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The sex dependence of Deaf1 function in mice is consistent with a greater role for 5-HT1A autoreceptors in sensitivity to depression in men.
These data suggest that during the progression of type 1 diabetes, inflammation and hyperglycemia mediate the splicing of DEAF1 and loss of peripheral tissue antigen expression.
DEAF1 binds to the IFNbeta promoter and to IRF3 and IRF7, that it is required for the transcription of the IFNbeta gene and IFNbeta secretion
reduced DEAF1 function, and subsequent loss of Eif4g3 transcription may affect peripheral tissue antigen (PTA) expression in LNSCs and contribute to the pathology of T1D.
LMO4 modulates the activity of the DEAF NES, causing nuclear accumulation of a construct containing the LMO4-interaction region of DEAF1.
Reduced raphe 5-HT content in Deaf-1(-/-) mice indicate its importance in regulation of 5-HT1A gene expression and the role of the 5-HT1A G(-1019) allele in reducing serotonergic neurotransmission by derepression of 5-HT1A autoreceptors.
These results suggest that transcription factors such as Aire and Deaf1, which exert global transcriptional regulatory functions, may play important roles in self-renewal of ESCs and maintaining ESC in a transcriptionally hyperactive state.
Data indicate an important role for LMO4 and Deaf-1 in pathways affecting neural tube closure and skeletal patterning, most likely reflecting their presence in a functional complex in vivo.
Lower peripheral tissue antigens (PTA) expression resulting from the alternative splicing of DEAF1 may contribute to the pathogenesis of type 1 diabetes.
The results demonstrate that variants located within the neurodevelopmental disorder (DAND)or NLS domains significantly reduce DEAF1 transcriptional regulatory activities and are thus, likely to contribute to the underlying clinical concerns in DAND patients.
identified pathogenic de novo variants in two cases, a nonsense variant in IQSEC2 and a missense variant in the SAND domain of DEAF1
We conclude that this DEAF1 gene alteration caused this patient's symptoms and that white matter disease should not be considered a obligate feature of this syndrome.
RAI1 polymorphisms rs4925102 and rs9907986 are predicted to disrupt the binding of retinoic acid RXR-RAR receptors and the transcription factor DEAF1, respectively, in Smith-Magenis and Potocki-Lupski syndromes patients.
an autosomal recessive splice acceptor mutation in DEAF1 (c.997+4A>C, p.G292Pfs*) in all affected individuals, which led to exon skipping, and reduced the normal full-length mRNA copy number in the patients with epilepsy and extrapyramidal symptoms
Data show that deformed epidermal autoregulatory factor-1 (DEAF1) was located in the nucleus under the fluorescence microscope.
This study indicates, for the first time, a hereditary role of DEAF1 in white matter abnormalities, microcephaly and syndromic intellectual disability.
these results demonstrate that mutations in DEAF1 cause ID and behavioral problems, most likely as a result of impaired transcriptional regulation by DEAF1.
Pellino1 interacts with the transcription factor Deformed Epidermal Autoregulatory Factor 1 (DEAF1).
Non-genomic downregulation of 5-HT1A receptor by 17beta-estradiol does not involve NUDR and Freud-1 proteins.
DEAF1 can interact with the DNA-PK complex through interactions of its DNA binding domain with the carboxy-terminal region of Ku70 that contains the Bax binding domain, and that DEAF1 is a potential substrate for DNA-PK.
Data identify DEAF1 as an interactor and in vitro substrate of GSK3A and GSK3B that interacts with the phosphatidylinositol 3-kinase-mammalian target of rapamycin pathway.
The spn gene was mutated in the primary CRC, the expression of SPN was primarily cytoplasmic in nonmucinous CRCs and nuclear in mucinous CRCs.
DEAF1 has nuclear export signal and protein interaction domains
Cell-specific regulation by Deaf-1 could underlie region-specific alterations in 5-HT1A receptor expression in different mood disorders.
In this study the NUDR immunoreactivity as measured by Western blot was significantly decreased in the prefrontal cortex of female depressed subjects (42%, p=0.02) and unchanged in male depressed subjects relative to gender-matched control subjects.
Overexpression of transgenic DEAF-1 in human breast epithelial cells enhances cell proliferation.
DEAF-1 is a trans-acting factor that merits further investigation as a potential tool for modulating GDF5 expression.
effects of loss or gain of DEAF-1 function on Drosophila development
DEAF-1 is a regulator of Drosophila immunity; it activates the expression of Mtk and Drs promoter.
Transcription factor that binds the homeotic Deformed (Dfd) response element. High affinity binding sites contain at least 1 TTCG motif surrounded by additional TCG sequences. May be involved in the selective action of Dfd on these sites without binding directly to the Dfd protein. Requirement of DEAF1 activity may be a common feature of enhancers targeted by Dfd.
deformed epidermal autoregulatory factor 1 homolog
, nuclear DEAF-1-related transcriptional regulator
, zinc finger MYND domain-containing protein 5
, nuclear DEAF-1 related transcriptional regulator
, zinc finger MYND domain containing 5
, DEAF-1 related transcriptional regulator
, DEAF-1 related transcriptional regulator (NUDR)
, deformed epidermal autoregulatory factor 1 (Drosophila)
, deformed epidermal autoregulatory factor 1 homolog-like
, deformed epidermal autoregulatory factor 1
, deformed epidermal autoregulatory factor-1