ID:RRAGD_HUMAN DESCRIPTION: RecName: Full=Ras-related GTP-binding protein D; Short=Rag D; Short=RagD; FUNCTION: Has guanine nucleotide-binding activity but lacks intrinsic GTPase activity. Probably required for the amino acid- induced relocalization of mTORC1 to the lysosomes and its subsequent activation by the GTPase RHEB. This is a crucial step in the activation of the TOR signaling cascade by amino acids. SUBUNIT: Binds GTP. Forms a heterodimer with RRAGA in a sequence- independent manner and RRAGB. Heterodimerization stabilizes PPAG proteins. In complex with RRAGB, interacts with RPTOR; this interaction is particularly efficient with GTP-loaded RRAGB and GDP-loaded RRAGC. Interacts with NOL8. INTERACTION: Q9P2J5:LARS; NbExp=13; IntAct=EBI-992949, EBI-356077; Q7L523:RRAGA; NbExp=7; IntAct=EBI-992949, EBI-752376; Q5VZM2:RRAGB; NbExp=7; IntAct=EBI-992949, EBI-993049; SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Lysosome. Note=Predominantly cytoplasmic. May shuttle between the cytoplasm and nucleus, depending on the bound nucleotide state of associated RRAGA. SIMILARITY: Belongs to the GTR/RAG GTP-binding protein family. SEQUENCE CAUTION: Sequence=AAH03088.1; Type=Erroneous initiation; Note=Translation N-terminally extended;
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.
Pfam Domains: PF00025 - ADP-ribosylation factor family PF04670 - Gtr1/RagA G protein conserved region PF09439 - Signal recognition particle receptor beta subunit
ModBase Predicted Comparative 3D Structure on Q9NQL2
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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.