Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment

Objectives The glucocorticoid receptor (GR) is a well-studied, ligand-activated transcription factor and a common target of anti-inflammatory treatments. Recently, several studies have drawn attention the effects of binding of GR to RNA rather than DNA and the potential implications of this activity...
Ausführliche Beschreibung

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Autor*in:	Lammer, Nickolaus C. [verfasserIn] Allen, Mary A. Batey, Robert T. Wuttke, Deborah S.

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Transcription factor Glucocorticoid receptor RNA binding RNA sequencing Transcriptomics 4-thiouridine NR3C1

Anmerkung:	© The Author(s) 2023

Übergeordnetes Werk:	Enthalten in: BMC Research Notes - London, 2008, 16(2023), 1 vom: 22. Aug.
Übergeordnetes Werk:	volume:16 ; year:2023 ; number:1 ; day:22 ; month:08

Links:	Volltext

DOI / URN:	10.1186/s13104-023-06446-4

Katalog-ID:	SPR052831396

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520			\|a Objectives The glucocorticoid receptor (GR) is a well-studied, ligand-activated transcription factor and a common target of anti-inflammatory treatments. Recently, several studies have drawn attention the effects of binding of GR to RNA rather than DNA and the potential implications of this activity for GR function. The objective of our study was to further characterize the relationship between GR function and RNA binding by measuring changes in the glucocorticoid-driven transcriptome in the presence of a GR mutant that exhibited reduced RNA affinity. Data description GR was activated in three cell lines containing GR constructs (GR-HaloTag). One of the cell lines contained a wild-type GR-HaloTag. Another contained GR-HaloTag with a mutation that reduced RNA affinity and slightly reduced DNA affinity. The third cell line contained GR-HaloTag with a mutation that only slightly reduced DNA affinity. All three cell lines were treated with dexamethasone, a GR agonist. RNA-seq samples were collected every hour for 3 h. Moreover, transcriptome quantification was accomplished via labeling of RNAs transcribed in the final hour of dexamethasone treatment using 4-thiouridine. These labeled RNAs were then purified and sequenced. This data set is the first of its kind for GR and contains valuable insights into the function of RNA binding by GR.
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allfields	10.1186/s13104-023-06446-4 doi (DE-627)SPR052831396 (SPR)s13104-023-06446-4-e DE-627 ger DE-627 rakwb eng Lammer, Nickolaus C. verfasserin aut Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Objectives The glucocorticoid receptor (GR) is a well-studied, ligand-activated transcription factor and a common target of anti-inflammatory treatments. Recently, several studies have drawn attention the effects of binding of GR to RNA rather than DNA and the potential implications of this activity for GR function. The objective of our study was to further characterize the relationship between GR function and RNA binding by measuring changes in the glucocorticoid-driven transcriptome in the presence of a GR mutant that exhibited reduced RNA affinity. Data description GR was activated in three cell lines containing GR constructs (GR-HaloTag). One of the cell lines contained a wild-type GR-HaloTag. Another contained GR-HaloTag with a mutation that reduced RNA affinity and slightly reduced DNA affinity. The third cell line contained GR-HaloTag with a mutation that only slightly reduced DNA affinity. All three cell lines were treated with dexamethasone, a GR agonist. RNA-seq samples were collected every hour for 3 h. Moreover, transcriptome quantification was accomplished via labeling of RNAs transcribed in the final hour of dexamethasone treatment using 4-thiouridine. These labeled RNAs were then purified and sequenced. This data set is the first of its kind for GR and contains valuable insights into the function of RNA binding by GR. Transcription factor (dpeaa)DE-He213 Glucocorticoid receptor (dpeaa)DE-He213 RNA binding (dpeaa)DE-He213 RNA sequencing (dpeaa)DE-He213 Transcriptomics (dpeaa)DE-He213 4-thiouridine (dpeaa)DE-He213 NR3C1 (dpeaa)DE-He213 Allen, Mary A. aut Batey, Robert T. aut Wuttke, Deborah S. aut Enthalten in BMC Research Notes London, 2008 16(2023), 1 vom: 22. Aug. (DE-627)559431805 (DE-600)2413336-X 1756-0500 nnns volume:16 year:2023 number:1 day:22 month:08 https://dx.doi.org/10.1186/s13104-023-06446-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2023 1 22 08
spelling	10.1186/s13104-023-06446-4 doi (DE-627)SPR052831396 (SPR)s13104-023-06446-4-e DE-627 ger DE-627 rakwb eng Lammer, Nickolaus C. verfasserin aut Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Objectives The glucocorticoid receptor (GR) is a well-studied, ligand-activated transcription factor and a common target of anti-inflammatory treatments. Recently, several studies have drawn attention the effects of binding of GR to RNA rather than DNA and the potential implications of this activity for GR function. The objective of our study was to further characterize the relationship between GR function and RNA binding by measuring changes in the glucocorticoid-driven transcriptome in the presence of a GR mutant that exhibited reduced RNA affinity. Data description GR was activated in three cell lines containing GR constructs (GR-HaloTag). One of the cell lines contained a wild-type GR-HaloTag. Another contained GR-HaloTag with a mutation that reduced RNA affinity and slightly reduced DNA affinity. The third cell line contained GR-HaloTag with a mutation that only slightly reduced DNA affinity. All three cell lines were treated with dexamethasone, a GR agonist. RNA-seq samples were collected every hour for 3 h. Moreover, transcriptome quantification was accomplished via labeling of RNAs transcribed in the final hour of dexamethasone treatment using 4-thiouridine. These labeled RNAs were then purified and sequenced. This data set is the first of its kind for GR and contains valuable insights into the function of RNA binding by GR. Transcription factor (dpeaa)DE-He213 Glucocorticoid receptor (dpeaa)DE-He213 RNA binding (dpeaa)DE-He213 RNA sequencing (dpeaa)DE-He213 Transcriptomics (dpeaa)DE-He213 4-thiouridine (dpeaa)DE-He213 NR3C1 (dpeaa)DE-He213 Allen, Mary A. aut Batey, Robert T. aut Wuttke, Deborah S. aut Enthalten in BMC Research Notes London, 2008 16(2023), 1 vom: 22. Aug. (DE-627)559431805 (DE-600)2413336-X 1756-0500 nnns volume:16 year:2023 number:1 day:22 month:08 https://dx.doi.org/10.1186/s13104-023-06446-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2023 1 22 08
allfields_unstemmed	10.1186/s13104-023-06446-4 doi (DE-627)SPR052831396 (SPR)s13104-023-06446-4-e DE-627 ger DE-627 rakwb eng Lammer, Nickolaus C. verfasserin aut Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Objectives The glucocorticoid receptor (GR) is a well-studied, ligand-activated transcription factor and a common target of anti-inflammatory treatments. Recently, several studies have drawn attention the effects of binding of GR to RNA rather than DNA and the potential implications of this activity for GR function. The objective of our study was to further characterize the relationship between GR function and RNA binding by measuring changes in the glucocorticoid-driven transcriptome in the presence of a GR mutant that exhibited reduced RNA affinity. Data description GR was activated in three cell lines containing GR constructs (GR-HaloTag). One of the cell lines contained a wild-type GR-HaloTag. Another contained GR-HaloTag with a mutation that reduced RNA affinity and slightly reduced DNA affinity. The third cell line contained GR-HaloTag with a mutation that only slightly reduced DNA affinity. All three cell lines were treated with dexamethasone, a GR agonist. RNA-seq samples were collected every hour for 3 h. Moreover, transcriptome quantification was accomplished via labeling of RNAs transcribed in the final hour of dexamethasone treatment using 4-thiouridine. These labeled RNAs were then purified and sequenced. This data set is the first of its kind for GR and contains valuable insights into the function of RNA binding by GR. Transcription factor (dpeaa)DE-He213 Glucocorticoid receptor (dpeaa)DE-He213 RNA binding (dpeaa)DE-He213 RNA sequencing (dpeaa)DE-He213 Transcriptomics (dpeaa)DE-He213 4-thiouridine (dpeaa)DE-He213 NR3C1 (dpeaa)DE-He213 Allen, Mary A. aut Batey, Robert T. aut Wuttke, Deborah S. aut Enthalten in BMC Research Notes London, 2008 16(2023), 1 vom: 22. Aug. (DE-627)559431805 (DE-600)2413336-X 1756-0500 nnns volume:16 year:2023 number:1 day:22 month:08 https://dx.doi.org/10.1186/s13104-023-06446-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2023 1 22 08
allfieldsGer	10.1186/s13104-023-06446-4 doi (DE-627)SPR052831396 (SPR)s13104-023-06446-4-e DE-627 ger DE-627 rakwb eng Lammer, Nickolaus C. verfasserin aut Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Objectives The glucocorticoid receptor (GR) is a well-studied, ligand-activated transcription factor and a common target of anti-inflammatory treatments. Recently, several studies have drawn attention the effects of binding of GR to RNA rather than DNA and the potential implications of this activity for GR function. The objective of our study was to further characterize the relationship between GR function and RNA binding by measuring changes in the glucocorticoid-driven transcriptome in the presence of a GR mutant that exhibited reduced RNA affinity. Data description GR was activated in three cell lines containing GR constructs (GR-HaloTag). One of the cell lines contained a wild-type GR-HaloTag. Another contained GR-HaloTag with a mutation that reduced RNA affinity and slightly reduced DNA affinity. The third cell line contained GR-HaloTag with a mutation that only slightly reduced DNA affinity. All three cell lines were treated with dexamethasone, a GR agonist. RNA-seq samples were collected every hour for 3 h. Moreover, transcriptome quantification was accomplished via labeling of RNAs transcribed in the final hour of dexamethasone treatment using 4-thiouridine. These labeled RNAs were then purified and sequenced. This data set is the first of its kind for GR and contains valuable insights into the function of RNA binding by GR. Transcription factor (dpeaa)DE-He213 Glucocorticoid receptor (dpeaa)DE-He213 RNA binding (dpeaa)DE-He213 RNA sequencing (dpeaa)DE-He213 Transcriptomics (dpeaa)DE-He213 4-thiouridine (dpeaa)DE-He213 NR3C1 (dpeaa)DE-He213 Allen, Mary A. aut Batey, Robert T. aut Wuttke, Deborah S. aut Enthalten in BMC Research Notes London, 2008 16(2023), 1 vom: 22. Aug. (DE-627)559431805 (DE-600)2413336-X 1756-0500 nnns volume:16 year:2023 number:1 day:22 month:08 https://dx.doi.org/10.1186/s13104-023-06446-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2023 1 22 08
allfieldsSound	10.1186/s13104-023-06446-4 doi (DE-627)SPR052831396 (SPR)s13104-023-06446-4-e DE-627 ger DE-627 rakwb eng Lammer, Nickolaus C. verfasserin aut Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Objectives The glucocorticoid receptor (GR) is a well-studied, ligand-activated transcription factor and a common target of anti-inflammatory treatments. Recently, several studies have drawn attention the effects of binding of GR to RNA rather than DNA and the potential implications of this activity for GR function. The objective of our study was to further characterize the relationship between GR function and RNA binding by measuring changes in the glucocorticoid-driven transcriptome in the presence of a GR mutant that exhibited reduced RNA affinity. Data description GR was activated in three cell lines containing GR constructs (GR-HaloTag). One of the cell lines contained a wild-type GR-HaloTag. Another contained GR-HaloTag with a mutation that reduced RNA affinity and slightly reduced DNA affinity. The third cell line contained GR-HaloTag with a mutation that only slightly reduced DNA affinity. All three cell lines were treated with dexamethasone, a GR agonist. RNA-seq samples were collected every hour for 3 h. Moreover, transcriptome quantification was accomplished via labeling of RNAs transcribed in the final hour of dexamethasone treatment using 4-thiouridine. These labeled RNAs were then purified and sequenced. This data set is the first of its kind for GR and contains valuable insights into the function of RNA binding by GR. Transcription factor (dpeaa)DE-He213 Glucocorticoid receptor (dpeaa)DE-He213 RNA binding (dpeaa)DE-He213 RNA sequencing (dpeaa)DE-He213 Transcriptomics (dpeaa)DE-He213 4-thiouridine (dpeaa)DE-He213 NR3C1 (dpeaa)DE-He213 Allen, Mary A. aut Batey, Robert T. aut Wuttke, Deborah S. aut Enthalten in BMC Research Notes London, 2008 16(2023), 1 vom: 22. Aug. (DE-627)559431805 (DE-600)2413336-X 1756-0500 nnns volume:16 year:2023 number:1 day:22 month:08 https://dx.doi.org/10.1186/s13104-023-06446-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2023 1 22 08
language	English
source	Enthalten in BMC Research Notes 16(2023), 1 vom: 22. Aug. volume:16 year:2023 number:1 day:22 month:08
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institution	findex.gbv.de
topic_facet	Transcription factor Glucocorticoid receptor RNA binding RNA sequencing Transcriptomics 4-thiouridine NR3C1
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container_title	BMC Research Notes
authorswithroles_txt_mv	Lammer, Nickolaus C. @@aut@@ Allen, Mary A. @@aut@@ Batey, Robert T. @@aut@@ Wuttke, Deborah S. @@aut@@
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author	Lammer, Nickolaus C.
spellingShingle	Lammer, Nickolaus C. misc Transcription factor misc Glucocorticoid receptor misc RNA binding misc RNA sequencing misc Transcriptomics misc 4-thiouridine misc NR3C1 Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment
authorStr	Lammer, Nickolaus C.
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topic_title	Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment Transcription factor (dpeaa)DE-He213 Glucocorticoid receptor (dpeaa)DE-He213 RNA binding (dpeaa)DE-He213 RNA sequencing (dpeaa)DE-He213 Transcriptomics (dpeaa)DE-He213 4-thiouridine (dpeaa)DE-He213 NR3C1 (dpeaa)DE-He213
topic	misc Transcription factor misc Glucocorticoid receptor misc RNA binding misc RNA sequencing misc Transcriptomics misc 4-thiouridine misc NR3C1
topic_unstemmed	misc Transcription factor misc Glucocorticoid receptor misc RNA binding misc RNA sequencing misc Transcriptomics misc 4-thiouridine misc NR3C1
topic_browse	misc Transcription factor misc Glucocorticoid receptor misc RNA binding misc RNA sequencing misc Transcriptomics misc 4-thiouridine misc NR3C1
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title	Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment
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title_full	Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment
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author_browse	Lammer, Nickolaus C. Allen, Mary A. Batey, Robert T. Wuttke, Deborah S.
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title_sort	quantification of transcriptome changes to investigate the role of glucocorticoid receptor-rna binding during dexamethasone treatment
title_auth	Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment
abstract	Objectives The glucocorticoid receptor (GR) is a well-studied, ligand-activated transcription factor and a common target of anti-inflammatory treatments. Recently, several studies have drawn attention the effects of binding of GR to RNA rather than DNA and the potential implications of this activity for GR function. The objective of our study was to further characterize the relationship between GR function and RNA binding by measuring changes in the glucocorticoid-driven transcriptome in the presence of a GR mutant that exhibited reduced RNA affinity. Data description GR was activated in three cell lines containing GR constructs (GR-HaloTag). One of the cell lines contained a wild-type GR-HaloTag. Another contained GR-HaloTag with a mutation that reduced RNA affinity and slightly reduced DNA affinity. The third cell line contained GR-HaloTag with a mutation that only slightly reduced DNA affinity. All three cell lines were treated with dexamethasone, a GR agonist. RNA-seq samples were collected every hour for 3 h. Moreover, transcriptome quantification was accomplished via labeling of RNAs transcribed in the final hour of dexamethasone treatment using 4-thiouridine. These labeled RNAs were then purified and sequenced. This data set is the first of its kind for GR and contains valuable insights into the function of RNA binding by GR. © The Author(s) 2023
abstractGer	Objectives The glucocorticoid receptor (GR) is a well-studied, ligand-activated transcription factor and a common target of anti-inflammatory treatments. Recently, several studies have drawn attention the effects of binding of GR to RNA rather than DNA and the potential implications of this activity for GR function. The objective of our study was to further characterize the relationship between GR function and RNA binding by measuring changes in the glucocorticoid-driven transcriptome in the presence of a GR mutant that exhibited reduced RNA affinity. Data description GR was activated in three cell lines containing GR constructs (GR-HaloTag). One of the cell lines contained a wild-type GR-HaloTag. Another contained GR-HaloTag with a mutation that reduced RNA affinity and slightly reduced DNA affinity. The third cell line contained GR-HaloTag with a mutation that only slightly reduced DNA affinity. All three cell lines were treated with dexamethasone, a GR agonist. RNA-seq samples were collected every hour for 3 h. Moreover, transcriptome quantification was accomplished via labeling of RNAs transcribed in the final hour of dexamethasone treatment using 4-thiouridine. These labeled RNAs were then purified and sequenced. This data set is the first of its kind for GR and contains valuable insights into the function of RNA binding by GR. © The Author(s) 2023
abstract_unstemmed	Objectives The glucocorticoid receptor (GR) is a well-studied, ligand-activated transcription factor and a common target of anti-inflammatory treatments. Recently, several studies have drawn attention the effects of binding of GR to RNA rather than DNA and the potential implications of this activity for GR function. The objective of our study was to further characterize the relationship between GR function and RNA binding by measuring changes in the glucocorticoid-driven transcriptome in the presence of a GR mutant that exhibited reduced RNA affinity. Data description GR was activated in three cell lines containing GR constructs (GR-HaloTag). One of the cell lines contained a wild-type GR-HaloTag. Another contained GR-HaloTag with a mutation that reduced RNA affinity and slightly reduced DNA affinity. The third cell line contained GR-HaloTag with a mutation that only slightly reduced DNA affinity. All three cell lines were treated with dexamethasone, a GR agonist. RNA-seq samples were collected every hour for 3 h. Moreover, transcriptome quantification was accomplished via labeling of RNAs transcribed in the final hour of dexamethasone treatment using 4-thiouridine. These labeled RNAs were then purified and sequenced. This data set is the first of its kind for GR and contains valuable insights into the function of RNA binding by GR. © The Author(s) 2023
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title_short	Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment
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author2	Allen, Mary A. Batey, Robert T. Wuttke, Deborah S.
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Quantification of transcriptome changes to investigate the role of glucocorticoid receptor-RNA binding during dexamethasone treatment

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