scholarly journals Transcription Cofactor HES-6

2020 ◽  
Author(s):  
Keyword(s):  
Transcription Cofactor

5403712 Transcription cofactor assay

1996 ◽  
Vol 14 (2) ◽  
pp. 199
Keyword(s):  
Transcription Cofactor

Abstract 96: Inactivation of Neddylation Causes Left Ventricular Noncompaction Cardiomyopathy Through Suppressing YAP Signaling

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Jianqiu Zou ◽  
Wenxia Ma ◽  
Jie Li ◽  
Rodney Littlejohn ◽  
Il-man Kim ◽  
...  
Keyword(s):  
Cardiac Development ◽  
Heart Diseases ◽  
Left Ventricular ◽  
Late Gestation ◽  
Mouse Heart ◽  
Cardiomyocyte Proliferation ◽  
Transcription Cofactor ◽  
Wild Type Counterpart

Rationale: Cardiac development is orchestrated by a number of growth factors, transcription factors and epigenetic regulators, perturbation of which can lead to congenital heart diseases and cardiomyopathies. However, the role of novel ubiquitin-like protein modifiers, such as NEDD8 (neural precursor cells expressed developmentally downregulated 8), in cardiac development is unknown. Objectives: The objective of this study was to determine the significance of NEDD8 modification (neddylation) during perinatal cardiac development. Methods and Results: Neddylated proteins and NEDD8 enzymes were highly abundant in fetal and neonatal hearts but downregulated in adult hearts. We employed an αMHC Cre transgene to delete NAE1, a subunit of the NEDD8 E1 enzyme, in the perinatal mouse heart. Cardiac-specific deletion of NAE1 (NAE1 CKO ) significantly decreased neddylated proteins in the heart. The NAE1 CKO mice displayed cardiac hypoplasia, ventricular non-compaction and heart failure during late gestation, which became more pronounced by postnatal day 1 and led to perinatal lethality. Mechanistically, genetic deletion or pharmacological inhibition of NAE1 resulted in accumulation of Hippo kinases Mst1 and LATS1/2, which in turn phosphorylated and inactivated YAP, a transcription cofactor necessary for cardiomyocyte proliferation, leading to dysregulation of a number of cell cycle-regulatory genes and blockade of cardiomyocyte proliferation in vivo and in vitro . Reactivation of YAP signaling by overexpression of a constitutively-active YAP mutant (YAP 5SA ), but not its wild-type counterpart, overcame the blockade of cardiomyocyte proliferation induced by inhibition of NAE1. Conclusions: Our findings establish the importance of neddylation in the heart, more specifically, in ventricular chamber maturation, and identify neddylation as a novel regulator of Hippo-YAP signaling to promote cardiomyocyte proliferation.

scholarly journals TEADs, Yap, Taz, Vgll4s transcription factors control the establishment of Left-Right asymmetry in zebrafish

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Jonathan Fillatre ◽  
Jean-Daniel Fauny ◽  
Jasmine Alexandra Fels ◽  
Cheng Li ◽  
Mary Goll ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Signaling Pathways ◽  
Transcriptional Control ◽  
Hippo Pathway ◽  
Hippo Signaling ◽  
Zebrafish Model ◽  
Transcription Cofactor ◽  
Expression Of Genes ◽  
Epigenetic Programming ◽  
Left Right Asymmetry

In many vertebrates, establishment of Left-Right (LR) asymmetry results from the activity of a ciliated organ functioning as the LR Organizer (LRO). While regulation of the formation of this structure by major signaling pathways has been described, the transcriptional control of LRO formation is poorly understood. Using the zebrafish model, we show that the transcription factors and cofactors mediating or regulating the transcriptional outcome of the Hippo signaling pathway play a pivotal role in controlling the expression of genes essential to the formation of the LRO including ligands and receptors of signaling pathways involved in this process and most genes required for motile ciliogenesis. Moreover, the transcription cofactor, Vgll4l regulates epigenetic programming in LRO progenitors by controlling the expression of writers and readers of DNA methylation marks. Altogether, our study uncovers a novel and essential role for the transcriptional effectors and regulators of the Hippo pathway in establishing LR asymmetry.

5403712 Transcription cofactor assay

1996 ◽  
Vol 14 (2) ◽  
pp. 183
Keyword(s):  
Transcription Cofactor

scholarly journals AIRE's CARD Revealed, a New Structure for Central Tolerance Provokes Transcriptional Plasticity

2007 ◽  
Vol 283 (3) ◽  
pp. 1723-1731 ◽  
Author(s):  
Brian J. Ferguson ◽  
Clare Alexander ◽  
Simona W. Rossi ◽  
Ingrid Liiv ◽  
Ana Rebane ◽  
...  
Keyword(s):  
Hot Spot ◽  
Structural Basis ◽  
Central Tolerance ◽  
Aire Gene ◽  
Transcription Cofactor ◽  
Genome Wide ◽  
Regulator Protein ◽  
Specific Antigens

Developing T cells encounter peripheral self-antigens in the thymus in order to delete autoreactive clones. It is now known that the autoimmune regulator protein (AIRE), which is expressed in thymic medullary epithelial cells, plays a key role in regulating the thymic transcription of these peripheral tissue-specific antigens. Mutations in the AIRE gene are associated with a severe multiorgan autoimmune syndrome (APECED), and autoimmune reactivities are manifest in AIRE-deficient mice. Functional AIRE protein is expressed as distinct nuclear puncta, although no structural basis existed to explain their relevance to disease. In addressing the cell biologic basis for APECED, we made the unexpected discovery that an AIRE mutation hot spot lies in a caspase recruitment domain. Combined homology modeling and in vitro data now show how APECED mutations influence the activity of this transcriptional regulator. We also provide novel in vivo evidence for AIRE's association with a global transcription cofactor, which may underlie AIRE's focal, genome-wide, alteration of the transcriptome.

scholarly journals Purification of transcription cofactor complex CRSP

1999 ◽  
Vol 96 (13) ◽  
pp. 7137-7142 ◽  
Author(s):  
S. Ryu ◽  
R. Tjian
Keyword(s):  
Transcription Cofactor

scholarly journals Immunometabolic function of the transcription cofactor VGLL3 provides an evolutionary rationale for sexual dimorphism in autoimmunity

FEBS Letters ◽  
2020 ◽  
Vol 594 (20) ◽  
pp. 3371-3383
Author(s):  
Adam Pagenkopf ◽  
Yun Liang
Keyword(s):  
Sexual Dimorphism ◽  
Transcription Cofactor

scholarly journals Binding Model for the Interaction of Anticancer Arylsulfonamides with the p300 Transcription Cofactor

2012 ◽  
Vol 3 (8) ◽  
pp. 620-625 ◽  
Author(s):  
Qi Shi ◽  
Shaoman Yin ◽  
Stefan Kaluz ◽  
Nanting Ni ◽  
Narra Sarojini Devi ◽  
...  
Keyword(s):  
Binding Model ◽  
Transcription Cofactor

scholarly journals Role of NF-Y in In Vivo Regulation of the γ-Globin Gene

2001 ◽  
Vol 21 (9) ◽  
pp. 3083-3095 ◽  
Author(s):  
Zhijun Duan ◽  
George Stamatoyannopoulos ◽  
Qiliang Li
Keyword(s):  
Globin Gene ◽  
Gene Promoter ◽  
Transcriptional Factor ◽  
Proximal Promoter ◽  
Transcription Cofactor ◽  
Basal Transcriptional Machinery ◽  
Ccaat Box ◽  
Chromatin Opening

ABSTRACT The duplicated CCAAT box is required for γ gene expression. We report here that the transcriptional factor NF-Y is recruited to the duplicated CCAAT box in vivo. A mutation of the duplicated CCAAT box that severely disrupts the NF-Y binding also reduces the accessibility level of the γ gene promoter, affects the assembly of basal transcriptional machinery, and increases the recruitment of GATA-1 to the locus control region (LCR) and the proximal promoter and the recruitment of transcription cofactor CBP/p300 to the LCR. These findings suggest that recruitment of NF-Y to the duplicated CCAAT box plays a role in the chromatin opening of the γ gene promoter as well as in the communication between the γ gene promoter and the LCR.

Sign in / Sign up

Export Citation Format

Share Document