Association of Androgen Receptor CAG Repeat Polymorphism and Polycystic Ovary Syndrome
Context: Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the androgen receptor exon 1 polymorphic CAG repeat have produced conflicting results in PCOS. Objective: We tested the hypothesis that a lower number...
Saved in:
| Published in | The journal of clinical endocrinology and metabolism Vol. 93; no. 5; pp. 1939 - 1945 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Bethesda, MD
Oxford University Press
01.05.2008
Endocrine Society The Endocrine Society |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0021-972X 1945-7197 |
| DOI | 10.1210/jc.2008-0038 |
Cover
| Abstract | Context: Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the androgen receptor exon 1 polymorphic CAG repeat have produced conflicting results in PCOS.
Objective: We tested the hypothesis that a lower number of CAG repeats is associated with increased odds of PCOS. We also compared X-chromosome inactivation between cases and controls.
Design: Women with and without PCOS were genotyped for the CAG repeat and assessed for X-chromosome methylation. Association analyses were performed.
Setting: Subjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; controls were recruited from the surrounding community. Genotyping took place at Cedars-Sinai Medical Center in Los Angeles.
Participants: Participants included 330 women with PCOS and 289 controls (77% white, 23% black).
Main Measurements: Androgen receptor genotype, X-chromosome methylation, and phenotyping for PCOS were measured.
Results: A smaller biallelic mean of CAG repeats was associated with increased odds of PCOS. X-chromosome inactivation was not different comparing cases with controls; however, in the subset with nonrandom inactivation, the chromosome bearing the shorter CAG allele was preferentially active in PCOS women.
Conclusions: Association of shorter CAG repeats with PCOS is consistent with in vitro functional studies demonstrating higher activity of androgen receptors expressed from alleles with fewer CAG repeats, suggesting inherited alteration in androgen sensitivity may contribute to PCOS. In some women, such heightened sensitivity may also result from preferential expression of androgen receptors with shorter alleles. Thus, genetic and epigenetic changes may be involved in the pathogenesis of PCOS. |
|---|---|
| AbstractList | Context: Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the androgen receptor exon 1 polymorphic CAG repeat have produced conflicting results in PCOS. Objective: We tested the hypothesis that a lower number of CAG repeats is associated with increased odds of PCOS. We also compared X-chromosome inactivation between cases and controls. Design: Women with and without PCOS were genotyped for the CAG repeat and assessed for X-chromosome methylation. Association analyses were performed. Setting: Subjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; controls were recruited from the surrounding community. Genotyping took place at Cedars-Sinai Medical Center in Los Angeles. Participants: Participants included 330 women with PCOS and 289 controls (77% white, 23% black). Main Measurements: Androgen receptor genotype, X-chromosome methylation, and phenotyping for PCOS were measured. Results: A smaller biallelic mean of CAG repeats was associated with increased odds of PCOS. X-chromosome inactivation was not different comparing cases with controls; however, in the subset with nonrandom inactivation, the chromosome bearing the shorter CAG allele was preferentially active in PCOS women. Conclusions: Association of shorter CAG repeats with PCOS is consistent with in vitro functional studies demonstrating higher activity of androgen receptors expressed from alleles with fewer CAG repeats, suggesting inherited alteration in androgen sensitivity may contribute to PCOS. In some women, such heightened sensitivity may also result from preferential expression of androgen receptors with shorter alleles. Thus, genetic and epigenetic changes may be involved in the pathogenesis of PCOS. Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the androgen receptor exon 1 polymorphic CAG repeat have produced conflicting results in PCOS.CONTEXTGenetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the androgen receptor exon 1 polymorphic CAG repeat have produced conflicting results in PCOS.We tested the hypothesis that a lower number of CAG repeats is associated with increased odds of PCOS. We also compared X-chromosome inactivation between cases and controls.OBJECTIVEWe tested the hypothesis that a lower number of CAG repeats is associated with increased odds of PCOS. We also compared X-chromosome inactivation between cases and controls.Women with and without PCOS were genotyped for the CAG repeat and assessed for X-chromosome methylation. Association analyses were performed.DESIGNWomen with and without PCOS were genotyped for the CAG repeat and assessed for X-chromosome methylation. Association analyses were performed.Subjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; controls were recruited from the surrounding community. Genotyping took place at Cedars-Sinai Medical Center in Los Angeles.SETTINGSubjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; controls were recruited from the surrounding community. Genotyping took place at Cedars-Sinai Medical Center in Los Angeles.Participants included 330 women with PCOS and 289 controls (77% white, 23% black).PARTICIPANTSParticipants included 330 women with PCOS and 289 controls (77% white, 23% black).Androgen receptor genotype, X-chromosome methylation, and phenotyping for PCOS were measured.MAIN MEASUREMENTSAndrogen receptor genotype, X-chromosome methylation, and phenotyping for PCOS were measured.A smaller biallelic mean of CAG repeats was associated with increased odds of PCOS. X-chromosome inactivation was not different comparing cases with controls; however, in the subset with nonrandom inactivation, the chromosome bearing the shorter CAG allele was preferentially active in PCOS women.RESULTSA smaller biallelic mean of CAG repeats was associated with increased odds of PCOS. X-chromosome inactivation was not different comparing cases with controls; however, in the subset with nonrandom inactivation, the chromosome bearing the shorter CAG allele was preferentially active in PCOS women.Association of shorter CAG repeats with PCOS is consistent with in vitro functional studies demonstrating higher activity of androgen receptors expressed from alleles with fewer CAG repeats, suggesting inherited alteration in androgen sensitivity may contribute to PCOS. In some women, such heightened sensitivity may also result from preferential expression of androgen receptors with shorter alleles. Thus, genetic and epigenetic changes may be involved in the pathogenesis of PCOS.CONCLUSIONSAssociation of shorter CAG repeats with PCOS is consistent with in vitro functional studies demonstrating higher activity of androgen receptors expressed from alleles with fewer CAG repeats, suggesting inherited alteration in androgen sensitivity may contribute to PCOS. In some women, such heightened sensitivity may also result from preferential expression of androgen receptors with shorter alleles. Thus, genetic and epigenetic changes may be involved in the pathogenesis of PCOS. Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the androgen receptor exon 1 polymorphic CAG repeat have produced conflicting results in PCOS. We tested the hypothesis that a lower number of CAG repeats is associated with increased odds of PCOS. We also compared X-chromosome inactivation between cases and controls. Women with and without PCOS were genotyped for the CAG repeat and assessed for X-chromosome methylation. Association analyses were performed. Subjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; controls were recruited from the surrounding community. Genotyping took place at Cedars-Sinai Medical Center in Los Angeles. Participants included 330 women with PCOS and 289 controls (77% white, 23% black). Androgen receptor genotype, X-chromosome methylation, and phenotyping for PCOS were measured. A smaller biallelic mean of CAG repeats was associated with increased odds of PCOS. X-chromosome inactivation was not different comparing cases with controls; however, in the subset with nonrandom inactivation, the chromosome bearing the shorter CAG allele was preferentially active in PCOS women. Association of shorter CAG repeats with PCOS is consistent with in vitro functional studies demonstrating higher activity of androgen receptors expressed from alleles with fewer CAG repeats, suggesting inherited alteration in androgen sensitivity may contribute to PCOS. In some women, such heightened sensitivity may also result from preferential expression of androgen receptors with shorter alleles. Thus, genetic and epigenetic changes may be involved in the pathogenesis of PCOS. Context: Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the androgen receptor exon 1 polymorphic CAG repeat have produced conflicting results in PCOS. Objective: We tested the hypothesis that a lower number of CAG repeats is associated with increased odds of PCOS. We also compared X-chromosome inactivation between cases and controls. Design: Women with and without PCOS were genotyped for the CAG repeat and assessed for X-chromosome methylation. Association analyses were performed. Setting: Subjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; controls were recruited from the surrounding community. Genotyping took place at Cedars-Sinai Medical Center in Los Angeles. Participants: Participants included 330 women with PCOS and 289 controls (77% white, 23% black). Main Measurements: Androgen receptor genotype, X-chromosome methylation, and phenotyping for PCOS were measured. Results: A smaller biallelic mean of CAG repeats was associated with increased odds of PCOS. X-chromosome inactivation was not different comparing cases with controls; however, in the subset with nonrandom inactivation, the chromosome bearing the shorter CAG allele was preferentially active in PCOS women. Conclusions: Association of shorter CAG repeats with PCOS is consistent with in vitro functional studies demonstrating higher activity of androgen receptors expressed from alleles with fewer CAG repeats, suggesting inherited alteration in androgen sensitivity may contribute to PCOS. In some women, such heightened sensitivity may also result from preferential expression of androgen receptors with shorter alleles. Thus, genetic and epigenetic changes may be involved in the pathogenesis of PCOS. This study suggests that in addition to excess androgen production, the risk of polycystic ovary syndrome is associated with the inheritance of androgen receptors with shorter polyglutamine tracts, suggesting that genetic differences in androgen sensitivity may contribute to the development of the syndrome. Context: Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the androgen receptor exon 1 polymorphic CAG repeat have produced conflicting results in PCOS. Objective: We tested the hypothesis that a lower number of CAG repeats is associated with increased odds of PCOS. We also compared X-chromosome inactivation between cases and controls. Design: Women with and without PCOS were genotyped for the CAG repeat and assessed for X-chromosome methylation. Association analyses were performed. Setting: Subjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; controls were recruited from the surrounding community. Genotyping took place at Cedars-Sinai Medical Center in Los Angeles. Participants: Participants included 330 women with PCOS and 289 controls (77% white, 23% black). Main Measurements: Androgen receptor genotype, X-chromosome methylation, and phenotyping for PCOS were measured. Results: A smaller biallelic mean of CAG repeats was associated with increased odds of PCOS. X-chromosome inactivation was not different comparing cases with controls; however, in the subset with nonrandom inactivation, the chromosome bearing the shorter CAG allele was preferentially active in PCOS women. Conclusions: Association of shorter CAG repeats with PCOS is consistent with in vitro functional studies demonstrating higher activity of androgen receptors expressed from alleles with fewer CAG repeats, suggesting inherited alteration in androgen sensitivity may contribute to PCOS. In some women, such heightened sensitivity may also result from preferential expression of androgen receptors with shorter alleles. Thus, genetic and epigenetic changes may be involved in the pathogenesis of PCOS. |
| Author | Antoine, Heath J. Shah, Nissar A. Goodarzi, Mark O. Taylor, Kent D. Azziz, Ricardo Pall, Marita |
| Author_xml | – sequence: 1 givenname: Nissar A. surname: Shah fullname: Shah, Nissar A. organization: 1Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine (N.A.S., H.J.A., M.O.G.), Cedars-Sinai Medical Center, Los Angeles, California 90048 – sequence: 2 givenname: Heath J. surname: Antoine fullname: Antoine, Heath J. organization: 1Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine (N.A.S., H.J.A., M.O.G.), Cedars-Sinai Medical Center, Los Angeles, California 90048 – sequence: 3 givenname: Marita surname: Pall fullname: Pall, Marita organization: 2Department of Obstetrics and Gynecology (M.P., R.A., M.O.G.), Cedars-Sinai Medical Center, Los Angeles, California 90048 – sequence: 4 givenname: Kent D. surname: Taylor fullname: Taylor, Kent D. organization: 3Department of Medical Genetics Institute (K.D.T., M.O.G.), Cedars-Sinai Medical Center, Los Angeles, California 90048 – sequence: 5 givenname: Ricardo surname: Azziz fullname: Azziz, Ricardo organization: 2Department of Obstetrics and Gynecology (M.P., R.A., M.O.G.), Cedars-Sinai Medical Center, Los Angeles, California 90048 – sequence: 6 givenname: Mark O. surname: Goodarzi fullname: Goodarzi, Mark O. email: mark.goodarzi@cshs.org organization: 1Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine (N.A.S., H.J.A., M.O.G.), Cedars-Sinai Medical Center, Los Angeles, California 90048 |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20323528$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/18303071$$D View this record in MEDLINE/PubMed |
| BookMark | eNqFkt1rFDEUxYNU7Lb65rMMiPri1JuPSTIvwrK0VShUtIhvIZvJtFlmkmkyU9j_3uyHixbFp5Dkd09O7j0n6MgHbxF6ieEMEwwfVuaMAMgSgMonaIZrVpUC1-IIzQAILmtBfhyjk5RWAJixij5Dx1hSoCDwDH2fpxSM06MLvghtMfdNDLfWF1-tscMYYrGYX-bNYPVYfAndug9xuHOpL7RvtgdmnUZniusHHdfFt_WmvrfP0dNWd8m-2K-n6Obi_Gbxqby6vvy8mF-VhvFqLDlvCCOkJpRRXnHguKrlkhIK0DAspKTUtpharCuGa8zbiglTtaAlNKZa0lP0cSc7TMveNsb6MepODdH12Y0K2qk_b7y7U7fhQREqORE8C7zdC8RwP9k0qt4lY7tOexumpHiNayqyu_-BBKSoBYcMvn4ErsIUfW6CopgzWmcxkalXvxs_OP41mAy82QM6Gd21UXvj0oEjkJtUEZk5suNMDClF2yrjxu00839dpzCoTUrUyqhNStQmJbno_aOiw_t_x9_t8DAN_yK38aM_AZ2Kxzg |
| CODEN | JCEMAZ |
| CitedBy_id | crossref_primary_10_1016_j_mce_2015_11_030 crossref_primary_10_1186_s43042_022_00292_y crossref_primary_10_1586_eog_10_73 crossref_primary_10_1111_jsm_12268 crossref_primary_10_1007_s43032_021_00516_3 crossref_primary_10_1016_j_bpobgyn_2016_04_002 crossref_primary_10_1016_j_gyobfe_2010_08_021 crossref_primary_10_1007_s11033_013_2605_4 crossref_primary_10_1007_s40618_020_01215_7 crossref_primary_10_1080_09513590802342841 crossref_primary_10_1016_j_gene_2013_04_040 crossref_primary_10_1016_j_psyneuen_2008_12_007 crossref_primary_10_3390_biomedicines10030540 crossref_primary_10_1371_journal_pone_0012401 crossref_primary_10_1016_j_arr_2021_101488 crossref_primary_10_1038_s41598_020_65890_5 crossref_primary_10_1007_s10815_010_9485_5 crossref_primary_10_1016_j_atherosclerosis_2015_03_021 crossref_primary_10_1016_j_rbmo_2014_02_011 crossref_primary_10_2217_WHE_10_53 crossref_primary_10_25208_vdv982 crossref_primary_10_1530_JOE_14_0469 crossref_primary_10_1371_journal_pone_0017718 crossref_primary_10_1093_humrep_deq181 crossref_primary_10_1016_S0084_3741_08_79245_X crossref_primary_10_1186_s13048_023_01295_y crossref_primary_10_33589_23_3_0077 crossref_primary_10_1093_humrep_dep296 crossref_primary_10_1002_prp2_541 crossref_primary_10_1016_j_ijgo_2012_08_016 crossref_primary_10_2164_jandrol_111_014415 crossref_primary_10_1016_j_fertnstert_2009_10_020 crossref_primary_10_1111_j_1365_2265_2009_03598_x crossref_primary_10_1210_en_2017_03218 crossref_primary_10_1007_s11033_012_1688_7 crossref_primary_10_18311_jer_2023_34654 crossref_primary_10_3892_mmr_2016_5414 crossref_primary_10_1016_j_isci_2023_106131 crossref_primary_10_1093_molehr_gas024 crossref_primary_10_1093_humupd_dmq048 crossref_primary_10_1111_ddg_15630 crossref_primary_10_1016_j_psyneuen_2021_105604 crossref_primary_10_1111_ddg_15630_g crossref_primary_10_1210_en_2019_00389 crossref_primary_10_1371_journal_pone_0195046 crossref_primary_10_1210_en_2013_1764 crossref_primary_10_1371_journal_pone_0075709 crossref_primary_10_3390_biomedicines11082215 crossref_primary_10_1371_journal_pone_0148548 crossref_primary_10_1071_RD09190 crossref_primary_10_1586_eem_10_32 crossref_primary_10_1016_j_psyneuen_2013_12_003 crossref_primary_10_1073_pnas_1418216112 crossref_primary_10_1097_gme_0b013e31821b81b8 crossref_primary_10_18502_ijrm_v20i3_10711 crossref_primary_10_56543_aaeeu_2023_2_3_02 crossref_primary_10_1016_j_fertnstert_2015_09_043 crossref_primary_10_1007_s12013_013_9602_z crossref_primary_10_1007_s10815_014_0286_0 crossref_primary_10_1016_j_contraception_2011_10_007 crossref_primary_10_1016_j_mce_2017_09_007 crossref_primary_10_1177_1933719114565037 crossref_primary_10_1186_s13048_021_00879_w crossref_primary_10_1016_j_rbmo_2015_09_007 crossref_primary_10_1093_humrep_dep074 crossref_primary_10_3390_diagnostics12081922 crossref_primary_10_1016_j_reprotox_2022_04_010 crossref_primary_10_14341_probl201056648_54 crossref_primary_10_3109_09513590_2011_650744 crossref_primary_10_1080_15592294_2020_1754674 crossref_primary_10_1155_2018_7624932 crossref_primary_10_1530_EJE_10_0205 crossref_primary_10_1016_j_jsbmb_2011_11_006 crossref_primary_10_1155_2017_3507671 |
| Cites_doi | 10.1152/japplphysiol.00537.2004 10.1210/jc.2006-0227 10.1093/nar/22.15.3181 10.1210/jc.2006-0069 10.1177/120347549800300103 10.1210/jcem.85.9.6832 10.1530/EJE-06-0607 10.1210/jc.2002-021791 10.1111/j.1745-7262.2007.00250.x 10.1146/annurev.genet.31.1.571 10.1093/jnci/92.24.2009 10.1038/sj.ijo.0802191 10.1007/s00125-002-0980-9 10.1210/jcem.87.1.8137 10.1016/S0090-4295(98)00481-6 10.1016/j.fertnstert.2004.11.080 10.1073/pnas.96.15.8573 10.1530/eje.1.02195 10.1210/er.2007-0019 10.1182/blood.V88.1.59.59 10.1046/j.1365-2141.1997.2573078.x 10.1210/jc.2003-032046 10.1677/jme.0.0250085 10.1016/j.jsgi.2004.11.003 10.1016/j.fertnstert.2005.01.096 10.1158/1055-9965.1765.13.11 10.1126/science.3353727 10.1210/jc.2007-1110 10.1093/humrep/dem382 |
| ContentType | Journal Article |
| Copyright | Copyright © 2008 by The Endocrine Society 2008 2008 INIST-CNRS Copyright © 2008 by The Endocrine Society Copyright © 2008 by The Endocrine Society 2008 |
| Copyright_xml | – notice: Copyright © 2008 by The Endocrine Society 2008 – notice: 2008 INIST-CNRS – notice: Copyright © 2008 by The Endocrine Society – notice: Copyright © 2008 by The Endocrine Society 2008 |
| DBID | AAYXX CITATION IQODW CGR CUY CVF ECM EIF NPM 7QP 7T5 7TM H94 K9. 8FD FR3 P64 RC3 7X8 5PM |
| DOI | 10.1210/jc.2008-0038 |
| DatabaseName | CrossRef Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Calcium & Calcified Tissue Abstracts Immunology Abstracts Nucleic Acids Abstracts AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) Technology Research Database Engineering Research Database Biotechnology and BioEngineering Abstracts Genetics Abstracts MEDLINE - Academic PubMed Central (Full Participant titles) |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) Immunology Abstracts Calcium & Calcified Tissue Abstracts Nucleic Acids Abstracts Genetics Abstracts Engineering Research Database Technology Research Database Biotechnology and BioEngineering Abstracts MEDLINE - Academic |
| DatabaseTitleList | AIDS and Cancer Research Abstracts MEDLINE - Academic MEDLINE Genetics Abstracts |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1945-7197 |
| EndPage | 1945 |
| ExternalDocumentID | PMC2386276 18303071 20323528 10_1210_jc_2008_0038 10.1210/jc.2008-0038 |
| Genre | Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
| GrantInformation_xml | – fundername: NICHD NIH HHS grantid: R01 HD 29364 – fundername: NICHD NIH HHS grantid: K24 HD 01346 – fundername: NCRR NIH HHS grantid: M01 RR000425 – fundername: NICHD NIH HHS grantid: R01 HD029364 – fundername: NICHD NIH HHS grantid: K24 HD001346 – fundername: NCRR NIH HHS grantid: M01 RR 00425 |
| GroupedDBID | --- -~X .55 .XZ 08P 0R~ 18M 1TH 29K 2WC 34G 354 39C 4.4 48X 53G 5GY 5RS 5YH 8F7 AABZA AACZT AAIMJ AAPQZ AAPXW AARHZ AAUAY AAVAP AAWTL ABBLC ABDFA ABEJV ABGNP ABJNI ABLJU ABMNT ABNHQ ABOCM ABPMR ABPPZ ABPQP ABPTD ABQNK ABVGC ABWST ABXVV ACGFO ACGFS ACPRK ACUTJ ACYHN ADBBV ADGKP ADGZP ADHKW ADQBN ADRTK ADVEK AELWJ AEMDU AENEX AENZO AERZD AETBJ AEWNT AFCHL AFFNX AFFZL AFGWE AFOFC AFRAH AFXAL AGINJ AGKRT AGQXC AGUTN AHMBA AHMMS AJEEA ALMA_UNASSIGNED_HOLDINGS APIBT ARIXL ASPBG ATGXG AVWKF AZFZN BAWUL BAYMD BCRHZ BEYMZ BSWAC BTRTY C45 CDBKE CS3 D-I DAKXR DIK E3Z EBS EJD EMOBN ENERS F5P FECEO FHSFR FLUFQ FOEOM FOTVD FQBLK GAUVT GJXCC GX1 H13 HZ~ H~9 KBUDW KOP KQ8 KSI KSN L7B M5~ MHKGH MJL N4W N9A NLBLG NOMLY NOYVH NVLIB O9- OAUYM OBH OCB ODMLO OFXIZ OGEVE OHH OJZSN OK1 OPAEJ OVD OVIDX P2P P6G REU ROX ROZ TEORI TJX TLC TR2 TWZ VVN W8F WOQ X7M YBU YFH YHG YOC YSK ZY1 ~02 ~H1 AAYXX ABXZS ADNBA AEMQT AEOTA AFYAG AGORE ALXQX CITATION NU- .GJ 3O- 7X7 88E 8FI 8FJ AAJQQ AAKAS AAPGJ AAQQT AAUQX AAWDT AAYJJ ABDPE ABUWG ACFRR ACVCV ACZBC ADMTO ADZCM AFFQV AFKRA AGMDO AHGBF AI. AJBYB AJDVS APJGH AQDSO AQKUS AVNTJ BENPR BPHCQ BVXVI CCPQU EIHJH FEDTE FYUFA HMCUK HVGLF IAO IHR INH IQODW ITC J5H M1P MBLQV OBFPC PHGZM PHGZT PJZUB PPXIY PQQKQ PROAC PSQYO TMA UKHRP VH1 WHG X52 ZGI ZXP 3V. CGR CUY CVF ECM EIF NPM VXZ 7QP 7T5 7TM H94 K9. 8FD FR3 P64 RC3 7X8 5PM |
| ID | FETCH-LOGICAL-c465t-66d242292343656061598b32300d4178833ef13e1a541916f547c5f0a80dc5b3 |
| ISSN | 0021-972X |
| IngestDate | Tue Sep 02 05:54:45 EDT 2025 Thu Sep 04 19:17:45 EDT 2025 Mon Sep 08 17:45:30 EDT 2025 Mon Jun 30 12:42:06 EDT 2025 Wed Feb 19 01:51:28 EST 2025 Mon Jul 21 09:15:33 EDT 2025 Tue Jul 01 04:01:26 EDT 2025 Thu Apr 24 23:10:11 EDT 2025 Fri Feb 07 10:35:24 EST 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 5 |
| Keywords | Obesity Genetic variability Nutrition Nutrition disorder Female sterility Genotype Metabolic diseases Polycystic ovary Female genital diseases Ovarian diseases Association Microsatellite DNA Cyst Androgen receptor Benign neoplasm Endocrinology Nutritional status Polymorphism Hormonal receptor |
| Language | English |
| License | CC BY 4.0 |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c465t-66d242292343656061598b32300d4178833ef13e1a541916f547c5f0a80dc5b3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Address all correspondence and requests for reprints to: Mark O. Goodarzi, M.D., Ph.D., Division of Endocrinology, Diabetes, and Metabolism, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Room B-131, Los Angeles, California 90048. E-mail: mark.goodarzi@cshs.org. |
| PMID | 18303071 |
| PQID | 3164393437 |
| PQPubID | 2046206 |
| PageCount | 7 |
| ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_2386276 proquest_miscellaneous_69193734 proquest_miscellaneous_20879760 proquest_journals_3164393437 pubmed_primary_18303071 pascalfrancis_primary_20323528 crossref_citationtrail_10_1210_jc_2008_0038 crossref_primary_10_1210_jc_2008_0038 oup_primary_10_1210_jc_2008-0038 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2008-05-01 |
| PublicationDateYYYYMMDD | 2008-05-01 |
| PublicationDate_xml | – month: 05 year: 2008 text: 2008-05-01 day: 01 |
| PublicationDecade | 2000 |
| PublicationPlace | Bethesda, MD |
| PublicationPlace_xml | – name: Bethesda, MD – name: United States – name: Washington |
| PublicationTitle | The journal of clinical endocrinology and metabolism |
| PublicationTitleAlternate | J Clin Endocrinol Metab |
| PublicationYear | 2008 |
| Publisher | Oxford University Press Endocrine Society The Endocrine Society |
| Publisher_xml | – name: Oxford University Press – name: Endocrine Society – name: The Endocrine Society |
| References | Sawaya ( key 2019041114095908200_R11) 1998; 3 Lubahn ( key 2019041114095908200_R1) 1988; 240 Xita ( key 2019041114095908200_R21) 2008; 23 Gale ( key 2019041114095908200_R31) 1997; 98 Rajender ( key 2019041114095908200_R3) 2007; 9 Naumova ( key 2019041114095908200_R25) 1996; 58 Zitzmann ( key 2019041114095908200_R35) 2003; 46 Tut ( key 2019041114095908200_R5) 1997; 82 Mifsud ( key 2019041114095908200_R17) 2000; 85 Zawadzki ( key 2019041114095908200_R22) 1992 Azziz ( key 2019041114095908200_R23) 2004; 89 Westberg ( key 2019041114095908200_R28) 2001; 86 Walsh ( key 2019041114095908200_R34) 2005; 98 Busque ( key 2019041114095908200_R30) 1996; 88 Brum ( key 2019041114095908200_R29) 2005; 12 Brownstein ( key 2019041114095908200_R24) 1996 Heard ( key 2019041114095908200_R26) 1997; 31 Legro ( key 2019041114095908200_R9) 1994; 83 Sartor ( key 2019041114095908200_R37) 1999; 53 Zeegers ( key 2019041114095908200_R8) 2004; 13 Gustafson ( key 2019041114095908200_R32) 2003; 27 Mohlig ( key 2019041114095908200_R18) 2006; 155 Kim ( key 2019041114095908200_R20) 2008 Ibanez ( key 2019041114095908200_R10) 2003; 88 Hickey ( key 2019041114095908200_R15) 2006; 91 Heemers ( key 2019041114095908200_R38) 2007; 28 Lapauw ( key 2019041114095908200_R33) 2007; 156 Beilin ( key 2019041114095908200_R6) 2000; 25 Calvo ( key 2019041114095908200_R13) 2000; 85 Chamberlain ( key 2019041114095908200_R4) 1994; 22 Davis-Dao ( key 2019041114095908200_R7) 2007; 92 Platz ( key 2019041114095908200_R36) 2000; 92 Goodarzi ( key 2019041114095908200_R39) 2006; 91 Hickey ( key 2019041114095908200_R14) 2002; 87 Jaaskelainen ( key 2019041114095908200_R16) 2005; 83 Urbanek ( key 2019041114095908200_R19) 1999; 96 Brown ( key 2019041114095908200_R2) 1989; 44 Chang ( key 2019041114095908200_R12) 2005; 83 Vottero ( key 2019041114095908200_R27) 1999; 84 16793958 - Eur J Endocrinol. 2006 Jul;155(1):127-30 9332303 - Br J Haematol. 1997 Sep;98(3):512-9 10770223 - J Clin Endocrinol Metab. 2000 Apr;85(4):1735-40 7909364 - Obstet Gynecol. 1994 May;83(5 Pt 1):701-6 10411917 - Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8573-8 17684052 - J Clin Endocrinol Metab. 2007 Nov;92(11):4319-26 8065934 - Nucleic Acids Res. 1994 Aug 11;22(15):3181-6 12843184 - J Clin Endocrinol Metab. 2003 Jul;88(7):3333-8 12637980 - Diabetologia. 2003 Jan;46(1):31-9 8780871 - Biotechniques. 1996 Jun;20(6):1004-6, 1008-10 9360540 - J Clin Endocrinol Metab. 1997 Nov;82(11):3777-82 15533905 - Cancer Epidemiol Biomarkers Prev. 2004 Nov;13(11 Pt 1):1765-71 3353727 - Science. 1988 Apr 15;240(4850):327-30 17322500 - Eur J Endocrinol. 2007 Mar;156(3):395-401 17940184 - Endocr Rev. 2007 Dec;28(7):778-808 15377647 - J Appl Physiol (1985). 2005 Jan;98(1):132-7 11397855 - J Clin Endocrinol Metab. 2001 Jun;86(6):2562-8 18191848 - Fertil Steril. 2008 Dec;90(6):2318-23 15950641 - Fertil Steril. 2005 Jun;83(6):1717-23 15950642 - Fertil Steril. 2005 Jun;83(6):1724-8 10084600 - J Clin Endocrinol Metab. 1999 Mar;84(3):1091-5 17334586 - Asian J Androl. 2007 Mar;9(2):147-79 15181052 - J Clin Endocrinol Metab. 2004 Jun;89(6):2745-9 10915221 - J Mol Endocrinol. 2000 Aug;25(1):85-96 11788641 - J Clin Endocrinol Metab. 2002 Jan;87(1):161-5 10999852 - J Clin Endocrinol Metab. 2000 Sep;85(9):3484-8 2563196 - Am J Hum Genet. 1989 Feb;44(2):264-9 9677254 - J Cutan Med Surg. 1998 Jul;3(1):9-15 18192296 - Hum Reprod. 2008 Mar;23(3):693-8 8651287 - Am J Hum Genet. 1996 Jun;58(6):1111-9 16636126 - J Clin Endocrinol Metab. 2006 Jul;91(7):2789-91 11121463 - J Natl Cancer Inst. 2000 Dec 20;92(24):2009-17 9442908 - Annu Rev Genet. 1997;31:571-610 16849416 - J Clin Endocrinol Metab. 2006 Oct;91(10):4085-91 9933058 - Urology. 1999 Feb;53(2):378-80 8704202 - Blood. 1996 Jul 1;88(1):59-65 15695110 - J Soc Gynecol Investig. 2005 Feb;12(2):135-41 12532157 - Int J Obes Relat Metab Disord. 2003 Jan;27(1):75-81 |
| References_xml | – volume: 98 start-page: 132 year: 2005 ident: key 2019041114095908200_R34 article-title: Androgen receptor CAG repeat polymorphism is associated with fat-free mass in men. publication-title: J Appl Physiol doi: 10.1152/japplphysiol.00537.2004 – volume: 91 start-page: 4085 year: 2006 ident: key 2019041114095908200_R39 article-title: Variants in the 5α-reductase type 1 and type 2 genes are associated with polycystic ovary syndrome and the severity of hirsutism in affected women. publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2006-0227 – volume: 22 start-page: 3181 year: 1994 ident: key 2019041114095908200_R4 article-title: The length and location of CAG trinucleotide repeats in the androgen receptor N-terminal domain affect transactivation function. publication-title: Nucleic Acids Res doi: 10.1093/nar/22.15.3181 – volume: 91 start-page: 2789 year: 2006 ident: key 2019041114095908200_R15 article-title: Epigenetic modification of the X chromosome influences susceptibility to polycystic ovary syndrome. publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2006-0069 – volume: 84 start-page: 1091 year: 1999 ident: key 2019041114095908200_R27 article-title: Androgen receptor-mediated hypersensitivity to androgens in women with nonhyperandrogenic hirsutism: skewing of X-chromosome inactivation. publication-title: J Clin Endocrinol Metab – volume: 3 start-page: 9 year: 1998 ident: key 2019041114095908200_R11 article-title: Androgen receptor polymorphisms (CAG repeat lengths) in androgenetic alopecia, hirsutism, and acne. publication-title: J Cutan Med Surg doi: 10.1177/120347549800300103 – volume: 85 start-page: 3484 year: 2000 ident: key 2019041114095908200_R17 article-title: Androgen receptor gene CAG trinucleotide repeats in anovulatory infertility and polycystic ovaries. publication-title: J Clin Endocrinol Metab doi: 10.1210/jcem.85.9.6832 – volume: 44 start-page: 264 year: 1989 ident: key 2019041114095908200_R2 article-title: Androgen receptor locus on the human X chromosome: regional localization to Xq11–12 and description of a DNA polymorphism. publication-title: Am J Hum Genet – volume: 156 start-page: 395 year: 2007 ident: key 2019041114095908200_R33 article-title: Is the effect of testosterone on body composition modulated by the androgen receptor gene CAG repeat polymorphism in elderly men? publication-title: Eur J Endocrinol doi: 10.1530/EJE-06-0607 – volume: 88 start-page: 3333 year: 2003 ident: key 2019041114095908200_R10 article-title: Androgen receptor gene CAG repeat polymorphism in the development of ovarian hyperandrogenism. publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2002-021791 – volume: 9 start-page: 147 year: 2007 ident: key 2019041114095908200_R3 article-title: Phenotypic heterogeneity of mutations in androgen receptor gene. publication-title: Asian J Androl doi: 10.1111/j.1745-7262.2007.00250.x – volume: 31 start-page: 571 year: 1997 ident: key 2019041114095908200_R26 article-title: X-chromosome inactivation in mammals. publication-title: Annu Rev Genet doi: 10.1146/annurev.genet.31.1.571 – volume: 92 start-page: 2009 year: 2000 ident: key 2019041114095908200_R36 article-title: Racial variation in prostate cancer incidence and in hormonal system markers among male health professionals. publication-title: J Natl Cancer Inst doi: 10.1093/jnci/92.24.2009 – volume: 27 start-page: 75 year: 2003 ident: key 2019041114095908200_R32 article-title: Androgen receptor gene repeats and indices of obesity in older adults. publication-title: Int J Obes Relat Metab Disord doi: 10.1038/sj.ijo.0802191 – volume: 83 start-page: 701 year: 1994 ident: key 2019041114095908200_R9 article-title: Size polymorphisms of the androgen receptor among female Hispanics and correlation with androgenic characteristics. publication-title: Obstet Gynecol – volume: 46 start-page: 31 year: 2003 ident: key 2019041114095908200_R35 article-title: The CAG repeat polymorphism in the androgen receptor gene modulates body fat mass and serum concentrations of leptin and insulin in men. publication-title: Diabetologia doi: 10.1007/s00125-002-0980-9 – volume: 87 start-page: 161 year: 2002 ident: key 2019041114095908200_R14 article-title: The androgen receptor CAG repeat polymorphism and X-chromosome inactivation in Australian Caucasian women with infertility related to polycystic ovary syndrome. publication-title: J Clin Endocrinol Metab doi: 10.1210/jcem.87.1.8137 – volume: 53 start-page: 378 year: 1999 ident: key 2019041114095908200_R37 article-title: Androgen receptor gene CAG repeat length varies in a race-specific fashion in men without prostate cancer. publication-title: Urology doi: 10.1016/S0090-4295(98)00481-6 – volume: 83 start-page: 1724 year: 2005 ident: key 2019041114095908200_R16 article-title: Androgen receptor gene CAG length polymorphism in women with polycystic ovary syndrome. publication-title: Fertil Steril doi: 10.1016/j.fertnstert.2004.11.080 – volume: 86 start-page: 2562 year: 2001 ident: key 2019041114095908200_R28 article-title: Polymorphisms of the androgen receptor gene and the estrogen receptor β gene are associated with androgen levels in women. publication-title: J Clin Endocrinol Metab – volume: 96 start-page: 8573 year: 1999 ident: key 2019041114095908200_R19 article-title: Thirty-seven candidate genes for polycystic ovary syndrome: strongest evidence for linkage is with follistatin. publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.96.15.8573 – volume: 85 start-page: 1735 year: 2000 ident: key 2019041114095908200_R13 article-title: The role of the CAG repeat polymorphism in the androgen receptor gene and of skewed X-chromosome inactivation, in the pathogenesis of hirsutism. publication-title: J Clin Endocrinol Metab – volume: 155 start-page: 127 year: 2006 ident: key 2019041114095908200_R18 article-title: The androgen receptor CAG repeat modifies the impact of testosterone on insulin resistance in women with polycystic ovary syndrome. publication-title: Eur J Endocrinol doi: 10.1530/eje.1.02195 – volume: 28 start-page: 778 year: 2007 ident: key 2019041114095908200_R38 article-title: Androgen receptor (AR) coregulators: a diversity of functions converging on and regulating the AR transcriptional complex. publication-title: Endocr Rev doi: 10.1210/er.2007-0019 – start-page: 377 year: 1992 ident: key 2019041114095908200_R22 article-title: Diagnostic criteria for polycystic ovary syndrome: towards a rational approach publication-title: In: Dunaif A, Givens JR, Haseltine F, Merriam GR, eds. Polycystic ovary syndrome. Cambridge, UK: Blackwell Scientific Publications; – volume: 88 start-page: 59 year: 1996 ident: key 2019041114095908200_R30 article-title: Nonrandom X-inactivation patterns in normal females: lyonization ratios vary with age. publication-title: Blood doi: 10.1182/blood.V88.1.59.59 – volume: 98 start-page: 512 year: 1997 ident: key 2019041114095908200_R31 article-title: Acquired skewing of X-chromosome inactivation patterns in myeloid cells of the elderly suggests stochastic clonal loss with age. publication-title: Br J Haematol doi: 10.1046/j.1365-2141.1997.2573078.x – volume: 89 start-page: 2745 year: 2004 ident: key 2019041114095908200_R23 article-title: The prevalence and features of the polycystic ovary syndrome in an unselected population. publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2003-032046 – volume: 25 start-page: 85 year: 2000 ident: key 2019041114095908200_R6 article-title: Effect of the androgen receptor CAG repeat polymorphism on transcriptional activity: specificity in prostate and non-prostate cell lines. publication-title: J Mol Endocrinol doi: 10.1677/jme.0.0250085 – year: 2008 ident: key 2019041114095908200_R20 article-title: Androgen receptor gene CAG repeat polymorphism in women with polycystic ovary syndrome publication-title: Fertil Steril – volume: 12 start-page: 135 year: 2005 ident: key 2019041114095908200_R29 article-title: Association between androgen receptor gene CAG repeat polymorphism and plasma testosterone levels in postmenopausal women. publication-title: J Soc Gynecol Investig doi: 10.1016/j.jsgi.2004.11.003 – volume: 83 start-page: 1717 year: 2005 ident: key 2019041114095908200_R12 article-title: Phenotypic spectrum of polycystic ovary syndrome: clinical and biochemical characterization of the three major clinical subgroups. publication-title: Fertil Steril doi: 10.1016/j.fertnstert.2005.01.096 – volume: 13 start-page: 1765 year: 2004 ident: key 2019041114095908200_R8 article-title: How strong is the association between CAG and GGN repeat length polymorphisms in the androgen receptor gene and prostate cancer risk? publication-title: Cancer Epidemiol Biomarkers Prev doi: 10.1158/1055-9965.1765.13.11 – start-page: 1008 year: 1996 ident: key 2019041114095908200_R24 article-title: Modulation of non-templated nucleotide addition by Taq DNA polymerase: primer modifications that facilitate genotyping publication-title: Biotechniques 20:1004–1006, – volume: 58 start-page: 1111 year: 1996 ident: key 2019041114095908200_R25 article-title: Heritability of X chromosome—inactivation phenotype in a large family. publication-title: Am J Hum Genet – volume: 240 start-page: 327 year: 1988 ident: key 2019041114095908200_R1 article-title: Cloning of human androgen receptor complementary DNA and localization to the X chromosome. publication-title: Science doi: 10.1126/science.3353727 – volume: 92 start-page: 4319 year: 2007 ident: key 2019041114095908200_R7 article-title: Male infertility and variation in CAG repeat length in the androgen receptor gene: a meta-analysis. publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2007-1110 – volume: 82 start-page: 3777 year: 1997 ident: key 2019041114095908200_R5 article-title: Long polyglutamine tracts in the androgen receptor are associated with reduced trans-activation, impaired sperm production, and male infertility. publication-title: J Clin Endocrinol Metab – volume: 23 start-page: 693 year: 2008 ident: key 2019041114095908200_R21 article-title: The role of sex hormone-binding globulin and androgen receptor gene variants in the development of polycystic ovary syndrome. publication-title: Hum Reprod doi: 10.1093/humrep/dem382 – reference: 10770223 - J Clin Endocrinol Metab. 2000 Apr;85(4):1735-40 – reference: 9332303 - Br J Haematol. 1997 Sep;98(3):512-9 – reference: 15377647 - J Appl Physiol (1985). 2005 Jan;98(1):132-7 – reference: 7909364 - Obstet Gynecol. 1994 May;83(5 Pt 1):701-6 – reference: 10915221 - J Mol Endocrinol. 2000 Aug;25(1):85-96 – reference: 9933058 - Urology. 1999 Feb;53(2):378-80 – reference: 16636126 - J Clin Endocrinol Metab. 2006 Jul;91(7):2789-91 – reference: 12532157 - Int J Obes Relat Metab Disord. 2003 Jan;27(1):75-81 – reference: 3353727 - Science. 1988 Apr 15;240(4850):327-30 – reference: 8065934 - Nucleic Acids Res. 1994 Aug 11;22(15):3181-6 – reference: 2563196 - Am J Hum Genet. 1989 Feb;44(2):264-9 – reference: 9360540 - J Clin Endocrinol Metab. 1997 Nov;82(11):3777-82 – reference: 17940184 - Endocr Rev. 2007 Dec;28(7):778-808 – reference: 10999852 - J Clin Endocrinol Metab. 2000 Sep;85(9):3484-8 – reference: 11397855 - J Clin Endocrinol Metab. 2001 Jun;86(6):2562-8 – reference: 8651287 - Am J Hum Genet. 1996 Jun;58(6):1111-9 – reference: 11121463 - J Natl Cancer Inst. 2000 Dec 20;92(24):2009-17 – reference: 11788641 - J Clin Endocrinol Metab. 2002 Jan;87(1):161-5 – reference: 15181052 - J Clin Endocrinol Metab. 2004 Jun;89(6):2745-9 – reference: 15533905 - Cancer Epidemiol Biomarkers Prev. 2004 Nov;13(11 Pt 1):1765-71 – reference: 17684052 - J Clin Endocrinol Metab. 2007 Nov;92(11):4319-26 – reference: 9677254 - J Cutan Med Surg. 1998 Jul;3(1):9-15 – reference: 16849416 - J Clin Endocrinol Metab. 2006 Oct;91(10):4085-91 – reference: 17334586 - Asian J Androl. 2007 Mar;9(2):147-79 – reference: 15695110 - J Soc Gynecol Investig. 2005 Feb;12(2):135-41 – reference: 18192296 - Hum Reprod. 2008 Mar;23(3):693-8 – reference: 10084600 - J Clin Endocrinol Metab. 1999 Mar;84(3):1091-5 – reference: 15950641 - Fertil Steril. 2005 Jun;83(6):1717-23 – reference: 8704202 - Blood. 1996 Jul 1;88(1):59-65 – reference: 17322500 - Eur J Endocrinol. 2007 Mar;156(3):395-401 – reference: 12843184 - J Clin Endocrinol Metab. 2003 Jul;88(7):3333-8 – reference: 18191848 - Fertil Steril. 2008 Dec;90(6):2318-23 – reference: 8780871 - Biotechniques. 1996 Jun;20(6):1004-6, 1008-10 – reference: 15950642 - Fertil Steril. 2005 Jun;83(6):1724-8 – reference: 16793958 - Eur J Endocrinol. 2006 Jul;155(1):127-30 – reference: 9442908 - Annu Rev Genet. 1997;31:571-610 – reference: 12637980 - Diabetologia. 2003 Jan;46(1):31-9 – reference: 10411917 - Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8573-8 |
| SSID | ssj0014453 |
| Score | 2.2466686 |
| Snippet | Context: Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the... Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the androgen... CONTEXT: Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the... Context: Genetically determined heightened androgen sensitivity may influence the phenotype of polycystic ovary syndrome (PCOS). To date, studies of the... |
| SourceID | pubmedcentral proquest pubmed pascalfrancis crossref oup |
| SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 1939 |
| SubjectTerms | Adolescent Adult Alleles Androgen receptors Androgens Biological and medical sciences Endocrinology Endocrinopathies Epigenetics Feeding. Feeding behavior Female Fundamental and applied biological sciences. Psychology Gene polymorphism Genotyping Humans Medical sciences Methylation Middle Aged Original Ovaries Phenotypes Phenotyping Polycystic ovary syndrome Polycystic Ovary Syndrome - genetics Polyglutamine Polymorphism, Genetic Receptors, Androgen - genetics Trinucleotide Repeats Vertebrates: anatomy and physiology, studies on body, several organs or systems Vertebrates: endocrinology X Chromosome Inactivation X chromosomes |
| Title | Association of Androgen Receptor CAG Repeat Polymorphism and Polycystic Ovary Syndrome |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/18303071 https://www.proquest.com/docview/3164393437 https://www.proquest.com/docview/20879760 https://www.proquest.com/docview/69193734 https://pubmed.ncbi.nlm.nih.gov/PMC2386276 |
| Volume | 93 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9NAEF6FIiGkCvEmUMoe4GQ58mPXax-j8gitApUIqLdovfaqRcGOGqcS_Bp-KjNeP4sjFS5WZI8de-fz7sx45htCXjuB5n7qKjt2hcbQjbIjprUdJGEkhRsJnmDt8PxTMPvKjs_42Wj0u5O1tC3iifo1WFfyP1qFfaBXrJL9B802F4Ud8Bv0C1vQMGxvpOPO2JYWJZIPgDDagukanGnraPoBTWyMApzmK3DzYVTrrhi4Q_1Emmbr8xXmzn0ZIC9AFHXIJZo6yjRLcphvspbB6UdaAJ5WNSNhyfoozw3YNht5aU0nbcihyC9MJHWGFqh13Bw6leYzyFxi0OLvsMIJpi68nfRiFWGbGdjUDrh2JMoG6rD6mCk3YtxGVHTnZNM1scIe70ywYG9GncUaTx5cCMCTxYWgJKmE23AMhUyfb_vaOthkJ6JfBOcvv6uqSSecfYvc9oQwiQAfT5rvVIxVPKfVc1WlFVgX1f3vntFjCin313ID-tKmfcqQf3M9Tbdj9yzuk3uVw0KnBn0PyCjNHpI78yol4xH51gEhzTWtQUhrEFIAITUgpF0QUkANbUFISxDSGoSPyeL9u8XRzK6addiKBbywgyABa88Df4H5SOgElnIUxj54uE7CXIE9rVPtwrQgOXPBJ9GcCcW1I0MnUTz2n5C9LM_SZ4Q6MuU6AalQhEx7fgxzR6y4L3SopHSdMbHqwVyqisge-6mslkOKG5M3jfTaELjskKOgl10ithE57CmtEfYceE7ugcBBrcVl9W5ulr6LRj-MihiTV81hmMTxy5zM0ny7gQuEAvwCZ7dEEAHyhc_G5KkBRXunoY8LtTsmogeXRgAJ5PtHsovzkkgezPXAE8HzGw7RC3K3fakPyF5xuU1fgklexIflW_EHB63fcQ |
| linkProvider | Flying Publisher |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Association+of+Androgen+Receptor+CAG+Repeat+Polymorphism+and+Polycystic+Ovary+Syndrome&rft.jtitle=The+journal+of+clinical+endocrinology+and+metabolism&rft.au=Shah%2C+Nissar+A.&rft.au=Antoine%2C+Heath+J.&rft.au=Pall%2C+Marita&rft.au=Taylor%2C+Kent+D.&rft.date=2008-05-01&rft.issn=0021-972X&rft.eissn=1945-7197&rft.volume=93&rft.issue=5&rft.spage=1939&rft.epage=1945&rft_id=info:doi/10.1210%2Fjc.2008-0038&rft.externalDBID=n%2Fa&rft.externalDocID=10_1210_jc_2008_0038 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0021-972X&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0021-972X&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0021-972X&client=summon |