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RAI1 is located within the Smith-Magenis syndrome region on chromosome 17. Zusätzlich bieten wir Ihnen Retinoic Acid Induced 1 Antikörper (30) und Retinoic Acid Induced 1 Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
we report molecular and clinical characterizations of six subjects with the reciprocal phenomenon of deletions spanning both genes, i.e., PMP22 (zeige PMP22 ELISA Kits)-RAI1 (zeige DOM3Z ELISA Kits) deletions. Systematic clinical studies revealed features consistent with SMS (zeige SMS ELISA Kits), including features of intellectual disability, speech and gross motor delays, behavioral problems and ocular abnormalities.
RAI1 (zeige DOM3Z ELISA Kits) polymorphisms rs4925102 and rs9907986 are predicted to disrupt the binding of retinoic acid RXR-RAR (zeige RARA ELISA Kits) receptors and the transcription factor DEAF1 (zeige DEAF1 ELISA Kits), respectively, in Smith-Magenis and Potocki-Lupski syndromes patients.
Mutations in RAI1 (zeige DOM3Z ELISA Kits), OTOF (zeige OTOF ELISA Kits), and SLC26A4 (zeige SLC26A4 ELISA Kits) 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 (zeige DOM3Z ELISA Kits), CACNA1A (zeige CACNA1A ELISA Kits), ATXN3 (zeige ATXN3 ELISA Kits), and ATXN7 (zeige ATXN7 ELISA Kits) genes
RAI1 (zeige DOM3Z ELISA Kits) Gene Duplication is associated with Potocki-Lupski syndrome.
Results show that when MBD5 (zeige MBD5 ELISA Kits) and RAI1 (zeige DOM3Z ELISA Kits) are haploinsufficient, they perturb several common pathways that are linked to neuronal and behavioral development.
Human RAI1 (zeige DOM3Z ELISA Kits) protein was found to be a highly expressed neuronal protein (zeige LRCH1 ELISA Kits) whose distribution matches well with its role in cognitive and motor skills.
RAI1 (zeige DOM3Z ELISA Kits) 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 (zeige TCF20 ELISA Kits) and RAI1 (zeige DOM3Z ELISA Kits)
The Shc (zeige SHC1 ELISA Kits) family protein adaptor, Rai (zeige RNH1 ELISA Kits), acts as a negative regulator of Th17 and Th1 (zeige TH1L ELISA Kits) cell development.
Rai1 preferentially occupies DNA regions near active promoters and promotes the expression of a group of genes involved in circuit assembly and neuronal communication. Behavioral analyses demonstrated that pan-neural loss of Rai1 causes deficits in motor function, learning, and food intake.
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 (zeige DDX58 ELISA Kits) 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 (zeige SHC1 ELISA Kits) family protein adaptor, Rai (zeige SHC3 ELISA Kits), acts as a negative regulator of Th17 and Th1 (zeige HAND1 ELISA Kits) 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 (zeige BDNF ELISA Kits)
transcriptional regulator, deficiency is responsible for obesity and craniofacial phenotypes in mice with SMS (zeige SMS ELISA Kits) deletions
Activation of the host response by RIG-I (zeige DDX58 ELISA Kits) early in infection is important for controlling replication of West Nile virus NY
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