Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation
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
Published 2018
Rockefeller University Press
Published 2018
Publication Date: |
2018-05-08
|
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Publisher: |
Rockefeller University Press
|
Print ISSN: |
0022-1007
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Electronic ISSN: |
1540-9538
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Topics: |
Medicine
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Published by: |
_version_ | 1836398921633497088 |
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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 |