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anti-Human CITED2 Antibodies:
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Human Monoclonal CITED2 Primary Antibody for ICC, IF - ABIN151069
Bamforth, Bragança, Farthing, Schneider, Broadbent, Michell, Clarke, Neubauer, Norris, Brown, Anderson, Bhattacharya: Cited2 controls left-right patterning and heart development through a Nodal-Pitx2c pathway. in Nature genetics 2004
Show all 15 Pubmed References
Monoclonal CITED2 Primary Antibody for WB - ABIN534076
Bhattacharya, Michels, Leung, Arany, Kung, Livingston: Functional role of p35srj, a novel p300/CBP binding protein, during transactivation by HIF-1. in Genes & development 1999
Show all 5 Pubmed References
Dog (Canine) Polyclonal CITED2 Primary Antibody for ELISA - ABIN547597
Weninger, Lopes Floro, Bennett, Withington, Preis, Barbera, Mohun, Dunwoodie: Cited2 is required both for heart morphogenesis and establishment of the left-right axis in mouse development. in Development (Cambridge, England) 2005
The results showed that the core promoter area of MUC5AC was located within the 935/+48 region and that P300 reduced the expression of MUC5AC in A549 cells.
Observations identify CITED2 as a novel negative regulator of macrophage proinflammatory activation that protects the host from inflammatory insults.
CITED2 acts as a molecular chaperone to guide PRMT5 and p300 to nucleolin, thereby activating nucleolin. Informatics and experimental data suggest that the CITED2-nucleolin axis is involved in prostate cancer metastasis.
Knockdown of CITED2 led to a decreased interaction of p53 with its inhibitor MDM2, which results in increased amounts of total p53 protein. Data indicate that CITED2 functions in pathways regulating p53 activity.
CITED2 regulates primary breast tumor growth, likely by influencing tumor vasculature via TGF-beta-dependent regulation of VEGFA.
The results suggest that CITED2 mutations in conserved regions lead to disease-causing biological and functional changes and may contribute to the occurrence of conotruncal heart defects in Chinese children.
CITED2 gene mutation may play a significant role in the development of pediatric congenital heart disease.
CITED2 supports gastric cancer cell colony formation and proliferation while inhibiting apoptosis making it a potential gene therapy target for gastric cancer.
Through allosteric enhancement of HIF-1alpha release, CITED2 activates a highly responsive negative feedback circuit that rapidly and efficiently attenuates the hypoxic response, even at modest CITED2 concentrations.
down-regulation of Cited2 was associated with high glucose-induced apoptosis in cardiomyocytes in vitro
High Cited2 level in cumulus cells was associated with low embryo quality and pregnancy outcome in in vitro fertilization patients.
the downregulation of CITED2 contributes to TGFbeta-mediated senescence.
CITED2 plays important roles in the progression and chemoresistance of breast carcinoma and that CITED2 status is a potent prognostic factor in breast cancer patients.
Intrinsic protein disorder plays a prominent role in the function and interactions of the transcriptional co-activators CBP and p300. (Review)
FBXL5-mediated degradation of CITED2 leads to the activation of HIF-1 alpha.
The increased CITED2 expression in acute myeloid leukemia results in better hematopoietic stem cell survival, lower PU.1 levels, and perturbed myeloid differentiation program that contributes to leukemia persistence.
CITED2 has a potential causative impact on congenital heart disease
Our study suggests that CITED2 gene mutations and methylation may play an important role in the development of pediatric congenital heart disease.
data indicate that CITED2 functions as a transcriptional co-activator of ER in breast cancer cells and that its increased expression in tumors may result in estrogen-independent ER activation
CITED2 is a direct effector of PPARgamma for tumor suppression.
Data suggest that tumor suppressor gene Cited2 is direct target of microRNA-182-5p; here, carcinogenic solvent trichloroethylene (TCE) up-regulates expression of microRNA-182-5p in liver; TCE-induced hepatocyte cell proliferation is mediated by microRNA-182-5p overexpression and down-regulation of Cited2 expression.
CITED2 and ISL1 proteins interact physically and cooperate to promote embryonic stem cell differentiation toward cardiomyocytes.
ectopic CITED2 expression at the onset of the reprogramming process in combination with the reprogramming factors promotes a complete and homogeneous conversion of somatic cells into induced pluripotent stem cells
This study demonstrated that Cited2 Regulates Neocortical Layer II/III Generation and Somatosensory Callosal Projection Neuron Development and Connectivity in mice.
Study showed a novel function of miR-200b and CITED2 in high glucose-induced unfolded protein response and ER stress, suggesting that miR-200b and CITED2 are critical for ER homeostasis and neural tube defect formation in the developing embryo.
MicroRNAs in the Myocyte Enhancer Factor 2 (MEF2)-regulated Gtl2-Dio3 Noncoding RNA Locus Promote Cardiomyocyte Proliferation by Targeting the Transcriptional Coactivator Cited2.
Cited2 is required for and enhances reprogramming of mouse embryonic fibroblasts to induced pluripotent stem cells.
Cited2 is required for the maintenance of adult hematopoietic stem cell glycolytic metabolism likely through regulating Pdk2, Pdk4, lactate dehydrogenases B and D, and Akt activity.
Cited2 in sinusoidal trophoblast giant cells and syncytiotrophoblasts is likely to have a non-cell autonomous role in patterning of the pericytes associated with the embryonic capillaries.
a deletion of Cited2 in mESCs results in abnormal mitochondrial morphology and impaired glucose metabolism, which correlates with a defective cell fate decision.
CITED2 is phosphorylated by MAPK1 in vitro at T166, and that MAPK1 activation enhances the coactivation function of CITED2 but not of CITED2-T166N.
Cited2 controls ESC pluripotency and differentiation via direct regulation of Oct4 gene expression.
This study demonistrated that loss of hepatic CITED2 function suppresses gluconeogenesis in diabetic mice, suggesting it as a therapeutic target for hyperglycemia
Our results suggest that Cited2 regulates hematopoietic stem cell quiescence through both HIF-1-dependent and HIF-1-independent pathways
Loss of Cited2 causes congenital heart disease by perturbing left-right patterning of the body axis.
Lipopolysaccharide induces CITED2 expression via nuclear factor (NF)-kappaB in J774 cultured cells and bone-marrow-derived macrophages.
High-fat diet reduces Pitx2c levels in Cited2-deficient embryos and enhance penetrance of left-right patterning defects.
Data indicated that there is a genetic interaction between Cited2 and Lmo4 in control of thymus development.
The protein encoded by this gene inhibits transactivation of HIF1A-induced genes by competing with binding of hypoxia-inducible factor 1-alpha to p300-CH1. Mutations in this gene are a cause of cardiac septal defects. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
, cbp/p300-interacting transactivator 2
, Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 2
, similar to Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal
, Cbp/p300-interacting transactivator 2
, MSG-related protein 1
, MSG1-related gene 1
, melanocyte-specific gene 1-related gene 1
, melanocyte specific gene 2
, cited2/melanocyte specific gene-related gene 1 MRG1