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Disruption of the CREBBP gene and decreased expression of CREB, NFκB p65, c-JUN, c-FOS, BCL2 and c-MYC suggest immune dysregulation.

Abstract：

:Genomic aberrations in the CREBBP (CREB-binding protein - CREBBP or CBP) gene such as point mutations, small insertions or exonic copy number changes are usually associated with Rubinstein-Taybi syndrome (RTs). In this study, the disruption of the CREBBP gene on chromosome 16p13.3, as revealed by CGH-array and FISH, suggests immune dysregulation in a patient with the Rubinstein Taybi syndrome (RTs) phenotype. Further investigation with Western blot techniques demonstrated decreased expression of CREB, NFκB, c-Jun, c-Fos, BCL2 and cMyc in peripheral blood mononuclear cells, thus indicating that the CREBBP gene is essential for the normal expression of these proteins and the regulation of immune responses.

journal_name

Hum Immunol

journal_title

Human immunology

authors

Torres LC,Kulikowski LD,Ramos PL,Sugayama SM,Moreira-Filho CA,Carneiro-Sampaio M

doi

10.1016/j.humimm.2013.04.024

subject

Has Abstract

pub_date

2013-08-01 00:00:00

pages

911-5

issue

8

eissn

0198-8859

issn

1879-1166

pii

S0198-8859(13)00110-9

journal_volume

74

pub_type

杂志文章

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