CITED2: Transcriptional coactivator of the p300/CBP-mediated trancription complex. Acts as a bridge, linking TFAP2 transcription factors and the p300/CBP transcriptional coactivator complex in order to stimulate TFAP2-mediated transcriptional activation. Positively regulates TGF-beta signaling through its association with the SMAD/p300/CBP-mediated transcriptional coactivator complex. Stimulates the peroxisome proliferator- activated receptors PPARA transcriptional activity. Enhances estrogen-dependent transactivation mediated by estrogen receptors. Acts also as a transcriptional corepressor; interferes with the binding of the transcription factors HIF1A or STAT2 and the p300/CBP transcriptional coactivator complex. Participates in sex determination and early gonad development by stimulating transcription activation of SRY. Plays a role in controlling left- right patterning during embryogenesis; potentiates transcriptional activation of NODAL-mediated gene transcription in the left lateral plate mesoderm (LPM). Plays an essential role in differentiation of the adrenal cortex from the adrenogonadal primordium (AGP); stimulates WT1-mediated transcription activation thereby up-regulating the nuclear hormone receptor NR5A1 promoter activity. Associates with chromatin to the PITX2 P1 promoter region. Defects in CITED2 are a cause of ventricular septal defect type 2 (VSD2). VSD2 is a common form of congenital cardiovascular anomaly that may occur alone or in combination with other cardiac malformations. It can affect any portion of the ventricular septum, resulting in abnormal communications between the two lower chambers of the heart. Classification is based on location of the communication, such as perimembranous, inlet, outlet (infundibular), central muscular, marginal muscular, or apical muscular defect. Large defects that go unrepaired may give rise to cardiac enlargement, congestive heart failure, pulmonary hypertension, Eisenmenger's syndrome, delayed fetal brain development, arrhythmias, and even sudden cardiac death. Defects in CITED2 are a cause of atrial septal defect type 8 (ASD8). ASD8 is a congenital heart malformation characterized by incomplete closure of the wall between the atria resulting in blood flow from the left to the right atria. Belongs to the CITED family. 2 isoforms of the human protein are produced by alternative splicing.
Protein type: Nuclear receptor co-regulator; Apoptosis; Transcription, coactivator/corepressor; Cell cycle regulation; Motility/polarity/chemotaxis
Cellular Component: cytoplasm; nuclear chromatin; nucleus
Molecular Function: histone acetyltransferase binding; protein binding; transcription coactivator activity; LBD domain binding; transcription cofactor activity; chromatin binding; SMAD binding; transcription factor activity; transcription corepressor activity
Biological Process: transcription from RNA polymerase II promoter; erythrocyte development; embryonic placenta development; central nervous system development; multicellular organismal development; positive regulation of transcription, DNA-dependent; heart development; negative regulation of transcription from RNA polymerase II promoter; decidualization; regulation of transcription, DNA-dependent; vasculature development; cranial nerve morphogenesis; transforming growth factor beta receptor signaling pathway; positive regulation of cell-cell adhesion; morphogenesis of an epithelium; heart looping; cell differentiation; vasculogenesis; kidney development; negative regulation of cell migration; spleen development; blood vessel development; granulocyte differentiation; transcription, DNA-dependent; thymus development; adrenal gland development; in utero embryonic development; leukocyte differentiation; embryonic process involved in female pregnancy; male gonad development; positive regulation of transforming growth factor beta receptor signaling pathway; positive regulation of cell cycle; liver development; trophectodermal cell differentiation; peripheral nervous system development; regulation of transcription from RNA polymerase II promoter; sex determination; cell proliferation; response to estrogen stimulus; ureteric bud branching; neural tube closure; response to hypoxia; hemopoietic progenitor cell differentiation; positive regulation of transcription from RNA polymerase II promoter; lens morphogenesis in camera-type eye; embryonic camera-type eye morphogenesis; determination of left/right symmetry; negative regulation of transcription, DNA-dependent; neural tube formation; negative regulation of apoptosis
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