neurone disease. polyglutamine 45-58 androgen receptor Homo sapiens 159-163 10643885-3 1999 Here we show that the size of this polyglutamine tract influences both c-Jun regulation of androgen receptor-mediated transcription and androgen receptor regulation of c-Jun activity. polyglutamine 35-48 androgen receptor Homo sapiens 91-108 10643885-3 1999 Here we show that the size of this polyglutamine tract influences both c-Jun regulation of androgen receptor-mediated transcription and androgen receptor regulation of c-Jun activity. polyglutamine 35-48 androgen receptor Homo sapiens 136-153 10999852-3 2000 All androgens act through the X-linked androgen receptor (AR), the N-terminal domain of which contains a polyglutamine tract encoded by a highly polymorphic CAG trinucleotide repeat tract. polyglutamine 105-118 androgen receptor Homo sapiens 39-56 10928291-2 2000 At least nine disorders result from a CAG trinucleotide repeat expansion which is translated into a polyglutamine stretch in the respective proteins: Huntington"s disease (HD), dentatorubral pallidolysian atrophy (DRPLA), spinal bulbar muscular atrophy (SBMA), and several of the spinocerebellar ataxias (SCA1, 2, 3, 6, 7 and 12). polyglutamine 100-113 androgen receptor Homo sapiens 254-258 10769019-0 2000 Cytoplasmic localization and the choice of ligand determine aggregate formation by androgen receptor with amplified polyglutamine stretch. polyglutamine 116-129 androgen receptor Homo sapiens 83-100 10722721-0 2000 Chaperones Hsp70 and Hsp40 suppress aggregate formation and apoptosis in cultured neuronal cells expressing truncated androgen receptor protein with expanded polyglutamine tract. polyglutamine 158-171 androgen receptor Homo sapiens 118-135 10722721-1 2000 Spinal and bulbar muscular atrophy (SBMA) is one of a group of human inherited neurodegenerative diseases caused by polyglutamine expansion. polyglutamine 116-129 androgen receptor Homo sapiens 36-40 10694266-1 2000 The androgen receptor (AR) gene, located on the X-chromosome at Xq11-12, contains in exon 1 a polymorphic CAG repeat which codes for a polyglutamine tract. polyglutamine 135-148 androgen receptor Homo sapiens 4-21 10694266-1 2000 The androgen receptor (AR) gene, located on the X-chromosome at Xq11-12, contains in exon 1 a polymorphic CAG repeat which codes for a polyglutamine tract. polyglutamine 135-148 androgen receptor Homo sapiens 23-25 10502720-1 1999 Several reports have suggested that one or both of the trinucleotide repeat polymorphisms in the human androgen receptor (hAR) gene, (CAG)n coding for polyglutamine and (GGC)n coding for polyglycine, may be associated with prostate cancer risk; but no study has investigated their association with disease progression. polyglutamine 151-164 androgen receptor Homo sapiens 103-120 10400640-0 1999 The linkage of Kennedy"s neuron disease to ARA24, the first identified androgen receptor polyglutamine region-associated coactivator. polyglutamine 89-102 androgen receptor Homo sapiens 71-88 10400640-1 1999 Although the linkage of polyglutamine (poly-Q) repeat expansion in the androgen receptor (AR) to Kennedy"s disease (X-linked spinal and bulbar muscular atrophy) was a major step forward, the detailed molecular mechanism of how the change in poly-Q length contributes to the disease remains unclear. polyglutamine 24-37 androgen receptor Homo sapiens 71-88 10400640-1 1999 Although the linkage of polyglutamine (poly-Q) repeat expansion in the androgen receptor (AR) to Kennedy"s disease (X-linked spinal and bulbar muscular atrophy) was a major step forward, the detailed molecular mechanism of how the change in poly-Q length contributes to the disease remains unclear. polyglutamine 24-37 androgen receptor Homo sapiens 90-92 10400640-1 1999 Although the linkage of polyglutamine (poly-Q) repeat expansion in the androgen receptor (AR) to Kennedy"s disease (X-linked spinal and bulbar muscular atrophy) was a major step forward, the detailed molecular mechanism of how the change in poly-Q length contributes to the disease remains unclear. polyglutamine 39-45 androgen receptor Homo sapiens 71-88 10400640-1 1999 Although the linkage of polyglutamine (poly-Q) repeat expansion in the androgen receptor (AR) to Kennedy"s disease (X-linked spinal and bulbar muscular atrophy) was a major step forward, the detailed molecular mechanism of how the change in poly-Q length contributes to the disease remains unclear. polyglutamine 39-45 androgen receptor Homo sapiens 90-92 10400640-1 1999 Although the linkage of polyglutamine (poly-Q) repeat expansion in the androgen receptor (AR) to Kennedy"s disease (X-linked spinal and bulbar muscular atrophy) was a major step forward, the detailed molecular mechanism of how the change in poly-Q length contributes to the disease remains unclear. polyglutamine 241-247 androgen receptor Homo sapiens 71-88 10400640-1 1999 Although the linkage of polyglutamine (poly-Q) repeat expansion in the androgen receptor (AR) to Kennedy"s disease (X-linked spinal and bulbar muscular atrophy) was a major step forward, the detailed molecular mechanism of how the change in poly-Q length contributes to the disease remains unclear. polyglutamine 241-247 androgen receptor Homo sapiens 90-92 10400640-2 1999 Here we report the identification of a nuclear G-protein, Ras-related nuclear protein/ARA24, as the first AR coactivator that can bind differentially with different lengths of poly-Q within AR. polyglutamine 176-182 androgen receptor Homo sapiens 86-88 10400640-2 1999 Here we report the identification of a nuclear G-protein, Ras-related nuclear protein/ARA24, as the first AR coactivator that can bind differentially with different lengths of poly-Q within AR. polyglutamine 176-182 androgen receptor Homo sapiens 106-108 10400640-3 1999 In the yeast and mammalian reciprocal interacting assays, our data suggested the interaction of AR N-terminal domain with ARA24 diminishes as the poly-Q length increases. polyglutamine 146-152 androgen receptor Homo sapiens 96-98 10400640-4 1999 The coactivation of ARA24 also diminishes with the poly-Q expansion within AR. polyglutamine 51-57 androgen receptor Homo sapiens 20-22 10222781-5 1999 Therefore the expansion in the polyglutamine stretch may induce some pathological aberrations in transcriptional regulation and translocation of AR in SBMA. polyglutamine 31-44 androgen receptor Homo sapiens 151-155 10434308-1 1999 Kennedy"s disease is an X-linked form of motor neuron disease caused by an expanded polyglutamine repeat in the androgen receptor. polyglutamine 84-97 androgen receptor Homo sapiens 112-129 10495104-5 1999 Even when specific deficits have been identified, for example, mutations of the superoxide dismutase-1 gene in familial amyotrophic sclerosis and polyglutamine expansion of the androgen receptor in spinal and bulbar muscular atrophy, the mechanisms by which somatic motor neuronal degeneration occurs remain unclear. polyglutamine 146-159 androgen receptor Homo sapiens 177-194 10196362-1 1999 Spinal bulbar muscular atrophy is a neurodegenerative disorder caused by a polyglutamine expansion in the androgen receptor (AR). polyglutamine 75-88 androgen receptor Homo sapiens 106-123 10196362-1 1999 Spinal bulbar muscular atrophy is a neurodegenerative disorder caused by a polyglutamine expansion in the androgen receptor (AR). polyglutamine 75-88 androgen receptor Homo sapiens 125-127 10222782-1 1999 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motor caused by expansion of a polyglutamine repeat within the androgen receptor(AR). polyglutamine 88-101 androgen receptor Homo sapiens 36-40 10222782-1 1999 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motor caused by expansion of a polyglutamine repeat within the androgen receptor(AR). polyglutamine 88-101 androgen receptor Homo sapiens 120-137 10222782-4 1999 These results indicate that the polyglutamine repeat length-dependent aggregation may be a likely molecular basis for the toxic gain of AR function that produces neuronal degeneration in SBMA. polyglutamine 32-45 androgen receptor Homo sapiens 187-191 9537231-10 1998 No germ-line AR mutations were found in the present material, but the number of AR polyglutamine repeats tended to be lower among mutation carriers. polyglutamine 83-96 androgen receptor Homo sapiens 80-82 9886069-1 1999 X-linked spinal and bulbar muscular atrophy (SBMA), Kennedy"s disease, is a degenerative disease of the motor neurons that is associated with an increase in the number of CAG repeats encoding a polyglutamine stretch within the androgen receptor (AR). polyglutamine 194-207 androgen receptor Homo sapiens 45-49 9886069-1 1999 X-linked spinal and bulbar muscular atrophy (SBMA), Kennedy"s disease, is a degenerative disease of the motor neurons that is associated with an increase in the number of CAG repeats encoding a polyglutamine stretch within the androgen receptor (AR). polyglutamine 194-207 androgen receptor Homo sapiens 227-244 9886069-1 1999 X-linked spinal and bulbar muscular atrophy (SBMA), Kennedy"s disease, is a degenerative disease of the motor neurons that is associated with an increase in the number of CAG repeats encoding a polyglutamine stretch within the androgen receptor (AR). polyglutamine 194-207 androgen receptor Homo sapiens 246-248 9886069-4 1999 Here, we report the first conclusive evidence that caspase cleavage is a critical step in cytotoxicity; the expression of the AR with an expanded polyglutamine stretch enhances its ability to induce apoptosis when compared with the normal AR. polyglutamine 146-159 androgen receptor Homo sapiens 126-128 9813160-0 1998 Caspase-3 cleaves the expanded androgen receptor protein of spinal and bulbar muscular atrophy in a polyglutamine repeat length-dependent manner. polyglutamine 100-113 androgen receptor Homo sapiens 31-48 9813160-1 1998 Spinal and bulbar muscular atrophy (SBMA) is one of a group of human inherited neurodegenerative diseases caused by polyglutamine expansion. polyglutamine 116-129 androgen receptor Homo sapiens 36-40 9813160-4 1998 We now report that in vitro translated full-length AR proteins containing different sized polyglutamine repeats (24, 65 and 97 repeats, respectively) are specifically cleaved by recombinant caspase-3, liberating a polyglutamine containing fragment, and that the susceptibility to cleavage is polyglutamine repeat length-dependent. polyglutamine 90-103 androgen receptor Homo sapiens 51-53 9813160-4 1998 We now report that in vitro translated full-length AR proteins containing different sized polyglutamine repeats (24, 65 and 97 repeats, respectively) are specifically cleaved by recombinant caspase-3, liberating a polyglutamine containing fragment, and that the susceptibility to cleavage is polyglutamine repeat length-dependent. polyglutamine 214-227 androgen receptor Homo sapiens 51-53 9813160-4 1998 We now report that in vitro translated full-length AR proteins containing different sized polyglutamine repeats (24, 65 and 97 repeats, respectively) are specifically cleaved by recombinant caspase-3, liberating a polyglutamine containing fragment, and that the susceptibility to cleavage is polyglutamine repeat length-dependent. polyglutamine 214-227 androgen receptor Homo sapiens 51-53 9733433-2 1998 To further define the subregions/genes in the Y chromosome causing male infertility and its relationship to polymorphisms of the AR polyglutamine tract, we screened the genomic DNA of 202 subfertile males and 101 healthy fertile controls of predominantly Chinese ethnic origin. polyglutamine 132-145 androgen receptor Homo sapiens 129-131 9733433-10 1998 Y microdeletions and long AR polyglutamine tracts appear to be independent contributors to male infertility. polyglutamine 29-42 androgen receptor Homo sapiens 26-28 9829547-5 1998 Up to 20% of infertile males have reduced androgenicity caused by an increase in length of a polymorphic trinucleotide (CAG) repeat segment, encoding a polyglutamine tract, of the androgen receptor. polyglutamine 152-165 androgen receptor Homo sapiens 180-197 9499423-1 1998 Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by the expansion of a polyglutamine repeat within the androgen receptor (AR). polyglutamine 102-115 androgen receptor Homo sapiens 36-40 9499423-1 1998 Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by the expansion of a polyglutamine repeat within the androgen receptor (AR). polyglutamine 102-115 androgen receptor Homo sapiens 134-151 9499423-1 1998 Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by the expansion of a polyglutamine repeat within the androgen receptor (AR). polyglutamine 102-115 androgen receptor Homo sapiens 153-155 9499423-2 1998 We have studied the mutant AR in an in vitro system, and find both aggregation and proteolytic processing of the AR protein to occur in a polyglutamine repeat length-dependent manner. polyglutamine 138-151 androgen receptor Homo sapiens 113-115 9360540-0 1997 Long polyglutamine tracts in the androgen receptor are associated with reduced trans-activation, impaired sperm production, and male infertility. polyglutamine 5-18 androgen receptor Homo sapiens 33-50 9360540-1 1997 The X-linked androgen receptor (AR) gene contains two polymorphic trinucleotide repeat segments that code for polyglutamine and polyglycine tracts in the N-terminal trans-activation domain of the AR protein. polyglutamine 110-123 androgen receptor Homo sapiens 32-34 9360540-1 1997 The X-linked androgen receptor (AR) gene contains two polymorphic trinucleotide repeat segments that code for polyglutamine and polyglycine tracts in the N-terminal trans-activation domain of the AR protein. polyglutamine 110-123 androgen receptor Homo sapiens 196-198 9360540-11 1997 The data indicate a direct relation between length of the AR polyglutamine tract and the risk of defective spermatogenesis that is attributable to the decreased functional competence of AR with longer glutamine tracts. polyglutamine 61-74 androgen receptor Homo sapiens 58-60 9360540-11 1997 The data indicate a direct relation between length of the AR polyglutamine tract and the risk of defective spermatogenesis that is attributable to the decreased functional competence of AR with longer glutamine tracts. polyglutamine 61-74 androgen receptor Homo sapiens 186-188 9360540-1 1997 The X-linked androgen receptor (AR) gene contains two polymorphic trinucleotide repeat segments that code for polyglutamine and polyglycine tracts in the N-terminal trans-activation domain of the AR protein. polyglutamine 110-123 androgen receptor Homo sapiens 13-30 7641413-6 1995 The purpose of this study was to evaluate the use of the polyglutamine and polyglycine trinucleotide repeat polymorphisms in the first exon of the androgen receptor gene for carrier status determination in three CAIS families. polyglutamine 57-70 androgen receptor Homo sapiens 147-164 9211187-2 1997 The disease mechanism likely involves toxicity of an expanded polyglutamine tract in the androgen receptor protein. polyglutamine 62-75 androgen receptor Homo sapiens 89-106 8732995-10 1996 The molecular cause of spinal and bulbar muscle atrophy is an expanded length (> 40 residues) of one of the polyglutamine stretches in the N-terminal domain of the androgen receptor. polyglutamine 108-121 androgen receptor Homo sapiens 164-181 8867072-1 1996 The mutation in X-linked bulbospinal muscular atrophy (XBSMA) is an increased CAG triplet repeat coding for a polyglutamine domain in the gene for the androgen receptor. polyglutamine 110-123 androgen receptor Homo sapiens 151-168 7626493-10 1995 The X-linked spinal and bulbar muscle atrophy (SBMA; Kennedy"s disease) is associated with an expanded length (> 40 residues) of one of the polyglutamine stretches in the N-terminal domain of the androgen receptor. polyglutamine 140-153 androgen receptor Homo sapiens 47-51 7626493-10 1995 The X-linked spinal and bulbar muscle atrophy (SBMA; Kennedy"s disease) is associated with an expanded length (> 40 residues) of one of the polyglutamine stretches in the N-terminal domain of the androgen receptor. polyglutamine 140-153 androgen receptor Homo sapiens 196-213 34417184-1 2021 Spinal and bulbar muscular atrophy (SBMA) is an X-linked, adult-onset neuromuscular condition caused by an abnormal polyglutamine (polyQ) tract expansion in androgen receptor (AR) protein. polyglutamine 116-129 androgen receptor Homo sapiens 36-40 1423334-8 1992 A considerable variation in the length of one of the polyglutamine repeats has been reported in the aminoterminal transcription regulating domain of the wild type androgen receptor. polyglutamine 53-66 androgen receptor Homo sapiens 163-180 34723064-2 2021 There is a polymorphism site in exon 1 of the gene encoding this receptor that can have different frequencies of CAG trinucleotide repeats and leads to the formation of polyglutamine chains of different lengths in the N-terminal domain of the AR protein and reduced sperm production by affecting spermatogenesis. polyglutamine 169-182 androgen receptor Homo sapiens 243-245 18407238-3 1994 The resulting androgen receptor (AR) protein has an expanded polyglutamine tract in its NH(2)-terminal modulatory domain, and is postulated to lose a basic, intrinsic function that causes a mild form of androgen insensitivity; however, almost certainly, it also gains a novel, extrinsic function that is selectively neuronotoxic. polyglutamine 61-74 androgen receptor Homo sapiens 14-31 18407238-3 1994 The resulting androgen receptor (AR) protein has an expanded polyglutamine tract in its NH(2)-terminal modulatory domain, and is postulated to lose a basic, intrinsic function that causes a mild form of androgen insensitivity; however, almost certainly, it also gains a novel, extrinsic function that is selectively neuronotoxic. polyglutamine 61-74 androgen receptor Homo sapiens 33-35 34417184-1 2021 Spinal and bulbar muscular atrophy (SBMA) is an X-linked, adult-onset neuromuscular condition caused by an abnormal polyglutamine (polyQ) tract expansion in androgen receptor (AR) protein. polyglutamine 131-136 androgen receptor Homo sapiens 36-40 35204656-5 2022 Here, we performed a mirror image phage display selection on the polyglutamine containing a fragment of the androgen receptor. polyglutamine 65-78 androgen receptor Homo sapiens 108-125 35204656-7 2022 The selected D-enantiomeric peptides were tested for their ability to inhibit polyglutamine-induced androgen receptor aggregation. polyglutamine 78-91 androgen receptor Homo sapiens 100-117 34986150-0 2022 Poly-glutamine-dependent self-association as a potential mechanism for regulation of androgen receptor activity. polyglutamine 0-14 androgen receptor Homo sapiens 85-102 35052449-2 2022 Spinal and bulbar muscular atrophy (SBMA) is an X-linked and adult-onset neurodegenerative disorder caused by the expansion of trinucleotide cytosine-adenine-guanine repeats, which encodes a polyglutamine tract in the androgen receptor gene. polyglutamine 191-204 androgen receptor Homo sapiens 36-40 35052449-2 2022 Spinal and bulbar muscular atrophy (SBMA) is an X-linked and adult-onset neurodegenerative disorder caused by the expansion of trinucleotide cytosine-adenine-guanine repeats, which encodes a polyglutamine tract in the androgen receptor gene. polyglutamine 191-204 androgen receptor Homo sapiens 218-235 34986150-7 2022 We also show that the AR-NTD can undergo liquid-liquid phase separation in vitro, with longer polyQ sequences phase separating more readily. polyglutamine 94-99 androgen receptor Homo sapiens 22-24 34986150-8 2022 Moreover, longer polyQ sequences hinder nuclear localization in the absence of hormone and increase the propensity for formation of AR-containing puncta in the nucleus of cells treated with dihydrotestosterone. polyglutamine 17-22 androgen receptor Homo sapiens 132-134 34986150-9 2022 These results lead us to hypothesize that polyQ-dependent liquid-liquid phase separation may provide a mechanism to decrease the transcriptional activity of AR, potentially opening new opportunities to design effective therapies against CRPC and muscular atrophy. polyglutamine 42-47 androgen receptor Homo sapiens 157-159 32019272-1 2020 Polyglutamine (polyQ) expansions in the androgen receptor (AR) gene cause spinal and bulbar muscular atrophy (SBMA), a neuromuscular disease characterized by lower motor neuron (MN) loss and skeletal muscle atrophy, with an unknown mechanism. polyglutamine 0-13 androgen receptor Homo sapiens 110-114 34021780-1 2021 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansions in the androgen receptor (AR) gene. polyglutamine 79-92 androgen receptor Homo sapiens 36-40 34021780-1 2021 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansions in the androgen receptor (AR) gene. polyglutamine 79-92 androgen receptor Homo sapiens 119-136 34021780-1 2021 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansions in the androgen receptor (AR) gene. polyglutamine 79-92 androgen receptor Homo sapiens 138-140 34021780-1 2021 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansions in the androgen receptor (AR) gene. polyglutamine 94-99 androgen receptor Homo sapiens 36-40 34021780-1 2021 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansions in the androgen receptor (AR) gene. polyglutamine 94-99 androgen receptor Homo sapiens 119-136 34021780-1 2021 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansions in the androgen receptor (AR) gene. polyglutamine 94-99 androgen receptor Homo sapiens 138-140 34021780-5 2021 Here, we unveil that ionic current alterations induced by the expression of polyQ-expanded AR in motor neuron-derived MN-1 cells are attenuated by the administration of clenbuterol. polyglutamine 76-81 androgen receptor Homo sapiens 91-93 32583490-1 2020 CAG trinucleotide repeats are coded for the polyglutamine tract in the N-terminal of the androgen receptor (AR) gene which varies in normal individuals from 6 to 36 residues. polyglutamine 44-57 androgen receptor Homo sapiens 89-106 32583490-1 2020 CAG trinucleotide repeats are coded for the polyglutamine tract in the N-terminal of the androgen receptor (AR) gene which varies in normal individuals from 6 to 36 residues. polyglutamine 44-57 androgen receptor Homo sapiens 108-110 32934110-5 2020 Androgen-dependent nuclear accumulation of the polyglutamine-expanded AR is an essential step in the pathogenesis, providing therapeutic opportunities via hormonal manipulation and gene silencing with antisense oligonucleotides. polyglutamine 47-60 androgen receptor Homo sapiens 70-72 32854182-4 2020 Polymorphic polyglutamine (polyQ) tracts in the androgen receptor (AR/NR3C4) and nuclear receptor coactivator 3 (NCOA3) genes were investigated in control and OSA patients using polymerase chain reaction (PCR), Sanger sequencing and fragment analysis (n = 1019 Rottweilers, 379 Irish Wolfhounds). polyglutamine 12-25 androgen receptor Homo sapiens 48-65 32854182-4 2020 Polymorphic polyglutamine (polyQ) tracts in the androgen receptor (AR/NR3C4) and nuclear receptor coactivator 3 (NCOA3) genes were investigated in control and OSA patients using polymerase chain reaction (PCR), Sanger sequencing and fragment analysis (n = 1019 Rottweilers, 379 Irish Wolfhounds). polyglutamine 12-25 androgen receptor Homo sapiens 70-75 32854182-4 2020 Polymorphic polyglutamine (polyQ) tracts in the androgen receptor (AR/NR3C4) and nuclear receptor coactivator 3 (NCOA3) genes were investigated in control and OSA patients using polymerase chain reaction (PCR), Sanger sequencing and fragment analysis (n = 1019 Rottweilers, 379 Irish Wolfhounds). polyglutamine 27-32 androgen receptor Homo sapiens 48-65 32854182-4 2020 Polymorphic polyglutamine (polyQ) tracts in the androgen receptor (AR/NR3C4) and nuclear receptor coactivator 3 (NCOA3) genes were investigated in control and OSA patients using polymerase chain reaction (PCR), Sanger sequencing and fragment analysis (n = 1019 Rottweilers, 379 Irish Wolfhounds). polyglutamine 27-32 androgen receptor Homo sapiens 70-75 32641584-1 2020 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disorder caused by a polyglutamine expansion in the androgen receptor (AR). polyglutamine 82-95 androgen receptor Homo sapiens 36-40 32641584-1 2020 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disorder caused by a polyglutamine expansion in the androgen receptor (AR). polyglutamine 82-95 androgen receptor Homo sapiens 113-130 32641584-1 2020 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disorder caused by a polyglutamine expansion in the androgen receptor (AR). polyglutamine 82-95 androgen receptor Homo sapiens 132-134 32089544-0 2020 Androgen receptor with short polyglutamine tract preferably enhances Wnt/beta-catenin-mediated prostatic tumorigenesis. polyglutamine 29-42 androgen receptor Homo sapiens 0-17 32089544-1 2020 Polyglutamine (polyQ) tract polymorphism within the human androgen receptor (AR) shows population heterogeneity. polyglutamine 0-13 androgen receptor Homo sapiens 58-75 32089544-1 2020 Polyglutamine (polyQ) tract polymorphism within the human androgen receptor (AR) shows population heterogeneity. polyglutamine 0-13 androgen receptor Homo sapiens 77-79 32089544-1 2020 Polyglutamine (polyQ) tract polymorphism within the human androgen receptor (AR) shows population heterogeneity. polyglutamine 15-20 androgen receptor Homo sapiens 58-75 32089544-1 2020 Polyglutamine (polyQ) tract polymorphism within the human androgen receptor (AR) shows population heterogeneity. polyglutamine 15-20 androgen receptor Homo sapiens 77-79 33714752-4 2021 In particular, individual variations in polyglutamine (CAG) length in the androgen receptor (AR) gene could alter androgenic activity in brain regions associated with cognitive processes including memory and executive functions. polyglutamine 40-53 androgen receptor Homo sapiens 74-91 33714752-4 2021 In particular, individual variations in polyglutamine (CAG) length in the androgen receptor (AR) gene could alter androgenic activity in brain regions associated with cognitive processes including memory and executive functions. polyglutamine 40-53 androgen receptor Homo sapiens 93-95 33647767-0 2021 Shorter androgen receptor polyQ alleles protect against life-threatening COVID-19 disease in European males. polyglutamine 26-31 androgen receptor Homo sapiens 8-25 32631678-2 2020 SBMA is caused by trinucleotide repeat expansion in the first exon of the androgen receptor (AR) gene on chromosome X that encodes a polyglutamine (polyQ) tract in the AR protein. polyglutamine 133-146 androgen receptor Homo sapiens 0-4 32631678-2 2020 SBMA is caused by trinucleotide repeat expansion in the first exon of the androgen receptor (AR) gene on chromosome X that encodes a polyglutamine (polyQ) tract in the AR protein. polyglutamine 133-146 androgen receptor Homo sapiens 74-91 32631678-2 2020 SBMA is caused by trinucleotide repeat expansion in the first exon of the androgen receptor (AR) gene on chromosome X that encodes a polyglutamine (polyQ) tract in the AR protein. polyglutamine 133-146 androgen receptor Homo sapiens 93-95 32631678-2 2020 SBMA is caused by trinucleotide repeat expansion in the first exon of the androgen receptor (AR) gene on chromosome X that encodes a polyglutamine (polyQ) tract in the AR protein. polyglutamine 133-146 androgen receptor Homo sapiens 168-170 32631678-2 2020 SBMA is caused by trinucleotide repeat expansion in the first exon of the androgen receptor (AR) gene on chromosome X that encodes a polyglutamine (polyQ) tract in the AR protein. polyglutamine 148-153 androgen receptor Homo sapiens 0-4 32631678-2 2020 SBMA is caused by trinucleotide repeat expansion in the first exon of the androgen receptor (AR) gene on chromosome X that encodes a polyglutamine (polyQ) tract in the AR protein. polyglutamine 148-153 androgen receptor Homo sapiens 74-91 32631678-2 2020 SBMA is caused by trinucleotide repeat expansion in the first exon of the androgen receptor (AR) gene on chromosome X that encodes a polyglutamine (polyQ) tract in the AR protein. polyglutamine 148-153 androgen receptor Homo sapiens 93-95 32631678-2 2020 SBMA is caused by trinucleotide repeat expansion in the first exon of the androgen receptor (AR) gene on chromosome X that encodes a polyglutamine (polyQ) tract in the AR protein. polyglutamine 148-153 androgen receptor Homo sapiens 168-170 32019272-1 2020 Polyglutamine (polyQ) expansions in the androgen receptor (AR) gene cause spinal and bulbar muscular atrophy (SBMA), a neuromuscular disease characterized by lower motor neuron (MN) loss and skeletal muscle atrophy, with an unknown mechanism. polyglutamine 15-20 androgen receptor Homo sapiens 110-114 32019272-6 2020 Finally, we found that two-week induction of expression of polyQ-expanded AR in adult mice was sufficient to cause premature death, body weight loss and muscle atrophy, but not aggregation, metabolic alterations, motor coordination and fiber-type switch, indicating that expression of the disease protein in the adulthood is sufficient to recapitulate several, but not all SBMA manifestations in mice. polyglutamine 59-64 androgen receptor Homo sapiens 373-377 32019272-7 2020 These results imply that chronic expression of polyQ-expanded AR, i.e. during development and prepuberty, is key to induce the full SBMA muscle pathology observed in patients. polyglutamine 47-52 androgen receptor Homo sapiens 132-136 31551920-1 2019 Background: Spinal and Bulbar Muscular Atrophy (SBMA) is caused by the extension of the polyglutamine tract within the androgen receptor (AR) gene, and results in a multisystem presentation, including the degeneration of lower motor neurons. polyglutamine 88-101 androgen receptor Homo sapiens 119-136 31310754-2 2019 Spinal and bulbar muscular atrophy (SBMA) is a late-onset neurodegenerative neuromuscular disease without effective therapy, and the protein toxicity of androgen-dependent polyglutamine-expanded androgen receptor is thought to contribute to its etiology. polyglutamine 172-185 androgen receptor Homo sapiens 36-40 31686397-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by a polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 81-94 androgen receptor Homo sapiens 36-40 31686397-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by a polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 81-94 androgen receptor Homo sapiens 120-137 31686397-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by a polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 81-94 androgen receptor Homo sapiens 139-141 31686397-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by a polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 96-101 androgen receptor Homo sapiens 36-40 31686397-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by a polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 96-101 androgen receptor Homo sapiens 120-137 31686397-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by a polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 96-101 androgen receptor Homo sapiens 139-141 31686397-3 2019 In the current review, we provide an overview of the system-wide clinical features of SBMA, summarize the structure and function of the AR, discuss both gain-of-function and loss-of-function mechanisms of toxicity caused by polyQ-expanded AR, and describe the cell and animal models utilized in the study of SBMA. polyglutamine 224-229 androgen receptor Homo sapiens 86-90 31686397-3 2019 In the current review, we provide an overview of the system-wide clinical features of SBMA, summarize the structure and function of the AR, discuss both gain-of-function and loss-of-function mechanisms of toxicity caused by polyQ-expanded AR, and describe the cell and animal models utilized in the study of SBMA. polyglutamine 224-229 androgen receptor Homo sapiens 239-241 32696359-7 2020 Here, we present a protocol to prepare monomeric samples of isotope-enriched short helical polyQ peptides based on the sequence of the androgen receptor (AR) suitable for NMR characterization and suggest different ways to adapt it for the production and monomerization of other relatively short IDR sequences and SLiMs. polyglutamine 91-96 androgen receptor Homo sapiens 135-152 32696359-7 2020 Here, we present a protocol to prepare monomeric samples of isotope-enriched short helical polyQ peptides based on the sequence of the androgen receptor (AR) suitable for NMR characterization and suggest different ways to adapt it for the production and monomerization of other relatively short IDR sequences and SLiMs. polyglutamine 91-96 androgen receptor Homo sapiens 154-156 31551920-1 2019 Background: Spinal and Bulbar Muscular Atrophy (SBMA) is caused by the extension of the polyglutamine tract within the androgen receptor (AR) gene, and results in a multisystem presentation, including the degeneration of lower motor neurons. polyglutamine 88-101 androgen receptor Homo sapiens 138-140 30940675-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a polyglutamine-mediated neuromuscular disease caused by a CAG repeat expansion in the androgen receptor (AR) gene. polyglutamine 47-60 androgen receptor Homo sapiens 36-40 31481932-1 2019 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron disease (MND) caused by a mutant androgen receptor (AR) containing an elongated polyglutamine (polyQ) tract. polyglutamine 148-161 androgen receptor Homo sapiens 36-40 31481932-1 2019 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron disease (MND) caused by a mutant androgen receptor (AR) containing an elongated polyglutamine (polyQ) tract. polyglutamine 148-161 androgen receptor Homo sapiens 101-118 31481932-1 2019 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron disease (MND) caused by a mutant androgen receptor (AR) containing an elongated polyglutamine (polyQ) tract. polyglutamine 148-161 androgen receptor Homo sapiens 120-122 31481932-1 2019 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron disease (MND) caused by a mutant androgen receptor (AR) containing an elongated polyglutamine (polyQ) tract. polyglutamine 163-168 androgen receptor Homo sapiens 36-40 31481932-1 2019 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron disease (MND) caused by a mutant androgen receptor (AR) containing an elongated polyglutamine (polyQ) tract. polyglutamine 163-168 androgen receptor Homo sapiens 101-118 31481932-1 2019 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron disease (MND) caused by a mutant androgen receptor (AR) containing an elongated polyglutamine (polyQ) tract. polyglutamine 163-168 androgen receptor Homo sapiens 120-122 30996158-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a progressive hereditary neuromuscular disease caused by the testosterone-dependent accumulation of pathogenic polyglutamine-expanded androgen receptor protein. polyglutamine 156-169 androgen receptor Homo sapiens 36-40 30996158-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a progressive hereditary neuromuscular disease caused by the testosterone-dependent accumulation of pathogenic polyglutamine-expanded androgen receptor protein. polyglutamine 156-169 androgen receptor Homo sapiens 179-196 30391288-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by the expansion of polyglutamine region in the androgen receptor. polyglutamine 100-113 androgen receptor Homo sapiens 36-40 30391288-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by the expansion of polyglutamine region in the androgen receptor. polyglutamine 100-113 androgen receptor Homo sapiens 128-145 30713477-1 2018 CAG trinucleotide repeats in androgen receptor (AR) gene encode a polyglutamine tract in AR N-terminal transactivation domain. polyglutamine 66-79 androgen receptor Homo sapiens 29-46 30707359-7 2019 We show its usefulness by performing a comparative study of the interactome of the nine polyglutamine (polyQ) disease proteins, namely androgen receptor (AR), atrophin-1 (ATN1), ataxin 1 (ATXN1), ataxin 2 (ATXN2), ataxin 3 (ATXN3), ataxin 7 (ATXN7), calcium voltage-gated channel subunit alpha1 A (CACNA1A), Huntingtin (HTT), and TATA-binding protein (TBP). polyglutamine 88-101 androgen receptor Homo sapiens 135-152 30707359-7 2019 We show its usefulness by performing a comparative study of the interactome of the nine polyglutamine (polyQ) disease proteins, namely androgen receptor (AR), atrophin-1 (ATN1), ataxin 1 (ATXN1), ataxin 2 (ATXN2), ataxin 3 (ATXN3), ataxin 7 (ATXN7), calcium voltage-gated channel subunit alpha1 A (CACNA1A), Huntingtin (HTT), and TATA-binding protein (TBP). polyglutamine 88-101 androgen receptor Homo sapiens 154-156 30644418-0 2019 Impaired Nuclear Export of Polyglutamine-Expanded Androgen Receptor in Spinal and Bulbar Muscular Atrophy. polyglutamine 27-40 androgen receptor Homo sapiens 50-67 30644418-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 79-92 androgen receptor Homo sapiens 36-40 30644418-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 79-92 androgen receptor Homo sapiens 118-135 30644418-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 79-92 androgen receptor Homo sapiens 137-139 30644418-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 94-99 androgen receptor Homo sapiens 36-40 30644418-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 94-99 androgen receptor Homo sapiens 118-135 30644418-1 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansion in the androgen receptor (AR). polyglutamine 94-99 androgen receptor Homo sapiens 137-139 30644418-3 2019 We demonstrate here that the nuclear export of polyQ-expanded AR is impaired, even prior to the formation of intranuclear inclusions of aggregated AR. polyglutamine 47-52 androgen receptor Homo sapiens 62-64 30644418-3 2019 We demonstrate here that the nuclear export of polyQ-expanded AR is impaired, even prior to the formation of intranuclear inclusions of aggregated AR. polyglutamine 47-52 androgen receptor Homo sapiens 147-149 30713477-1 2018 CAG trinucleotide repeats in androgen receptor (AR) gene encode a polyglutamine tract in AR N-terminal transactivation domain. polyglutamine 66-79 androgen receptor Homo sapiens 48-50 30713477-1 2018 CAG trinucleotide repeats in androgen receptor (AR) gene encode a polyglutamine tract in AR N-terminal transactivation domain. polyglutamine 66-79 androgen receptor Homo sapiens 89-91 28688959-1 2018 Abnormal polyglutamine expansions in the androgen receptor (AR) cause a muscular condition, known as Kennedy"s disease or spinal and bulbar muscular atrophy (SBMA). polyglutamine 9-22 androgen receptor Homo sapiens 41-58 28688959-1 2018 Abnormal polyglutamine expansions in the androgen receptor (AR) cause a muscular condition, known as Kennedy"s disease or spinal and bulbar muscular atrophy (SBMA). polyglutamine 9-22 androgen receptor Homo sapiens 60-62 28688959-1 2018 Abnormal polyglutamine expansions in the androgen receptor (AR) cause a muscular condition, known as Kennedy"s disease or spinal and bulbar muscular atrophy (SBMA). polyglutamine 9-22 androgen receptor Homo sapiens 158-162 28334513-3 2017 N-terminal transactivation domain of the encoded AR protein harbours two polymorphic stretches of identical amino acids, a polyglutamine tract (encoded by 8-37 CAG-repeats) and a polyglycine tract (encoded by 10-30 GGN-repeats). polyglutamine 123-136 androgen receptor Homo sapiens 49-51 28782227-0 2018 Short androgen receptor poly-glutamine-promoted endometrial cancer is associated with benzo[a]pyrene-mediated aryl hydrocarbon receptor activation. polyglutamine 24-38 androgen receptor Homo sapiens 6-23 28782227-1 2018 The androgen receptor (AR) poly-glutamine polymorphism (AR-Q) was reported to play role in endometrial cancer (EMCA) development, yet controversial. polyglutamine 27-41 androgen receptor Homo sapiens 4-21 28782227-1 2018 The androgen receptor (AR) poly-glutamine polymorphism (AR-Q) was reported to play role in endometrial cancer (EMCA) development, yet controversial. polyglutamine 27-41 androgen receptor Homo sapiens 23-25 28782227-1 2018 The androgen receptor (AR) poly-glutamine polymorphism (AR-Q) was reported to play role in endometrial cancer (EMCA) development, yet controversial. polyglutamine 27-41 androgen receptor Homo sapiens 56-58 28782227-11 2018 A large-scale epidemiology and public health survey on the interaction of environmental toxin and AR poly-Q in EMCA is suggested. polyglutamine 101-107 androgen receptor Homo sapiens 98-100 28511915-1 2017 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a motor neuron disease caused by the expansion of a polymorphic CAG tandem repeat encoding a polyglutamine (polyQ) tract in the androgen receptor (AR) gene. polyglutamine 172-185 androgen receptor Homo sapiens 36-40 28511915-1 2017 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a motor neuron disease caused by the expansion of a polymorphic CAG tandem repeat encoding a polyglutamine (polyQ) tract in the androgen receptor (AR) gene. polyglutamine 172-185 androgen receptor Homo sapiens 207-224 28511915-1 2017 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a motor neuron disease caused by the expansion of a polymorphic CAG tandem repeat encoding a polyglutamine (polyQ) tract in the androgen receptor (AR) gene. polyglutamine 172-185 androgen receptor Homo sapiens 226-228 28511915-1 2017 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a motor neuron disease caused by the expansion of a polymorphic CAG tandem repeat encoding a polyglutamine (polyQ) tract in the androgen receptor (AR) gene. polyglutamine 187-192 androgen receptor Homo sapiens 36-40 28511915-1 2017 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a motor neuron disease caused by the expansion of a polymorphic CAG tandem repeat encoding a polyglutamine (polyQ) tract in the androgen receptor (AR) gene. polyglutamine 187-192 androgen receptor Homo sapiens 207-224 28511915-1 2017 Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy"s disease, is a motor neuron disease caused by the expansion of a polymorphic CAG tandem repeat encoding a polyglutamine (polyQ) tract in the androgen receptor (AR) gene. polyglutamine 187-192 androgen receptor Homo sapiens 226-228 28629183-0 2017 An Amyloidogenic Sequence at the N-Terminus of the Androgen Receptor Impacts Polyglutamine Aggregation. polyglutamine 77-90 androgen receptor Homo sapiens 51-68 28453707-0 2017 The role of AR polyQ tract in male breast carcinoma: lesson from an SBMA case. polyglutamine 15-20 androgen receptor Homo sapiens 68-72 29427100-1 2018 Spinal and Bulbar Muscular Atrophy (SBMA) is an inherited neuromuscular disorder caused by a CAG-polyglutamine (polyQ) repeat expansion in the androgen receptor (AR) gene. polyglutamine 112-117 androgen receptor Homo sapiens 36-40 29427100-1 2018 Spinal and Bulbar Muscular Atrophy (SBMA) is an inherited neuromuscular disorder caused by a CAG-polyglutamine (polyQ) repeat expansion in the androgen receptor (AR) gene. polyglutamine 112-117 androgen receptor Homo sapiens 143-160 29427100-1 2018 Spinal and Bulbar Muscular Atrophy (SBMA) is an inherited neuromuscular disorder caused by a CAG-polyglutamine (polyQ) repeat expansion in the androgen receptor (AR) gene. polyglutamine 112-117 androgen receptor Homo sapiens 162-164 28948156-2 2017 Although great intraspecific length polymorphisms in poly glutamine (poly-Q) and poly glycine (poly-G) regions of the androgen receptor in humans, apes and several Old World monkeys have been reported, little is known about the characteristics of these regions in New World monkeys. polyglutamine 53-67 androgen receptor Homo sapiens 118-135 28948156-2 2017 Although great intraspecific length polymorphisms in poly glutamine (poly-Q) and poly glycine (poly-G) regions of the androgen receptor in humans, apes and several Old World monkeys have been reported, little is known about the characteristics of these regions in New World monkeys. polyglutamine 69-75 androgen receptor Homo sapiens 118-135 27188284-1 2016 An expanded polyglutamine (polyQ) tract at the amino-terminus of the androgen receptor (AR) confers toxic properties responsible for neuronal and non-neuronal degeneration in spinal and bulbar muscular atrophy (SBMA), one of nine polyQ expansion diseases. polyglutamine 12-25 androgen receptor Homo sapiens 69-86 28087734-1 2017 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disorder caused by polyglutamine expansion in the androgen receptor (AR) and characterized by the loss of lower motor neurons. polyglutamine 80-93 androgen receptor Homo sapiens 36-40 28087734-1 2017 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disorder caused by polyglutamine expansion in the androgen receptor (AR) and characterized by the loss of lower motor neurons. polyglutamine 80-93 androgen receptor Homo sapiens 111-128 28087734-1 2017 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disorder caused by polyglutamine expansion in the androgen receptor (AR) and characterized by the loss of lower motor neurons. polyglutamine 80-93 androgen receptor Homo sapiens 130-132 28087734-5 2017 Polyglutamine-expanded AR expression was decreased in whole muscle, yet enriched in the nucleus, and localized to mitochondria. polyglutamine 0-13 androgen receptor Homo sapiens 23-25 28087734-9 2017 These observations suggest a causative link between nuclear polyglutamine-expanded AR accumulation, depletion of mitochondrial mass, increased mitophagy and altered mitochondrial membrane composition in SBMA muscle patients. polyglutamine 60-73 androgen receptor Homo sapiens 83-85 28087734-9 2017 These observations suggest a causative link between nuclear polyglutamine-expanded AR accumulation, depletion of mitochondrial mass, increased mitophagy and altered mitochondrial membrane composition in SBMA muscle patients. polyglutamine 60-73 androgen receptor Homo sapiens 203-207 27794482-3 2017 Less is known about genetic variation"s role in individual psychobiological responses to partnering and fathering, particularly as related to T. We examined the exon 1 CAG (polyglutamine) repeat (CAGn) within the androgen receptor (AR) gene. polyglutamine 173-186 androgen receptor Homo sapiens 213-230 27794482-3 2017 Less is known about genetic variation"s role in individual psychobiological responses to partnering and fathering, particularly as related to T. We examined the exon 1 CAG (polyglutamine) repeat (CAGn) within the androgen receptor (AR) gene. polyglutamine 173-186 androgen receptor Homo sapiens 232-234 27188284-1 2016 An expanded polyglutamine (polyQ) tract at the amino-terminus of the androgen receptor (AR) confers toxic properties responsible for neuronal and non-neuronal degeneration in spinal and bulbar muscular atrophy (SBMA), one of nine polyQ expansion diseases. polyglutamine 12-25 androgen receptor Homo sapiens 88-90 27188284-1 2016 An expanded polyglutamine (polyQ) tract at the amino-terminus of the androgen receptor (AR) confers toxic properties responsible for neuronal and non-neuronal degeneration in spinal and bulbar muscular atrophy (SBMA), one of nine polyQ expansion diseases. polyglutamine 12-25 androgen receptor Homo sapiens 211-215 27188284-1 2016 An expanded polyglutamine (polyQ) tract at the amino-terminus of the androgen receptor (AR) confers toxic properties responsible for neuronal and non-neuronal degeneration in spinal and bulbar muscular atrophy (SBMA), one of nine polyQ expansion diseases. polyglutamine 27-32 androgen receptor Homo sapiens 69-86 27188284-1 2016 An expanded polyglutamine (polyQ) tract at the amino-terminus of the androgen receptor (AR) confers toxic properties responsible for neuronal and non-neuronal degeneration in spinal and bulbar muscular atrophy (SBMA), one of nine polyQ expansion diseases. polyglutamine 27-32 androgen receptor Homo sapiens 88-90 27188284-1 2016 An expanded polyglutamine (polyQ) tract at the amino-terminus of the androgen receptor (AR) confers toxic properties responsible for neuronal and non-neuronal degeneration in spinal and bulbar muscular atrophy (SBMA), one of nine polyQ expansion diseases. polyglutamine 27-32 androgen receptor Homo sapiens 211-215 27188284-1 2016 An expanded polyglutamine (polyQ) tract at the amino-terminus of the androgen receptor (AR) confers toxic properties responsible for neuronal and non-neuronal degeneration in spinal and bulbar muscular atrophy (SBMA), one of nine polyQ expansion diseases. polyglutamine 230-235 androgen receptor Homo sapiens 69-86 27188284-1 2016 An expanded polyglutamine (polyQ) tract at the amino-terminus of the androgen receptor (AR) confers toxic properties responsible for neuronal and non-neuronal degeneration in spinal and bulbar muscular atrophy (SBMA), one of nine polyQ expansion diseases. polyglutamine 230-235 androgen receptor Homo sapiens 88-90 26971100-1 2016 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by the expansion of a polyglutamine tract in the androgen receptor (AR). polyglutamine 98-111 androgen receptor Homo sapiens 36-40 27520369-2 2016 Using these immunoassays, we now report that polyglutamine expansion influences the conformational properties of other polyglutamine disease proteins, exemplified by the androgen receptor (associated with spinal bulbar muscular atrophy) and TATA binding protein (associated with spinocerebellar ataxia 17). polyglutamine 45-58 androgen receptor Homo sapiens 170-187 26971100-1 2016 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by the expansion of a polyglutamine tract in the androgen receptor (AR). polyglutamine 98-111 androgen receptor Homo sapiens 125-142 26971100-1 2016 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by the expansion of a polyglutamine tract in the androgen receptor (AR). polyglutamine 98-111 androgen receptor Homo sapiens 144-146 26971100-2 2016 The mechanism by which expansion of polyglutamine in AR causes muscle atrophy is unknown. polyglutamine 36-49 androgen receptor Homo sapiens 53-55 26755334-1 2016 Spinal and bulbar muscular atrophy (SBMA) is a currently untreatable adult-onset neuromuscular disease caused by expansion of a polyglutamine repeat in the androgen receptor (AR). polyglutamine 128-141 androgen receptor Homo sapiens 36-40 27276254-3 2016 We used solution NMR to study at single-residue resolution a 156-residue proteolytic fragment of the androgen receptor that contains a polyQ tract associated with the disease spinobulbar muscular atrophy, also known as Kennedy disease. polyglutamine 135-140 androgen receptor Homo sapiens 101-118 26755334-1 2016 Spinal and bulbar muscular atrophy (SBMA) is a currently untreatable adult-onset neuromuscular disease caused by expansion of a polyglutamine repeat in the androgen receptor (AR). polyglutamine 128-141 androgen receptor Homo sapiens 156-173 26755334-1 2016 Spinal and bulbar muscular atrophy (SBMA) is a currently untreatable adult-onset neuromuscular disease caused by expansion of a polyglutamine repeat in the androgen receptor (AR). polyglutamine 128-141 androgen receptor Homo sapiens 175-177 26901084-2 2016 It is caused by a poly-glutamine tract expansion in the androgen receptor (AR) which generates protein aggregates that cannot be processed by proteasomes. polyglutamine 18-32 androgen receptor Homo sapiens 56-73 27854206-1 2016 Spinal and bulbar muscular atrophy is caused by polyglutamine expansion in the androgen receptor. polyglutamine 48-61 androgen receptor Homo sapiens 79-96 26563449-1 2016 Spinal-bulbar muscle atrophy (SBMA) or also named Kennedy"s Disease is caused by a polyglutamine expansion (PolyQ) of the coding region of the androgen receptor (AR). polyglutamine 83-96 androgen receptor Homo sapiens 30-34 26563449-1 2016 Spinal-bulbar muscle atrophy (SBMA) or also named Kennedy"s Disease is caused by a polyglutamine expansion (PolyQ) of the coding region of the androgen receptor (AR). polyglutamine 83-96 androgen receptor Homo sapiens 143-160 26563449-1 2016 Spinal-bulbar muscle atrophy (SBMA) or also named Kennedy"s Disease is caused by a polyglutamine expansion (PolyQ) of the coding region of the androgen receptor (AR). polyglutamine 83-96 androgen receptor Homo sapiens 162-164 26563449-4 2016 The PolyQ triggers a misfolding in the AR-PolyQ and leads to protein aggregation in spinal cord motoneurons and muscle cells. polyglutamine 4-9 androgen receptor Homo sapiens 39-41 26563449-4 2016 The PolyQ triggers a misfolding in the AR-PolyQ and leads to protein aggregation in spinal cord motoneurons and muscle cells. polyglutamine 42-47 androgen receptor Homo sapiens 39-41 26563449-7 2016 SBMA has been modeled in AR-overexpressing and AR-PolyQ-knock-in animals, but precisely how the PolyQ expansion leads to neurodegeneration is unclear. polyglutamine 50-55 androgen receptor Homo sapiens 0-4 26563449-7 2016 SBMA has been modeled in AR-overexpressing and AR-PolyQ-knock-in animals, but precisely how the PolyQ expansion leads to neurodegeneration is unclear. polyglutamine 50-55 androgen receptor Homo sapiens 47-49 26576772-1 2016 Spinal and bulbar muscular atrophy (SBMA) is a late-onset neuromuscular disease caused by a polyglutamine expansion in the androgen receptor gene which results in progressive spinal and bulbar motor neuron degeneration, and muscle atrophy. polyglutamine 92-105 androgen receptor Homo sapiens 36-40 26576772-1 2016 Spinal and bulbar muscular atrophy (SBMA) is a late-onset neuromuscular disease caused by a polyglutamine expansion in the androgen receptor gene which results in progressive spinal and bulbar motor neuron degeneration, and muscle atrophy. polyglutamine 92-105 androgen receptor Homo sapiens 123-140 26875173-3 2016 Expansion of polyglutamine in the AR results in selective lower motor neuron degeneration and skeletal muscle atrophy. polyglutamine 13-26 androgen receptor Homo sapiens 34-36 26875173-7 2016 Indeed, the polyglutamine-expanded AR is converted to a neurotoxic species upon binding to androgens. polyglutamine 12-25 androgen receptor Homo sapiens 35-37 26901084-2 2016 It is caused by a poly-glutamine tract expansion in the androgen receptor (AR) which generates protein aggregates that cannot be processed by proteasomes. polyglutamine 18-32 androgen receptor Homo sapiens 75-77 26673324-1 2015 Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by a polyglutamine expansion in the androgen receptor (AR) and is associated with misfolding and aggregation of the mutant AR. polyglutamine 85-98 androgen receptor Homo sapiens 36-40 26673324-3 2015 Male transgenic mice expressing polyQ-expanded AR with a mutation in the FxxLF motif (F23A) to prevent the N/C interaction displayed substantially improved motor function compared with N/C-intact AR-expressing mice and showed reduced pathological features of SBMA. polyglutamine 32-37 androgen receptor Homo sapiens 259-263 26453288-2 2015 In spinal and bulbar muscular atrophy (SBMA), polyglutamine expansion within the androgen receptor (AR) causes progressive debilitating muscular atrophy and lower motor neuron loss in males. polyglutamine 46-59 androgen receptor Homo sapiens 39-43 26453288-2 2015 In spinal and bulbar muscular atrophy (SBMA), polyglutamine expansion within the androgen receptor (AR) causes progressive debilitating muscular atrophy and lower motor neuron loss in males. polyglutamine 46-59 androgen receptor Homo sapiens 81-98 26453288-2 2015 In spinal and bulbar muscular atrophy (SBMA), polyglutamine expansion within the androgen receptor (AR) causes progressive debilitating muscular atrophy and lower motor neuron loss in males. polyglutamine 46-59 androgen receptor Homo sapiens 100-102 26453288-4 2015 Here we identify novel polyglutamine-expanded AR aggregates that are SDS-soluble and bind the toxicity-predicting antibody 3B5H10. polyglutamine 23-36 androgen receptor Homo sapiens 46-48