NDLI: Global transcriptional coactivators CREB-binding protein and p300 are highly essential collectively but not individually in peripheral B cells

Content Provider	PubMed Central
Author	Xu, Wu Fukuyama, Tomofusa Ney, Paul A. Wang, Demin Rehg, Jerold Boyd, Kelli Deursen, Jan M. A. Van Brindle, Paul K.
Copyright Year	2006
Abstract	CREB-binding protein (CBP) and its para-log p300 are transcriptional coactivators that physically or functionally interact with over 320 mammalian and viral proteins, including 36 that are essential for B cells in mice. CBP and p300 are generally considered limiting for transcription, yet their roles in adult cell lineages are largely unknown since homozygous null mutations in either gene or compound heterozygosity cause early embryonic lethality in mice. We tested the hypotheses that CBP and p300 are limiting and that each has unique properties in B cells, by using mice with Cre/LoxP conditional knockout alleles for CBP (CBPflox ) and p300 (p300flox ), which carry CD19Cre that initiates floxed gene recombination at the pro–B-cell stage. CD19Cre -mediated loss of CBP or p300 led to surprisingly modest deficits in B-cell numbers, whereas inactivation of both genes was not tolerated by peripheral B cells. There was a moderate decrease in B-cell receptor (BCR)–responsive gene expression in CBP or p300 homozygous null B cells, suggesting that CBP and p300 are essential for this signaling pathway that is crucial for B-cell homeostasis. These results indicate that individually CBP and p300 are partially limiting beyond the pro-B-cell stage and that other coactivators in B cells cannot replace their combined loss.
Related Links	http://dx.doi.org/10.1182/blood-2005-08-3263
Starting Page	4407
File Format	PDF
ISSN	15280020
e-ISSN	15280020
Journal	Blood
Issue Number	11
Volume Number	107
Language	English
Publisher	The American Society of Hematology
Publisher Date	2006-06-01
Access Restriction	Open
Rights Holder	The American Society of Hematology
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Hematology Biochemistry Immunology

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