The roles of @entity28693 ( @entity28693 ) and @entity24105 in vascular endothelial cells are not completely understood. Here, we found a novel regulatory mechanism for @entity69749 function. @entity69749 tend to accumulate in the nucleus in arterial endothelial cells in vivo and @entity1 aortic endothelial cells (HAoECs) in vitro. In HAoECs, nuclear localization of @entity69749 was not significantly affected by @entity12223 or @entity11391 , primarily due to the reduced binding of @entity69749 to G-actin and in part, to the low level of @entity28693 phosphorylation by @entity3963 . @entity28693 /B downregulation by serum depletion or transfection of siRNA against @entity28693 and/or @entity24105 induced @entity2071 expression in HAoECs. It is known that nuclear import of nuclear factor-kB (NF-kB) plays a key role in @entity2071 gene transcription. However, nuclear accumulation of NF-kB p65 was not observed in @entity28693 /B-depleted HAoECs. Our present findings suggest that @entity69749 inhibit @entity2071 mRNA expression by forming a complex with NF-kB p65 in the nucleus. Conversely, downregulation of @entity28693 /B alleviates this negative regulation without further translocation of NF-kB p65 into the nucleus. These results reveal the novel roles of @entity69749 in the homeostasis of vascular endothelium.

A novel inhibitory mechanism of XXXX on the @entity2071 gene expression in vascular endothelial cells.

@entity1 :: ('9606', 'Species') :: ['human'] @entity69749 :: ('57591;57496', 'Gene') :: ['MRTF-A/B'] @entity28693 :: ('57591', 'Gene') :: ['myocardin-related transcription factor A', 'MRTF-A'] @entity3963 :: ('5594', 'Gene') :: ['ERK'] @entity12223 :: ('MESH:C108830', 'Chemical') :: ['Y27632'] @entity11391 :: ('MESH:C037068', 'Chemical') :: ['latrunculin B'] @entity2071 :: ('3383', 'Gene') :: ['ICAM-1'] @entity24105 :: ('57496', 'Gene') :: ['MRTF-B']
@entity69749 :: (57591;57496,Gene) :: ['MRTF-A/B']
