ID:PDE3B_HUMAN DESCRIPTION: RecName: Full=cGMP-inhibited 3',5'-cyclic phosphodiesterase B; EC=3.1.4.17; AltName: Full=CGIPDE1; Short=CGIP1; AltName: Full=Cyclic GMP-inhibited phosphodiesterase B; Short=CGI-PDE B; FUNCTION: Cyclic nucleotide phosphodiesterase with a dual- specificity for the second messengers cAMP and cGMP, which are key regulators of many important physiological processes. May play a role in fat metabolism. Regulates cAMP binding of RAPGEF3. Through simultaneous binding to RAPGEF3 and PIK3R6 assembles a signaling complex in which the PI3K gamma complex is activated by RAPGEF3 and which is involved in angiogenesis. CATALYTIC ACTIVITY: Nucleoside 3',5'-cyclic phosphate + H(2)O = nucleoside 5'-phosphate. COFACTOR: Binds 2 divalent metal cations per subunit. Site 1 may preferentially bind zinc ions, while site 2 has a preference for magnesium and/or manganese ions. ENZYME REGULATION: Inhibited by cGMP. SUBUNIT: Interacts with PIK3CG (By similarity). Interacts with RAPGEF3 and PIK3R6. INTERACTION: P48736:PIK3CG; NbExp=3; IntAct=EBI-6172856, EBI-1030384; Q5UE93:PIK3R6; NbExp=3; IntAct=EBI-6172856, EBI-6172907; O95398:RAPGEF3; NbExp=8; IntAct=EBI-6172856, EBI-6172806; SUBCELLULAR LOCATION: Membrane; Multi-pass membrane protein (Potential). TISSUE SPECIFICITY: Abundant in adipose tissues. SIMILARITY: Belongs to the cyclic nucleotide phosphodiesterase family. PDE3 subfamily.
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 Q13370
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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.