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Gene Review

OR3D1P  -  olfactory receptor, family 3, subfamily D,...

Homo sapiens

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Disease relevance of OR3D1P


High impact information on OR3D1P

  • The NCD3G [for nine-cysteine domain of family 3 G-protein-coupled receptors (GPCRs)] domain is a novel protein domain that is conserved in family 3 GPCRs, including metabotropic glutamate receptors, calcium-sensing receptors, pheromone receptors and taste receptors, with the exception of GABA(B) receptors [6].
  • Family 3 beta-D-glucan glucohydrolases are distributed widely in higher plants [7].
  • Here we provide evidence for full agonist activity mediated by the heptahelical domain of family 3 G protein-coupled receptors (which have mGluR-like structure) that may lead to drug development opportunities [8].
  • To elucidate the respective role of VFTM closure and the change in orientation of the VFTMs in family 3 GPCR activation, we analyzed the mechanism of action of the mGlu8 receptor antagonists ACPT-II and MAP4 [9].
  • Family 3 was informative for four RFLPs detected with dystrophin cDNA probes which span the entire gene [10].

Chemical compound and disease context of OR3D1P


Biological context of OR3D1P


Anatomical context of OR3D1P


Associations of OR3D1P with chemical compounds

  • The gamma-amino-n-butyric acid type B (GABA(B)) receptor is composed of two subunits, GABA(B)1 and GABA(B)2, belonging to the family 3 heptahelix receptors [22].
  • As has been found for other family 3 GPCRs, the large amino-terminal extracellular domain (ECD) of the Ca(2+) receptor is the primary Ca(2+) binding domain [23].
  • Although thromboxane synthase-II lacks the conserved cysteine that serves as the proximal heme ligand in the other cytochromes, significant sequence similarities exist among thromboxane synthase-I and -II and several P450s, particularly those in family 3 [24].
  • Unique among the residues in this region, Pro823, which is highly conserved in family 3 of the G protein-coupled receptors, when mutated to either alanine or glycine, despite good expression severely impaired CaR activation by Ca2+ [25].
  • The stereochemistry of cellobiose hydrolysis revealed that beta-glucosidase from T. aurantiacus is a retaining glycosidase, while N-terminal amino acid sequence alignment indicated that it is a member of glycoside hydrolase family 3 [26].

Physical interactions of OR3D1P


Other interactions of OR3D1P

  • Molecular analysis in all families demonstrated sequence changes within exon 14 of the TGFBI gene on chromosome 5q31, at codon 622 in family 3, and at codon 626 in families 1 and 2, which are presumed to be responsible for the disease [28].
  • Family-3 (SMUG1) enzymes have recently been identified and have a preference for uracil in single-stranded DNA when assayed in vitro [29].
  • Metabotropic glutamate receptors (mGlu receptors), the Ca2+-sensing receptor, gamma-aminobutyric acid type B receptors, and one group of pheromone receptors constitute a unique family (also called family 3) of heptahelical receptors [30].
  • Three novel germline mutations in PTCH were identified, including a missense mutation (p.S1089 > P) in family 1, a nonsense mutation (p.Q160X) in family 2 and a de novo mutation (c.768_777delGACAAACTTC) in family 3 [31].
  • In family 3, DXS159 (Xq12-q13) gave a lod score of 2.53 at theta = 0; results were compatible with localisation of the putative XLMR locus in this family proximal to DXYS1 (Xq21) [32].

Analytical, diagnostic and therapeutic context of OR3D1P

  • Electromyography (EMG) was performed in heterozygous carriers from family 1 and family 3 [33].
  • Specific rabbit anti-rCjaA antibody reacted not only with CjaA but also with other solute-binding protein (family 3), component of the ABC transport system (CjaC protein), was chosen as the protective antigen for animal experiments [34].
  • In family 3, no causative base change was found by the sequencing analysis, but a deletion involving exons 4-9 was suggested by multiplex PCR analysis [35].
  • Further sequence analysis of isolates in strain family 3 identified a new T529C SNP in NAT resulting in a histidine instead of a tyrosine at position 177 [36].


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  7. Structural basis for broad substrate specificity in higher plant beta-D-glucan glucohydrolases. Hrmova, M., De Gori, R., Smith, B.J., Fairweather, J.K., Driguez, H., Varghese, J.N., Fincher, G.B. Plant Cell (2002) [Pubmed]
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  11. Anti-sense trefoil factor family-3 (intestinal trefoil factor) inhibits cell growth and induces chemosensitivity to adriamycin in human gastric cancer cells. Chan, M.W., Chan, V.Y., Leung, W.K., Chan, K.K., To, K.F., Sung, J.J., Chan, F.K. Life Sci. (2005) [Pubmed]
  12. Cerebral X-linked adrenoleukodystrophy in a girl with Xq27-Ter deletion. Hershkovitz, E., Narkis, G., Shorer, Z., Moser, A.B., Watkins, P.A., Moser, H.W., Manor, E. Ann. Neurol. (2002) [Pubmed]
  13. Cloning, expression, and regulation of lithocholic acid 6 beta-hydroxylase. Teixeira, J., Gil, G. J. Biol. Chem. (1991) [Pubmed]
  14. Sudden cardiac death in hypertrophic cardiomyopathy. Variability in phenotypic expression of beta-myosin heavy chain mutations. Marian, A.J., Mares, A., Kelly, D.P., Yu, Q.T., Abchee, A.B., Hill, R., Roberts, R. Eur. Heart J. (1995) [Pubmed]
  15. Cloning and expression of the gene which encodes a tube precipitin antigen and wall-associated beta-glucosidase of Coccidioides immitis. Hung, C.Y., Yu, J.J., Lehmann, P.F., Cole, G.T. Infect. Immun. (2001) [Pubmed]
  16. Qualitative change in antibody responses of human immunodeficiency virus-infected individuals to pneumococcal capsular polysaccharide vaccination associated with highly active antiretroviral therapy. Subramaniam, K.S., Segal, R., Lyles, R.H., Rodriguez-Barradas, M.C., Pirofski, L.A. J. Infect. Dis. (2003) [Pubmed]
  17. Regulation and function of trefoil factor family 3 expression in the biliary tree. Nozaki, I., Lunz, J.G., Specht, S., Park, J.I., Giraud, A.S., Murase, N., Demetris, A.J. Am. J. Pathol. (2004) [Pubmed]
  18. Isolation, characterization, and cloning of {alpha}-L-Arabinofuranosidase expressed during fruit ripening of Japanese pear. Tateishi, A., Mori, H., Watari, J., Nagashima, K., Yamaki, S., Inoue, H. Plant Physiol. (2005) [Pubmed]
  19. beta-Glucosidase in cellulosome of the anaerobic fungus Piromyces sp. strain E2 is a family 3 glycoside hydrolase. Steenbakkers, P.J., Harhangi, H.R., Bosscher, M.W., van der Hooft, M.M., Keltjens, J.T., van der Drift, C., Vogels, G.D., op den Camp, H.J. Biochem. J. (2003) [Pubmed]
  20. Localization of TFF3 peptide in human esophageal submucosal glands and gastric cardia: differentiation of two types of gastric pit cells along the rostro-caudal axis. Kouznetsova, I., Kalinski, T., Peitz, U., Mönkemüller, K.E., Kalbacher, H., Vieth, M., Meyer, F., Roessner, A., Malfertheiner, P., Lippert, H., Hoffmann, W. Cell Tissue Res. (2007) [Pubmed]
  21. A gradient of TFF3 (trefoil factor family 3) peptide synthesis within the normal human gastric mucosa. Kouznetsova, I., Peitz, U., Vieth, M., Meyer, F., Vestergaard, E.M., Malfertheiner, P., Roessner, A., Lippert, H., Hoffmann, W. Cell Tissue Res. (2004) [Pubmed]
  22. Mapping the agonist-binding site of GABAB type 1 subunit sheds light on the activation process of GABAB receptors. Galvez, T., Prezeau, L., Milioti, G., Franek, M., Joly, C., Froestl, W., Bettler, B., Bertrand, H.O., Blahos, J., Pin, J.P. J. Biol. Chem. (2000) [Pubmed]
  23. Evidence for distinct cation and calcimimetic compound (NPS 568) recognition domains in the transmembrane regions of the human Ca2+ receptor. Ray, K., Northup, J. J. Biol. Chem. (2002) [Pubmed]
  24. Primary structure of human thromboxane synthase determined from the cDNA sequence. Ohashi, K., Ruan, K.H., Kulmacz, R.J., Wu, K.K., Wang, L.H. J. Biol. Chem. (1992) [Pubmed]
  25. A region in the seven-transmembrane domain of the human Ca2+ receptor critical for response to Ca2+. Hu, J., McLarnon, S.J., Mora, S., Jiang, J., Thomas, C., Jacobson, K.A., Spiegel, A.M. J. Biol. Chem. (2005) [Pubmed]
  26. Biochemical characterization and mechanism of action of a thermostable beta-glucosidase purified from Thermoascus aurantiacus. Parry, N.J., Beever, D.E., Owen, E., Vandenberghe, I., Van Beeumen , J., Bhat, M.K. Biochem. J. (2001) [Pubmed]
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  28. A mutation within exon 14 of the TGFBI (BIGH3) gene on chromosome 5q31 causes an asymmetric, late-onset form of lattice corneal dystrophy. Stewart, H., Black, G.C., Donnai, D., Bonshek, R.E., McCarthy, J., Morgan, S., Dixon, M.J., Ridgway, A.A. Ophthalmology (1999) [Pubmed]
  29. hSMUG1 can functionally compensate for Ung1 in the yeast Saccharomyces cerevisiae. Elateri, I., Tinkelenberg, B.A., Hansbury, M., Caradonna, S., Muller-Weeks, S., Ladner, R.D. DNA Repair (Amst.) (2003) [Pubmed]
  30. Extreme C terminus of G protein alpha-subunits contains a site that discriminates between Gi-coupled metabotropic glutamate receptors. Blahos, J., Mary, S., Perroy, J., de Colle, C., Brabet, I., Bockaert, J., Pin, J.P. J. Biol. Chem. (1998) [Pubmed]
  31. Germline mutations of the PTCH gene in families with odontogenic keratocysts and nevoid basal cell carcinoma syndrome. Song, Y.L., Zhang, W.F., Peng, B., Wang, C.N., Wang, Q., Bian, Z. Tumour Biol. (2006) [Pubmed]
  32. Linkage analysis suggests at least two loci for X-linked non-specific mental retardation. Arveiler, B., Alembik, Y., Hanauer, A., Jacobs, P., Tranebjaerg, L., Mikkelsen, M., Puissant, H., Piet, L.L., Mandel, J.L. Am. J. Med. Genet. (1988) [Pubmed]
  33. Giant axonal neuropathy: clinical and genetic study in six cases. Demir, E., Bomont, P., Erdem, S., Cavalier, L., Demirci, M., Kose, G., Muftuoglu, S., Cakar, A.N., Tan, E., Aysun, S., Topcu, M., Guicheney, P., Koenig, M., Topaloglu, H. J. Neurol. Neurosurg. Psychiatr. (2005) [Pubmed]
  34. Oral immunization of chickens with avirulent Salmonella vaccine strain carrying C. jejuni 72Dz/92 cjaA gene elicits specific humoral immune response associated with protection against challenge with wild-type Campylobacter. Wyszyńska, A., Raczko, A., Lis, M., Jagusztyn-Krynicka, E.K. Vaccine (2004) [Pubmed]
  35. Novel IRF6 mutations in Japanese patients with Van der Woude syndrome: two missense mutations (R45Q and P396S) and a 17-kb deletion. Kayano, S., Kure, S., Suzuki, Y., Kanno, K., Aoki, Y., Kondo, S., Schutte, B.C., Murray, J.C., Yamada, A., Matsubara, Y. J. Hum. Genet. (2003) [Pubmed]
  36. Mutational and expression analysis of tbnat and its response to isoniazid. Sholto-Douglas-Vernon, C., Sandy, J., Victor, T.C., Sim, E., Helden, P.D. J. Med. Microbiol. (2005) [Pubmed]
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