Human Gene CNRIP1 (ENST00000409559.7) from GENCODE V44
Description: Homo sapiens cannabinoid receptor interacting protein 1 (CNRIP1), transcript variant 2, mRNA. (from RefSeq NM_001111101) RefSeq Summary (NM_001111101): This gene encodes a protein that interacts with the C-terminal tail of cannabinoid receptor 1. Two transcript variants encoding different isoforms have been described for this gene. [provided by RefSeq, Jul 2013]. Sequence Note: The RefSeq transcript and protein were derived from genomic sequence to make the sequence consistent with the reference genome assembly. The genomic coordinates used for the transcript record were based on alignments. Gencode Transcript: ENST00000409559.7 Gencode Gene: ENSG00000119865.9 Transcript (Including UTRs) Position: hg38 chr2:68,284,171-68,319,400 Size: 35,230 Total Exon Count: 3 Strand: - Coding Region Position: hg38 chr2:68,284,428-68,319,400 Size: 34,973 Coding Exon Count: 3
ID:CNRP1_HUMAN DESCRIPTION: RecName: Full=CB1 cannabinoid receptor-interacting protein 1; Short=CRIP-1; FUNCTION: Isoform 1 suppresses cannabinoid receptor CNR1-mediated tonic inhibition of voltage-gated calcium channels. Isoform 2 does not have this effect. SUBUNIT: Interacts with the cannabinoid receptor CNR1 (via C- terminus). Does not interact with cannabinoid receptor CNR2. SIMILARITY: Belongs to the CNRIP family.
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.
Protein Domain and Structure Information
ModBase Predicted Comparative 3D Structure on Q96F85
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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.