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functional studies on NR2F1 transfected cells, during osteoblast differentiation in combination with TGFbeta1 and BMP-2, showed that TGFb1 does not recover osteoblast differentiation, whereas BMP-2 rescues osteoblast differentiation in NR2F1 siRNA transfected cells. Thus, our results showed that BMP-2 could intervene in NR2F1 down-regulated signaling pathways to recover osteoblast differentiation.
Findings from basic biological analysis of disseminated tumor cells (DTCs) dormancy to the clinical situation and supports further clinical studies of nuclear receptor subfamily 2 group F member 1 (NR2F1) as a marker of dormancy.
Whole-exome sequencing identified a novel missense NR2F1 variant in each case, Cys86Phe in the DNA-binding domain in Case 1, and a Leu372Pro in the ligand-binding domain in Case 2. Using molecular modeling we are also able to demonstrate the putative effect of the two missenses on protein function, generating a hitherto undescribed molecular model for the ligand-binding domain of NR2F1 in the process.
fifth of COUP-TFI cells also co-expressed COUP-TFII, and cells expressing either transcription factor followed posterior or anterio-lateral pathways into the cortex
Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS)encompasses a broad range of clinical phenotypes. Functional studies help determine the severity of novel NR2F1 variants. Some genotype-phenotype correlations seem to exist, with missense mutations in the DNA-binding domain causing the most severe phenotypes
COUP-TFII is expressed in a diverse subset of GABAergic interneurons predominantly innervating small dendritic shafts originating from both interneurons and pyramidal cells.
our mechanistic in vitro assays and in vivo results suggest that a reduction in chemokine CXCL12 expression, with an enhancement of CXCR4 expression, provoked by COUP-TFI, could be associated with an increase in the invasive potential of breast cancer
NR2F1 has an important role in the development of the visual system and that haploinsuffiency can lead to optic atrophy with intellectual impairment.
COUP-TFI and related NRs such as the COUPTFs and PNR can selectively associate with the developmental corepressor BCL11A via a conserved motif F/YSXXLXXL/Y within the RID1 and RID2 domains. The interaction with BCL11A facilitates COUP-TFII-mediated repression of the RARb2 gene.
a novel mechanism of MTP repression that involves binding of NR2F1 to the DR1 element and recruitment of corepressors
study identifies two unique corticotroph tumor populations which differ in their expression of COUP-TFI, the presence of which occurs more frequently in macroadenomas.
provide detailed experimental validation of each step and, as a proof of principle, utilize the methodology to identify novel direct targets of the orphan nuclear receptor NR2F1 (COUP-TFI)
Transcriptional and posttranscriptional mechanisms involving NR2F1 and IRE1beta ensure low microsomal triglyceride transfer protein expression in undifferentiated intestinal cells and avoid apolipoprotein B lipoprotein biosynthesis.
Inhibit aldehyde dehydrogenase 2 gene expression
Regulation of retinoic acid-induced inhibition of AP-1 activity by orphan receptor chicken ovalbumin upstream promoter-transcription factor.
Formation of an hER alpha-COUP-TFI complex enhances hER alpha AF-1 through Ser118 phosphorylation by MAPK.
regulates transcription of hepatitis B virus
Transcription of the LHR gene is repressed by EAR3.
COUP-TF may be involved in repression of the human MGP gene promoter at the myoblast stage
These results indicate that COUP-TF1 plays an important role in modulating the timing and magnitude of T3-stimulated gene expression required for normal corticogenesis.
COUP-TFI expression is required for functional organization of the hippocampal septo-temporal longitudinal axis
These data identify silencer elements of the Nr2f1-A830082K12Rik gene pair as new candidate loci for Waardenburg syndrome type 4.
Coup-TF1 and Coup-TF2 control subtype and laminar identity of MGE-derived neocortical interneurons
COUP-TFI is required predominantly in Dentate gyrus progenitors for modulating expression of the Cxcr4 receptor during granule cell neurogenesis and migration.
Transcription factors COUP-TFI and COUP-TFII are required for the production of granule cells in the mouse olfactory bulb.
Findings provide evidence that Sp8 and another transcription factor, COUP-TF1, mutually repress each other's cortical neuroepithelial expression along the anterior-posterior and dorsoventral axes
a novel tissue-dependent coregulatory network for NR2F1, miR-140, and Klf9 in the inner ear
odour deprivation, which is known to downregulate tyrosine hydroxylase expression in the olfactory bulb, also downregulates COUP-TFI in dopaminergic cells, indicating a correlation between tyrosine hydroxylase- and COUP-TFI-activity-dependent action.
CoupTFI collaborates with retinoic acid signaling to regulate both cortical ventricular zone progenitor cell behavior and cortical neurogenesis
Interaction of NSD1 with the NR2E/F subfamily including COUP-TFI, COUP-TFII, EAR2 and TLX requires a F/YSXXLXXL/Y motif. NSD1 interaction with liganded NRs is mediated by an overlapping LXXLL motif.
Our data suggest that the non-protein coding locus Mcs1a regulates Nr2f1, which is a candidate modifier of differentiation, proliferation, and mammary cancer risk.
study extends the pool of recognized putative AR targets and identifies a negatively regulated target of AR - COUP-TF1 - which could possibly play a role in human prostate cancer
Exogenous expression of COUP-TFI in AS cells, in a dose-dependent fashion, leads to growth inhibition.
Data demonstrate that COUP-TFI modulates late-born neuron migration and favours proper differentiation of callosal projection neurons by finely regulating Rnd2 expression levels.
LHbeta promoter activity is further regulated by the orphan nuclear receptors, chicken ovalbumin upstream promoter-transcription factors (COUP-TFI and COUP-TFII).
COUP-TFI controls the delicate balance between medial ganglionic eminence and caudal ganglionic eminence derived cortical interneurons by regulating intermediate progenitor divisions
This study demonstrated that kallistatin expression is repressed by triiodothyronine and modulated by the orphan nuclear receptor, chicken ovalbumin upstream promoter transcription factor 1 (COUP-TF1).
COUP-TFI exerts critical areal and temporal control over the precise differentiation of CSMN during corticogenesis, thereby enabling the area-specific functional features of motor and sensory areas to arise.
Using nr2f1a and nr2f2 mutants, we find that Nr2f1a and Nr2f2 have redundant requirements restricting ventricular cardiomyocyte number and promoting development of the posterior pharyngeal muscles.
Nr2f1a concomitantly coordinates atrial and atrial-atrioventricular canal size through both Bmp-dependent and independent mechanisms.
nr2f1b control venous specification and angiogenic patterning during zebrafish vascular development, which is mediated by Notch signalings.
nr2f1a plays a critical role for vascular development in zebrafish.
results suggest that COUP-TF exerts a tonic inhibition on steroidogenesis by repressing StAR protein expression and that activators of aldosterone biosynthesis lift this inhibition in part by repressing COUP-TF levels.
Coup (chicken ovalbumin upstream promoter) transcription factor binds to the ovalbumin promoter and, in conjunction with another protein (S300-II) stimulates initiation of transcription. Binds to both direct repeats and palindromes of the 5'-AGGTCA-3' motif. Represses transcriptional activity of LHCG.
COUP transcription factor 1
, COUP transcription factor I
, COUP-TF I
, V-erbA-related protein 3
, chicken ovalbumin upstream promoter-transcription factor I
, transcription factor COUP 1 (chicken ovalbumin upstream promoter 1, v-erb-a homolog-like 3)
, avian erythroblastic leukemia viral (v-erb-a) oncogene homolog-like 3
, COUP transcription factor 1-A
, nuclear receptor subfamily 2 group F member 1-A
, nuclear receptor subfamily 2, group F, member 1
, seven-up related 44
, steroid receptor homolog SVP 44
, chicken ovalbumin upstream promoter-transcription factor
, nuclear receptor subfamily 2 group F member 1
, COUP transcription factor 1-B
, nuclear receptor subfamily 2 group F member 1-B
, nuclear receptor subfamily 2, group F, member 1, like
, LOW QUALITY PROTEIN: COUP transcription factor 1