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RAI1 is located within the Smith-Magenis syndrome region on chromosome 17. Additionally we are shipping Retinoic Acid Induced 1 Antibodies (26) and many more products for this protein.
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RAI1 (show DOM3Z Proteins) polymorphisms rs4925102 and rs9907986 are predicted to disrupt the binding of retinoic acid RXR-RAR (show RARA Proteins) receptors and the transcription factor DEAF1 (show DEAF1 Proteins), respectively, in Smith-Magenis and Potocki-Lupski syndromes patients.
Mutations in RAI1 (show DOM3Z Proteins), OTOF, and SLC26A4 (show SLC26A4 Proteins) may have roles in nonsyndromic hearing loss in Altaian families in Siberia
South American cohort did not confirm the effect of the four candidate loci as modifier of onset age: mithocondrial A10398G polymorphism and CAGn at RAI1, CACNA1A, ATXN3, and ATXN7 genes
RAI1 (show DOM3Z Proteins) Gene Duplication is associated with Potocki-Lupski syndrome.
Results show that when MBD5 (show MBD5 Proteins) and RAI1 (show DOM3Z Proteins) are haploinsufficient, they perturb several common pathways that are linked to neuronal and behavioral development.
Human RAI1 (show DOM3Z Proteins) protein was found to be a highly expressed neuronal protein (show LRCH1 Proteins) whose distribution matches well with its role in cognitive and motor skills.
RAI1 (show DOM3Z Proteins) gene polyglutamine repeat has a different distribution in our population. The 14-repeat allele is associated with perinatal depression and more frequent experience of physical and psychological symptoms during menstrual period.
evolutionary conservation of chromatin binding of SPBP (show TCF20 Proteins) and RAI1 (show DOM3Z Proteins)
The Shc (show SHC1 Proteins) family protein adaptor, Rai (show RNH1 Proteins), acts as a negative regulator of Th17 and Th1 (show TH1L Proteins) cell development.
A reduction of total RAI1 (show DOM3Z Proteins) transcription factor activity is at the heart of the Smith-Magenis Syndrome clinical presentation.
Mice haploinsufficient for Rai1 fed a high carbohydrate or a high fat diet gained weight at a significantly faster rate than their wild type littermates.
Viral pseudo-enzymes activate RIG-I (show DDX58 Proteins) via deamidation to evade cytokine production.
Rai1 dosage in forebrain neurons is critical during the development and is related to body weight regulation, activity levels and learning and memory.
Rai1 is likely one of the main genes responsible for the circadian clock regulation
The Shc (show SHC1 Proteins) family protein adaptor, Rai (show SHC3 Proteins), acts as a negative regulator of Th17 and Th1 (show HAND1 Proteins) cell development.
RAI1 is a positive transcriptional regulator of CLOCK, pinpointing a novel and important role for this gene in the circadian oscillator
study provides evidence to show that Rai1 haploinsufficiency affects feeding, satiety and fat deposition patterns; RAI1 directly regulates the expression of BDNF (show BDNF Proteins)
transcriptional regulator, deficiency is responsible for obesity and craniofacial phenotypes in mice with SMS (show SMS Proteins) deletions
Activation of the host response by RIG-I (show DDX58 Proteins) early in infection is important for controlling replication of West Nile virus NY
Normal disomic Rai1 gene dosage was sufficient to rescue the complex physical and behavioral phenotypes observed in Dp(11)17/+ mice
This gene is located within the Smith-Magenis syndrome region on chromosome 17. It is highly similar to its mouse counterpart and is expressed at high levels mainly in neuronal tissues. The protein encoded by this gene includes a polymorphic polyglutamine tract in the N-terminal domain. Expression of the mouse counterpart in neurons is induced by retinoic acid. This gene is associated with both the severity of the phenotype and the response to medication in schizophrenic patients.
retinoic acid induced 1
, Smith-Magenis syndrome chromosome region
, retinoic acid-induced protein 1
, hypothetical protein