ID:SNIP1_HUMAN DESCRIPTION: RecName: Full=Smad nuclear-interacting protein 1; AltName: Full=FHA domain-containing protein SNIP1; FUNCTION: Down-regulates NF-kappa-B signaling by competing with RELA for CREBBP/EP300 binding. Involved in the microRNA (miRNA) biogenesis. SUBUNIT: Binds SMAD4 and CREBBP/EP300. Binds the SMAD1/OAZ1/PSMB4 complex. Interacts with DROSHA. INTERACTION: P01106:MYC; NbExp=9; IntAct=EBI-749336, EBI-447544; SUBCELLULAR LOCATION: Nucleus. TISSUE SPECIFICITY: Ubiquitous, with highest expression in heart and skeletal muscle. PTM: Degraded by the proteasome upon binding to the SMAD1/OAZ1/PSMB4 complex. PTM: Phosphorylated upon DNA damage, probably by ATM or ATR. DISEASE: Defects in SNIP1 are the cause of psychomotor retardation, epilepsy, and craniofacial dysmorphism (PMRED) [MIM:614501]. A disease characterized by severe psychomotor retardation, intractable seizures, dysmorphic features, and a lumpy skull surface. Patients are hypotonic and have poor feeding in the neonatal period. SIMILARITY: Contains 1 FHA domain.
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q8TAD8
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.
Biological Process: GO:0006355 regulation of transcription, DNA-templated GO:0007249 I-kappaB kinase/NF-kappaB signaling GO:0031047 gene silencing by RNA GO:0035196 production of miRNAs involved in gene silencing by miRNA
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Sequence and Links to Tools and Databases 
Common Gene Haplotype Alleles 
