Inhibition of p300 impairs Foxp3⁺ T regulatory cell function and promotes antitumor immunity.
Philadelphia, United States. In Nat Med, Sep 2013
We now report that conditional deletion or pharmacologic inhibition of one HAT, p300 (also known as Ep300 or KAT3B), in Foxp3(+) T(reg) cells increased T cell receptor-induced apoptosis in T(reg) cells, impaired T(reg) cell suppressive function and peripheral T(reg) cell induction, and limited tumor growth in immunocompetent but not in immunodeficient mice.
SET1 and p300 act synergistically, through coupled histone modifications, in transcriptional activation by p53.
New York City, United States. In Cell, Aug 2013
In vitro studies with recombinant chromatin and purified human factors demonstrate a robust SET1 complex (SET1C)-mediated H3K4 trimethylation that is dependent upon p53- and p300-mediated H3 acetylation, a corresponding SET1C-mediated enhancement of p53- and p300-dependent transcription that reflects a primary effect of SET1C through H3K4 trimethylation, and direct SET1C-p53 and SET1C-p300 interactions indicative of a targeted recruitment mechanism.
Early T-cell precursor acute lymphoblastic leukaemia.
New York City, United States. In Curr Opin Hematol, Jul 2013
Consistently, these leukaemias show lower frequencies of prototypical T-ALL lesions such as CDKN2A/B deletions and activating mutations in NOTCH1 and show a higher prevalence of mutations typically associated with the pathogenesis of acute myeloid leukaemias (AMLs).
Genetic and epigenetic basis of chronic lymphocytic leukemia.
Barcelona, Spain. In Curr Opin Hematol, Jul 2013
The mutated genes tend to cluster in different pathways that include NOTCH1 signaling, RNA splicing, processing and transport machinery, innate inflammatory response, and DNA damage and cell cycle control, among others.
The importance of diagnosing NUT midline carcinoma.
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Boston, United States. In Head Neck Pathol, Mar 2013
The oncogenic mechanism of the dual bromodomains and the p300-binding portion of BRD4-NUT is to sequester p300 to localized regions of chromatin, leading to global transcriptional repression and blockade of differentiation.