Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation

Publication Date:
2018-05-08
Publisher:
Rockefeller University Press
Print ISSN:
0022-1007
Electronic ISSN:
1540-9538
Topics:
Medicine
Published by:
http://www.rupress.org/
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autor Fang, D., Cui, K., Hu, G., Gurram, R. K., Zhong, C., Oler, A. J., Yagi, R., Zhao, M., Sharma, S., Liu, P., Sun, B., Zhao, K., Zhu, J.
beschreibung GATA-binding protein 3 (GATA3) acts as the master transcription factor for type 2 T helper (Th2) cell differentiation and function. However, it is still elusive how GATA3 function is precisely regulated in Th2 cells. Here, we show that the transcription factor B cell lymphoma 11b (Bcl11b), a previously unknown component of GATA3 transcriptional complex, is involved in GATA3-mediated gene regulation. Bcl11b binds to GATA3 through protein–protein interaction, and they colocalize at many important cis-regulatory elements in Th2 cells. The expression of type 2 cytokines, including IL-4, IL-5, and IL-13, is up-regulated in Bcl11b -deficient Th2 cells both in vitro and in vivo; such up-regulation is completely GATA3 dependent. Genome-wide analyses of Bcl11b- and GATA3-regulated genes (from RNA sequencing), cobinding patterns (from chromatin immunoprecipitation sequencing), and Bcl11b-modulated epigenetic modification and gene accessibility suggest that GATA3/Bcl11b complex is involved in limiting Th2 gene expression, as well as in inhibiting non-Th2 gene expression. Thus, Bcl11b controls both GATA3-mediated gene activation and repression in Th2 cells.
citation_standardnr 6253108
datenlieferant ipn_articles
feed_id 96
feed_publisher Rockefeller University Press
feed_publisher_url http://www.rupress.org/
insertion_date 2018-05-08
journaleissn 1540-9538
journalissn 0022-1007
publikationsjahr_anzeige 2018
publikationsjahr_facette 2018
publikationsjahr_intervall 7984:2015-2019
publikationsjahr_sort 2018
publisher Rockefeller University Press
quelle Journal of Experimental Medicine
relation http://jem.rupress.org/cgi/content/short/215/5/1449?rss=1
search_space articles
shingle_author_1 Fang, D., Cui, K., Hu, G., Gurram, R. K., Zhong, C., Oler, A. J., Yagi, R., Zhao, M., Sharma, S., Liu, P., Sun, B., Zhao, K., Zhu, J.
shingle_author_2 Fang, D., Cui, K., Hu, G., Gurram, R. K., Zhong, C., Oler, A. J., Yagi, R., Zhao, M., Sharma, S., Liu, P., Sun, B., Zhao, K., Zhu, J.
shingle_author_3 Fang, D., Cui, K., Hu, G., Gurram, R. K., Zhong, C., Oler, A. J., Yagi, R., Zhao, M., Sharma, S., Liu, P., Sun, B., Zhao, K., Zhu, J.
shingle_author_4 Fang, D., Cui, K., Hu, G., Gurram, R. K., Zhong, C., Oler, A. J., Yagi, R., Zhao, M., Sharma, S., Liu, P., Sun, B., Zhao, K., Zhu, J.
shingle_catch_all_1 Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
GATA-binding protein 3 (GATA3) acts as the master transcription factor for type 2 T helper (Th2) cell differentiation and function. However, it is still elusive how GATA3 function is precisely regulated in Th2 cells. Here, we show that the transcription factor B cell lymphoma 11b (Bcl11b), a previously unknown component of GATA3 transcriptional complex, is involved in GATA3-mediated gene regulation. Bcl11b binds to GATA3 through protein–protein interaction, and they colocalize at many important cis-regulatory elements in Th2 cells. The expression of type 2 cytokines, including IL-4, IL-5, and IL-13, is up-regulated in Bcl11b -deficient Th2 cells both in vitro and in vivo; such up-regulation is completely GATA3 dependent. Genome-wide analyses of Bcl11b- and GATA3-regulated genes (from RNA sequencing), cobinding patterns (from chromatin immunoprecipitation sequencing), and Bcl11b-modulated epigenetic modification and gene accessibility suggest that GATA3/Bcl11b complex is involved in limiting Th2 gene expression, as well as in inhibiting non-Th2 gene expression. Thus, Bcl11b controls both GATA3-mediated gene activation and repression in Th2 cells.
Fang, D., Cui, K., Hu, G., Gurram, R. K., Zhong, C., Oler, A. J., Yagi, R., Zhao, M., Sharma, S., Liu, P., Sun, B., Zhao, K., Zhu, J.
Rockefeller University Press
0022-1007
00221007
1540-9538
15409538
shingle_catch_all_2 Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
GATA-binding protein 3 (GATA3) acts as the master transcription factor for type 2 T helper (Th2) cell differentiation and function. However, it is still elusive how GATA3 function is precisely regulated in Th2 cells. Here, we show that the transcription factor B cell lymphoma 11b (Bcl11b), a previously unknown component of GATA3 transcriptional complex, is involved in GATA3-mediated gene regulation. Bcl11b binds to GATA3 through protein–protein interaction, and they colocalize at many important cis-regulatory elements in Th2 cells. The expression of type 2 cytokines, including IL-4, IL-5, and IL-13, is up-regulated in Bcl11b -deficient Th2 cells both in vitro and in vivo; such up-regulation is completely GATA3 dependent. Genome-wide analyses of Bcl11b- and GATA3-regulated genes (from RNA sequencing), cobinding patterns (from chromatin immunoprecipitation sequencing), and Bcl11b-modulated epigenetic modification and gene accessibility suggest that GATA3/Bcl11b complex is involved in limiting Th2 gene expression, as well as in inhibiting non-Th2 gene expression. Thus, Bcl11b controls both GATA3-mediated gene activation and repression in Th2 cells.
Fang, D., Cui, K., Hu, G., Gurram, R. K., Zhong, C., Oler, A. J., Yagi, R., Zhao, M., Sharma, S., Liu, P., Sun, B., Zhao, K., Zhu, J.
Rockefeller University Press
0022-1007
00221007
1540-9538
15409538
shingle_catch_all_3 Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
GATA-binding protein 3 (GATA3) acts as the master transcription factor for type 2 T helper (Th2) cell differentiation and function. However, it is still elusive how GATA3 function is precisely regulated in Th2 cells. Here, we show that the transcription factor B cell lymphoma 11b (Bcl11b), a previously unknown component of GATA3 transcriptional complex, is involved in GATA3-mediated gene regulation. Bcl11b binds to GATA3 through protein–protein interaction, and they colocalize at many important cis-regulatory elements in Th2 cells. The expression of type 2 cytokines, including IL-4, IL-5, and IL-13, is up-regulated in Bcl11b -deficient Th2 cells both in vitro and in vivo; such up-regulation is completely GATA3 dependent. Genome-wide analyses of Bcl11b- and GATA3-regulated genes (from RNA sequencing), cobinding patterns (from chromatin immunoprecipitation sequencing), and Bcl11b-modulated epigenetic modification and gene accessibility suggest that GATA3/Bcl11b complex is involved in limiting Th2 gene expression, as well as in inhibiting non-Th2 gene expression. Thus, Bcl11b controls both GATA3-mediated gene activation and repression in Th2 cells.
Fang, D., Cui, K., Hu, G., Gurram, R. K., Zhong, C., Oler, A. J., Yagi, R., Zhao, M., Sharma, S., Liu, P., Sun, B., Zhao, K., Zhu, J.
Rockefeller University Press
0022-1007
00221007
1540-9538
15409538
shingle_catch_all_4 Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
GATA-binding protein 3 (GATA3) acts as the master transcription factor for type 2 T helper (Th2) cell differentiation and function. However, it is still elusive how GATA3 function is precisely regulated in Th2 cells. Here, we show that the transcription factor B cell lymphoma 11b (Bcl11b), a previously unknown component of GATA3 transcriptional complex, is involved in GATA3-mediated gene regulation. Bcl11b binds to GATA3 through protein–protein interaction, and they colocalize at many important cis-regulatory elements in Th2 cells. The expression of type 2 cytokines, including IL-4, IL-5, and IL-13, is up-regulated in Bcl11b -deficient Th2 cells both in vitro and in vivo; such up-regulation is completely GATA3 dependent. Genome-wide analyses of Bcl11b- and GATA3-regulated genes (from RNA sequencing), cobinding patterns (from chromatin immunoprecipitation sequencing), and Bcl11b-modulated epigenetic modification and gene accessibility suggest that GATA3/Bcl11b complex is involved in limiting Th2 gene expression, as well as in inhibiting non-Th2 gene expression. Thus, Bcl11b controls both GATA3-mediated gene activation and repression in Th2 cells.
Fang, D., Cui, K., Hu, G., Gurram, R. K., Zhong, C., Oler, A. J., Yagi, R., Zhao, M., Sharma, S., Liu, P., Sun, B., Zhao, K., Zhu, J.
Rockefeller University Press
0022-1007
00221007
1540-9538
15409538
shingle_title_1 Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
shingle_title_2 Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
shingle_title_3 Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
shingle_title_4 Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
timestamp 2025-06-30T23:34:46.134Z
titel Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
titel_suche Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
topic WW-YZ
uid ipn_articles_6253108