Analysis of multiple transcription factor cistromes in transdifferentiated mouse HAFTL pre-B lymphocytes 

2019 ◽  
Author(s):  
Oevelen van
Keyword(s):  
Transcription Factor ◽  
B Lymphocytes ◽  
Multiple Transcription Factor

scholarly journals Induction of Immunoglobulin Heavy-Chain Transcription through the Transcription Factor Bright Requires TFII-I

2006 ◽  
Vol 26 (12) ◽  
pp. 4758-4768 ◽  
Author(s):  
Jaya Rajaiya ◽  
Jamee C. Nixon ◽  
Neil Ayers ◽  
Zana P. Desgranges ◽  
Ananda L. Roy ◽  
...  
Keyword(s):  
Transcription Factor ◽  
B Lymphocytes ◽  
Heavy Chain ◽  
In Vitro Model ◽  
Model System ◽  
Interaction Domain ◽  
Tyrosine Residues ◽  
Immunoglobulin Locus ◽  
Vitro Model

ABSTRACT Bright/ARID3a/Dril1, a member of the ARID family of transcription factors, is expressed in a highly regulated fashion in B lymphocytes, where it enhances immunoglobulin transcription three- to sixfold. Recent publications from our lab indicated that functional, but not kinase-inactive, Bruton's tyrosine kinase (Btk) is critical for Bright activity in an in vitro model system, yet Bright itself is not appreciably tyrosine phosphorylated. These data suggested that a third protein, and Btk substrate, must contribute to Bright-enhanced immunoglobulin transcription. The ubiquitously expressed transcription factor TFII-I was identified as a substrate for Btk several years ago. In this work, we show that TFII-I directly interacts with human Bright through amino acids in Bright's protein interaction domain and that specific tyrosine residues of TFII-I are essential for Bright-induced activity of an immunoglobulin reporter gene. Moreover, inhibition of TFII-I function in a B-cell line resulted in decreased heavy-chain transcript levels. These data suggest that Bright functions as a three-component protein complex in the immunoglobulin locus and tie together previous data indicating important roles for Btk and TFII-I in B lymphocytes.

scholarly journals Identification of a novel NF-kappaB p50-related protein in B lymphocytes.

1996 ◽  
Vol 16 (12) ◽  
pp. 7089-7097 ◽  
Author(s):  
R J Phillips ◽  
S Gustafson ◽  
S Ghosh
Keyword(s):  
Transcription Factor ◽  
B Lymphocytes ◽  
Plasma Cells ◽  
Protein Complexes ◽  
Cell Types ◽  
Related Protein ◽  
Active Complex ◽  
Inactive Form ◽  
Nf Kappab ◽  
Constitutively Active

In most cell types other than mature B lymphocytes and macrophages, the transcription factor NF-kappaB remains in an inactive form in the cytosol by being bound to the inhibitory proteins IkappaBalpha and IkappaBbeta. To investigate the regulation of constitutively active NF-kappaB in B lymphocytes, we have examined the composition of Rel protein complexes in different mouse B-cell lines. As reported previously, the constitutively active complex in mature B cells was predominantly p50:c-Rel. However, the kappaB binding complex in the plasmacytomas that were examined lacked c-Rel and instead contained only a p50-related protein. This p50-related protein (p55) cross-reacts with three different p50 antisera, exists in both the cytosol and the nucleus, and is the protein that binds to kappaB sites in plasma cells. Transfection of reporter constructs into plasma cells indicates that the p55 complex is also transcriptionally active. The p55 protein can be detected in splenocytes from mice lacking the p105/p50 gene, and therefore it appears to be the product of a distinct gene. The implications of the existence of a NF-kappaB p50-related protein in plasma cells that is capable of binding to kappaB sites and activating transcription are discussed.

D1Dopamine Receptor Activation of Multiple Transcription Factor Genes in Rat Striatum

1992 ◽  
Vol 58 (4) ◽  
pp. 1420-1426 ◽  
Author(s):  
Andrew J. Cole ◽  
Ratan V. Bhat ◽  
Cary Patt ◽  
Paul F. Worley ◽  
Jay M. Baraban
Keyword(s):  
Transcription Factor ◽  
Receptor Activation ◽  
Rat Striatum ◽  
Transcription Factor Genes ◽  
Multiple Transcription Factor

scholarly journals EBI2 expression in B lymphocytes is controlled by the Epstein–Barr virus transcription factor, BRRF1 (Na), during viral infection

2017 ◽  
Vol 98 (3) ◽  
pp. 435-446 ◽  
Author(s):  
Caleb Cornaby ◽  
Jillian L Jafek ◽  
Cameron Birrell ◽  
Vera Mayhew ◽  
Lauren Syndergaard ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Viral Infection ◽  
B Lymphocytes ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Virus Transcription ◽  
Epstein Barr
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