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Receptor de glicocorticoides

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Non confundir con receptor de glicocorticoides de membrana.
NR3C1
Estruturas dispoñibles
PDBBuscar ortólogos: PDBe, RCSB
Identificadores
Nomenclatura
SímbolosNR3C1 (HGNC: 7978) NR3C1, GCCR, GCR, GCRST, GR, GRL
Identificadores
externos
LocusCr. 5 q31.3
Padrón de expresión de ARNm
Máis información
Ortólogos
Especies
Humano Rato
Entrez
2908 14815
Ensembl
Véxase HS Véxase MM
UniProt
P04150 P06537
RefSeq
(ARNm)
NM_000176 NM_008173
RefSeq
(proteína) NCBI
NP_000167 NP_001348138
Localización (UCSC)
Cr. 5:
143.28 – 143.44 Mb 		Cr. 18:
39.54 – 39.65 Mb
PubMed (Busca)
2908


14815

O receptor de glicocorticoides (GCR ou GR), tamén chamado NR3C1 (receptor nuclear subfamilia 3, grupo C, membro 1), é o receptor citosólico ao cal se unen o cortisol e outros glicocorticoides.

O GCR exprésase en case todas as células do corpo e regula xenes que controlan o desenvolvemento, metabolismo e resposta inmune. Como o xene do receptor exprésase de varias formas, ten moitos efectos diferentes (pleiotrópicos) en diferentes partes do corpo.

Cando os glicocorticoides se unen a este receptor, o seu mecanimso primario de acción é a regulación da transcrición xénica.[1][2] O receptor non unido a ligando encóntrase no citosol da célula. Despois de que o receptor se une a un glicocorticoide, o complexo receptor-glicocorticoide pode tomar dous camiños posibles: o complexo do receptor activado regula á alza a expresión de proteínas antiinflamatorias no núcleo ou ben reprime a expresión de proteínas proinflamatorias no citosol (ao impedir a translocación doutros factores de transcrición do citosol ao núcleo).

En humanos, a proteína do receptor de glicocorticoides está codificada polo xene NR3C1 que está localizado no cromosoma 5 (5q31).[3][4]

Este receptor citosólico actúa por medio de mecanismos xenómicos, e non debe confundirse cos receptores de glicocorticoides de membrana, que se encontran na superficie celular e actúan por medio de cadoiros de sinalización.

Estrutura

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Como outros receptores de esteroides,[5] o receptor de glicocortocoides ten estrutura modular.[6] e contén os seguintes dominios (designados do A ao F):

Unión de ligandos e resposta

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En ausencia de hormona, o receptor de glicocorticoides (GCR) encóntrase no citosol formando un complexo con diversas proteínas, como a proteína de choque térmico 90 (hsp90), a proteína de choque térmico 70 (hsp70) e a proteína FKBP4 (proteína que se une a FK506 4).[7] A hormona glicocorticoide endóxena cortisol difunde a través da membrana plasmática ata o citoplasma e únese ao receptor de glicocorticoides, causando a liberación das proteínas de choque térmico que formaban o complexo. Como resultado o receptor queda activado e exhibe dous mecanismos principais de acción: transactivación e transrepresión,[8][9] que se describen máis abaixo.

Transactivación

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Un mecanismo directo de acción implica a homodimerización do receptor, a translocación vía transporte activo ao núcleo celular e a unión a elementos de resposta ao ADN específicos activadores da transcrición de xenes. Este mecanismo de acción denomínase transactivación. A resposta biolóxica depende do tipo celular.[10]

Transrepresión

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En ausencia de GCR activado, outros factores de transcrición como NF-κB ou AP-1 poden transactivar xenes diana.[11] Porén, o GCR activado pode formar complexos con estes outros factores de transcrición e impedirlles unirse aos seus xenes diana e así reprimir a expresión de xenes que normalmente son regulados á alza por NF-κB ou AP-1. Este mecanismo indirecto de acción denomínase transrepresión.[12] A transrepresión do GCR por medio de NF-κB e AP-1 está restrinxida a só certos tipos celulares e non se considera o mecanismo universal para a represión de IκBα (I kapaB alfa é unha proteína inhibidora que impide o transporte nuclear e activación do factor de transcrición NF-kapaB). [12][13]

Importancia clínica

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O GCR é anormal na resistencia a glicocorticoides familiar.[14]

En estruturas do sistema nervioso central, aumenta o interese polo receptor de glicocorticoides como novo representante da integración neuroendócrina, funcionando como un compoñente importante da influencia endócrina (especificamente a resposta ao estrés) sobre o cerebro. O receptor está agora implicado en adaptacións a curto e longo prazo observadas en resposta a estresantes e pode ser fundamental para comprender trastornos psicolóxicos, como algúns ou todos os subtipos de depresión e trastorno por estrés postraumático.[15] As observacións de longa duración como a desregulación do estado de ánimo típica da enfermidade de Cushing demostran o papel dos corticosteroides na regulación do estado psicolóxico; avances recentes demostraron interaccións coa norepinefrina e serotonina a nivel neural.[16][17]

Na preeclampsia (un trastorno hipertensivo que pode ocorrer en mulleres xestantes), o nivel de secuencias de microARN que posiblemente teñen como diana esta proteína é elevado no sangue da nai. A placenta eleva o nivel de exosomas que conteñen este microARN, o cal ten como resultado a inhibición da tradución da molécula. A importancia clínica desta información aínda non está clara.[18]

Agonistas e antagonistas

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A dexametasona e outros corticosteroides son agonistas, mentres que a mifepristona e cetoconazol son antagonistas do GCR. Os esteroides anabólicos tamén impiden que o cortisol se una ao GCR.

Interaccións

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O receptor de glicocorticoides presenta interaccións con:

Notas

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  1. ↑ Lu NZ, Wardell SE, Burnstein KL, Defranco D, Fuller PJ, Giguere V, et al. (decembro de 2006). "International Union of Pharmacology. LXV. The pharmacology and classification of the nuclear receptor superfamily: glucocorticoid, mineralocorticoid, progesterone, and androgen receptors". Pharmacological Reviews 58 (4): 782–797. PMID 17132855. doi:10.1124/pr.58.4.9.  [texto completo libre]
  2. ↑ Rhen T, Cidlowski JA (outubro de 2005). "Antiinflammatory action of glucocorticoids--new mechanisms for old drugs". The New England Journal of Medicine 353 (16): 1711–1723. PMID 16236742. doi:10.1056/NEJMra050541. 
  3. ↑ Hollenberg SM, Weinberger C, Ong ES, Cerelli G, Oro A, Lebo R, et al. (decembro de 1985). "Primary structure and expression of a functional human glucocorticoid receptor cDNA". Nature 318 (6047): 635–641. Bibcode:1985Natur.318..635H. PMC 6165583. PMID 2867473. doi:10.1038/318635a0. 
  4. ↑ Francke U, Foellmer BE (maio de 1989). "The glucocorticoid receptor gene is in 5q31-q32 [corrected]". Genomics 4 (4): 610–612. PMID 2744768. doi:10.1016/0888-7543(89)90287-5. 
  5. ↑ Kumar R, Thompson EB (maio de 1999). "The structure of the nuclear hormone receptors". Steroids 64 (5): 310–319. PMID 10406480. doi:10.1016/S0039-128X(99)00014-8. 
  6. ↑ Kumar R, Thompson EB (abril de 2005). "Gene regulation by the glucocorticoid receptor: structure:function relationship". The Journal of Steroid Biochemistry and Molecular Biology 94 (5): 383–394. PMID 15876404. doi:10.1016/j.jsbmb.2004.12.046. 
  7. ↑ Pratt WB, Morishima Y, Murphy M, Harrell M (2006). "Chaperoning of glucocorticoid receptors". Molecular Chaperones in Health and Disease. Handbook of Experimental Pharmacology 172. pp. 111–138. ISBN 978-3-540-25875-9. PMID 16610357. doi:10.1007/3-540-29717-0_5. 
  8. ↑ Buckingham JC (xaneiro de 2006). "Glucocorticoids: exemplars of multi-tasking". British Journal of Pharmacology 147 (Supplement 1): S258–S268. PMC 1760726. PMID 16402112. doi:10.1038/sj.bjp.0706456. 
  9. ↑ Hayashi R, Wada H, Ito K, Adcock IM (outubro de 2004). "Effects of glucocorticoids on gene transcription". European Journal of Pharmacology 500 (1–3): 51–62. PMID 15464020. doi:10.1016/j.ejphar.2004.07.011. 
  10. ↑ Gaurang C. Patel; J. Cameron Millar; Abbot F. Clark. Glucocorticoid Receptor Transactivation Is Required for Glucocorticoid-Induced Ocular Hypertension and Glaucoma. Investigative Ophthalmology & Visual Science., maio de 2019, Vol.60, 1967-1978. doi:https://doi.org/10.1167/iovs.18-26383
  11. ↑ Ray A, Prefontaine KE (xaneiro de 1994). "Physical association and functional antagonism between the p65 subunit of transcription factor NF-kappa B and the glucocorticoid receptor". Proceedings of the National Academy of Sciences of the United States of America 91 (2): 752–756. Bibcode:1994PNAS...91..752R. PMC 43027. PMID 8290595. doi:10.1073/pnas.91.2.752. 
  12. ↑ 12,0 12,1 Coutinho AE, Chapman KE (marzo de 2011). "The anti-inflammatory and immunosuppressive effects of glucocorticoids, recent developments and mechanistic insights". Molecular and Cellular Endocrinology 335 (1): 2–13. PMC 3047790. PMID 20398732. doi:10.1016/j.mce.2010.04.005. 
  13. ↑ Heck S, Bender K, Kullmann M, Göttlicher M, Herrlich P, Cato AC (agosto de 1997). "I kappaB alpha-independent downregulation of NF-kappaB activity by glucocorticoid receptor". The EMBO Journal 16 (15): 4698–4707. PMC 1170096. PMID 9303314. doi:10.1093/emboj/16.15.4698. 
  14. ↑ Mendonca BB, Leite MV, de Castro M, Kino T, Elias LL, Bachega TA, et al. (abril de 2002). "Female pseudohermaphroditism caused by a novel homozygous missense mutation of the GR gene". The Journal of Clinical Endocrinology and Metabolism 87 (4): 1805–1809. PMID 11932321. doi:10.1210/jcem.87.4.8379. 
  15. ↑ Maletic V, Robinson M, Oakes T, Iyengar S, Ball SG, Russell J (decembro de 2007). "Neurobiology of depression: an integrated view of key findings". International Journal of Clinical Practice 61 (12): 2030–2040. PMC 2228409. PMID 17944926. doi:10.1111/j.1742-1241.2007.01602.x.  [Texto completo libre]
  16. ↑ Savitz J, Lucki I, Drevets WC (maio de 2009). "5-HT(1A) receptor function in major depressive disorder". Progress in Neurobiology 88 (1): 17–31. PMC 2736801. PMID 19428959. doi:10.1016/j.pneurobio.2009.01.009.  [Texto completo libre]
  17. ↑ Schechter DS, Moser DA, Paoloni-Giacobino A, Stenz A, Gex-Fabry M, Aue T, Adouan W, Cordero MI, Suardi F, Manini A, Sancho Rossignol A, Merminod G, Ansermet F, Dayer AG, Rusconi Serpa S (epub May 29, 2015). Methylation of NR3C1 is related to maternal PTSD, parenting stress and maternal medial prefrontal cortical activity in response to child separation among mothers with histories of violence exposure. Frontiers in Psychology. http://www.frontiersin.org/Journal/Abstract.aspx?s=944&name=psychology_for_clinical_settings&ART_DOI=10.3389/fpsyg.2015.00690&field=&journalName=Frontiers_in_Psychology&id=139466
  18. ↑ Salomon C, Guanzon D, Scholz-Romero K, Longo S, Correa P, Illanes SE, Rice GE (setembro de 2017). "Placental Exosomes as Early Biomarker of Preeclampsia: Potential Role of Exosomal MicroRNAs Across Gestation". The Journal of Clinical Endocrinology and Metabolism 102 (9): 3182–3194. PMID 28531338. doi:10.1210/jc.2017-00672. 
  19. ↑ Kullmann M, Schneikert J, Moll J, Heck S, Zeiner M, Gehring U, Cato AC (xuño de 1998). "RAP46 is a negative regulator of glucocorticoid receptor action and hormone-induced apoptosis". The Journal of Biological Chemistry 273 (23): 14620–14625. PMID 9603979. doi:10.1074/jbc.273.23.14620. 
  20. ↑ Schneikert J, Hübner S, Langer G, Petri T, Jäättelä M, Reed J, Cato AC (decembro de 2000). "Hsp70-RAP46 interaction in downregulation of DNA binding by glucocorticoid receptor". The EMBO Journal 19 (23): 6508–6516. PMC 305849. PMID 11101523. doi:10.1093/emboj/19.23.6508. 
  21. ↑ Boruk M, Savory JG, Haché RJ (novembro de 1998). "AF-2-dependent potentiation of CCAAT enhancer binding protein beta-mediated transcriptional activation by glucocorticoid receptor". Molecular Endocrinology 12 (11): 1749–1763. PMID 9817600. doi:10.1210/mend.12.11.0191. 
  22. ↑ Almlöf T, Wallberg AE, Gustafsson JA, Wright AP (xuño de 1998). "Role of important hydrophobic amino acids in the interaction between the glucocorticoid receptor tau 1-core activation domain and target factors". Biochemistry 37 (26): 9586–9594. PMID 9649342. doi:10.1021/bi973029x. 
  23. ↑ 23,0 23,1 Hulkko SM, Wakui H, Zilliacus J (agosto de 2000). "The pro-apoptotic protein death-associated protein 3 (DAP3) interacts with the glucocorticoid receptor and affects the receptor function". The Biochemical Journal. 349 349 (3): 885–893. PMC 1221218. PMID 10903152. doi:10.1042/bj3490885. 
  24. ↑ Lin DY, Lai MZ, Ann DK, Shih HM (maio de 2003). "Promyelocytic leukemia protein (PML) functions as a glucocorticoid receptor co-activator by sequestering Daxx to the PML oncogenic domains (PODs) to enhance its transactivation potential". The Journal of Biological Chemistry 278 (18): 15958–15965. PMID 12595526. doi:10.1074/jbc.M300387200. 
  25. ↑ Jibard N, Meng X, Leclerc P, Rajkowski K, Fortin D, Schweizer-Groyer G, et al. (marzo de 1999). "Delimitation of two regions in the 90-kDa heat shock protein (Hsp90) able to interact with the glucocorticosteroid receptor (GR)". Experimental Cell Research 247 (2): 461–474. PMID 10066374. doi:10.1006/excr.1998.4375. 
  26. ↑ Kanelakis KC, Shewach DS, Pratt WB (setembro de 2002). "Nucleotide binding states of hsp70 and hsp90 during sequential steps in the process of glucocorticoid receptor.hsp90 heterocomplex assembly". The Journal of Biological Chemistry 277 (37): 33698–33703. PMID 12093808. doi:10.1074/jbc.M204164200. 
  27. ↑ Hecht K, Carlstedt-Duke J, Stierna P, Gustafsson J, Brönnegârd M, Wikström AC (outubro de 1997). "Evidence that the beta-isoform of the human glucocorticoid receptor does not act as a physiologically significant repressor". The Journal of Biological Chemistry 272 (42): 26659–26664. PMID 9334248. doi:10.1074/jbc.272.42.26659. 
  28. ↑ de Castro M, Elliot S, Kino T, Bamberger C, Karl M, Webster E, Chrousos GP (setembro de 1996). "The non-ligand binding beta-isoform of the human glucocorticoid receptor (hGR beta): tissue levels, mechanism of action, and potential physiologic role". Molecular Medicine 2 (5): 597–607. PMC 2230188. PMID 8898375. doi:10.1007/BF03401643. 
  29. ↑ van den Berg JD, Smets LA, van Rooij H (febreiro de 1996). "Agonist-free transformation of the glucocorticoid receptor in human B-lymphoma cells". The Journal of Steroid Biochemistry and Molecular Biology 57 (3–4): 239–249. PMID 8645634. doi:10.1016/0960-0760(95)00271-5. 
  30. ↑ Stancato LF, Silverstein AM, Gitler C, Groner B, Pratt WB (abril de 1996). "Use of the thiol-specific derivatizing agent N-iodoacetyl-3-[125I]iodotyrosine to demonstrate conformational differences between the unbound and hsp90-bound glucocorticoid receptor hormone binding domain". The Journal of Biological Chemistry 271 (15): 8831–8836. PMID 8621522. doi:10.1074/jbc.271.15.8831. 
  31. ↑ Eggert M, Michel J, Schneider S, Bornfleth H, Baniahmad A, Fackelmayer FO, et al. (novembro de 1997). "The glucocorticoid receptor is associated with the RNA-binding nuclear matrix protein hnRNP U". The Journal of Biological Chemistry 272 (45): 28471–28478. PMID 9353307. doi:10.1074/jbc.272.45.28471. 
  32. ↑ 32,0 32,1 32,2 32,3 32,4 Zilliacus J, Holter E, Wakui H, Tazawa H, Treuter E, Gustafsson JA (abril de 2001). "Regulation of glucocorticoid receptor activity by 14--3-3-dependent intracellular relocalization of the corepressor RIP140". Molecular Endocrinology 15 (4): 501–511. PMID 11266503. doi:10.1210/mend.15.4.0624. 
  33. ↑ 33,0 33,1 Hittelman AB, Burakov D, Iñiguez-Lluhí JA, Freedman LP, Garabedian MJ (outubro de 1999). "Differential regulation of glucocorticoid receptor transcriptional activation via AF-1-associated proteins". The EMBO Journal 18 (19): 5380–5388. PMC 1171607. PMID 10508170. doi:10.1093/emboj/18.19.5380. 
  34. ↑ Savory JG, Préfontaine GG, Lamprecht C, Liao M, Walther RF, Lefebvre YA, Haché RJ (febreiro de 2001). "Glucocorticoid receptor homodimers and glucocorticoid-mineralocorticoid receptor heterodimers form in the cytoplasm through alternative dimerization interfaces". Molecular and Cellular Biology 21 (3): 781–793. PMC 86670. PMID 11154266. doi:10.1128/MCB.21.3.781-793.2001. 
  35. ↑ Tazawa H, Osman W, Shoji Y, Treuter E, Gustafsson JA, Zilliacus J (xuño de 2003). "Regulation of subnuclear localization is associated with a mechanism for nuclear receptor corepression by RIP140". Molecular and Cellular Biology 23 (12): 4187–4198. PMC 156128. PMID 12773562. doi:10.1128/MCB.23.12.4187-4198.2003. 
  36. ↑ Subramaniam N, Treuter E, Okret S (xuño de 1999). "Receptor interacting protein RIP140 inhibits both positive and negative gene regulation by glucocorticoids". The Journal of Biological Chemistry 274 (25): 18121–18127. PMID 10364267. doi:10.1074/jbc.274.25.18121. 
  37. ↑ Stevens A, Garside H, Berry A, Waters C, White A, Ray D (maio de 2003). "Dissociation of steroid receptor coactivator 1 and nuclear receptor corepressor recruitment to the human glucocorticoid receptor by modification of the ligand-receptor interface: the role of tyrosine 735". Molecular Endocrinology 17 (5): 845–859. PMID 12569182. doi:10.1210/me.2002-0320. 
  38. ↑ Schulz M, Eggert M, Baniahmad A, Dostert A, Heinzel T, Renkawitz R (July 2002). "RU486-induced glucocorticoid receptor agonism is controlled by the receptor N terminus and by corepressor binding". The Journal of Biological Chemistry 277 (29): 26238–26243. PMID 12011091. doi:10.1074/jbc.M203268200. 
  39. ↑ Kucera T, Waltner-Law M, Scott DK, Prasad R, Granner DK (xullo de 2002). "A point mutation of the AF2 transactivation domain of the glucocorticoid receptor disrupts its interaction with steroid receptor coactivator 1". The Journal of Biological Chemistry 277 (29): 26098–26102. PMID 12118039. doi:10.1074/jbc.M204013200. 
  40. ↑ Bledsoe RK, Montana VG, Stanley TB, Delves CJ, Apolito CJ, McKee DD, et al. (xullo de 2002). "Crystal structure of the glucocorticoid receptor ligand binding domain reveals a novel mode of receptor dimerization and coactivator recognition". Cell 110 (1): 93–105. PMID 12151000. doi:10.1016/S0092-8674(02)00817-6. 
  41. ↑ 41,0 41,1 41,2 Hsiao PW, Fryer CJ, Trotter KW, Wang W, Archer TK (setembro de 2003). "BAF60a mediates critical interactions between nuclear receptors and the BRG1 chromatin-remodeling complex for transactivation". Molecular and Cellular Biology 23 (17): 6210–6220. PMC 180928. PMID 12917342. doi:10.1128/MCB.23.17.6210-6220.2003. 
  42. ↑ Préfontaine GG, Walther R, Giffin W, Lemieux ME, Pope L, Haché RJ (setembro 1999). "Selective binding of steroid hormone receptors to octamer transcription factors determines transcriptional synergism at the mouse mammary tumor virus promoter". The Journal of Biological Chemistry 274 (38): 26713–26719. PMID 10480874. doi:10.1074/jbc.274.38.26713. 
  43. ↑ Préfontaine GG, Lemieux ME, Giffin W, Schild-Poulter C, Pope L, LaCasse E, et al. (xuño de 1998). "Recruitment of octamer transcription factors to DNA by glucocorticoid receptor". Molecular and Cellular Biology 18 (6): 3416–3430. PMC 108923. PMID 9584182. doi:10.1128/MCB.18.6.3416. 
  44. ↑ 44,0 44,1 Rao MA, Cheng H, Quayle AN, Nishitani H, Nelson CC, Rennie PS (decembro de 2002). "RanBPM, a nuclear protein that interacts with and regulates transcriptional activity of androgen receptor and glucocorticoid receptor". The Journal of Biological Chemistry 277 (50): 48020–48027. PMID 12361945. doi:10.1074/jbc.M209741200. 
  45. ↑ Nissen RM, Yamamoto KR (setembro de 2000). "The glucocorticoid receptor inhibits NFkappaB by interfering with serine-2 phosphorylation of the RNA polymerase II carboxy-terminal domain". Genes & Development 14 (18): 2314–2329. PMC 316928. PMID 10995388. doi:10.1101/gad.827900. 
  46. ↑ Caldenhoven E, Liden J, Wissink S, Van de Stolpe A, Raaijmakers J, Koenderman L, et al. (abril de 1995). "Negative cross-talk between RelA and the glucocorticoid receptor: a possible mechanism for the antiinflammatory action of glucocorticoids". Molecular Endocrinology 9 (4): 401–412. PMID 7659084. doi:10.1210/mend.9.4.7659084. 
  47. ↑ Li G, Wang S, Gelehrter TD (outubro de 2003). "Identification of glucocorticoid receptor domains involved in transrepression of transforming growth factor-beta action". The Journal of Biological Chemistry 278 (43): 41779–41788. PMID 12902338. doi:10.1074/jbc.M305350200. 
  48. ↑ Song CZ, Tian X, Gelehrter TD (outubro de 1999). "Glucocorticoid receptor inhibits transforming growth factor-beta signaling by directly targeting the transcriptional activation function of Smad3". Proceedings of the National Academy of Sciences of the United States of America 96 (21): 11776–11781. Bibcode:1999PNAS...9611776S. PMC 18362. PMID 10518526. doi:10.1073/pnas.96.21.11776. 
  49. ↑ Wallberg AE, Neely KE, Hassan AH, Gustafsson JA, Workman JL, Wright AP (marzo de 2000). "Recruitment of the SWI-SNF chromatin remodeling complex as a mechanism of gene activation by the glucocorticoid receptor tau1 activation domain". Molecular and Cellular Biology 20 (6): 2004–2013. PMC 110817. PMID 10688647. doi:10.1128/MCB.20.6.2004-2013.2000. 
  50. ↑ Lerner L, Henriksen MA, Zhang X, Darnell JE (outubro de 2003). "STAT3-dependent enhanceosome assembly and disassembly: synergy with GR for full transcriptional increase of the alpha 2-macroglobulin gene". Genes & Development 17 (20): 2564–2577. PMC 218150. PMID 14522952. doi:10.1101/gad.1135003. 
  51. ↑ Zhang Z, Jones S, Hagood JS, Fuentes NL, Fuller GM (decembro de 1997). "STAT3 acts as a co-activator of glucocorticoid receptor signaling". The Journal of Biological Chemistry 272 (49): 30607–30610. PMID 9388192. doi:10.1074/jbc.272.49.30607. 
  52. ↑ Stöcklin E, Wissler M, Gouilleux F, Groner B (outubro de 1996). "Functional interactions between Stat5 and the glucocorticoid receptor" (PDF). Nature 383 (6602): 726–728. Bibcode:1996Natur.383..726S. PMID 8878484. doi:10.1038/383726a0. 
  53. ↑ Makino Y, Yoshikawa N, Okamoto K, Hirota K, Yodoi J, Makino I, Tanaka H (xaneiro de 1999). "Direct association with thioredoxin allows redox regulation of glucocorticoid receptor function". The Journal of Biological Chemistry 274 (5): 3182–3188. PMID 9915858. doi:10.1074/jbc.274.5.3182. 
  54. ↑ Chang CJ, Chen YL, Lee SC (outubro de 1998). "Coactivator TIF1beta interacts with transcription factor C/EBPbeta and glucocorticoid receptor to induce alpha1-acid glycoprotein gene expression". Molecular and Cellular Biology 18 (10): 5880–5887. PMC 109174. PMID 9742105. doi:10.1128/mcb.18.10.5880. 
  55. ↑ Wakui H, Wright AP, Gustafsson J, Zilliacus J (marzo de 1997). "Interaction of the ligand-activated glucocorticoid receptor with the 14-3-3 eta protein". The Journal of Biological Chemistry 272 (13): 8153–8156. PMID 9079630. doi:10.1074/jbc.272.13.8153. 

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