GTPBP4

From Wikipedia, the free encyclopedia


GTP binding protein 4
Identifiers
Symbol(s) GTPBP4; CRFG; FLJ10686; FLJ10690; FLJ39774; NGB
External IDs MGI1916487 HomoloGene7100
RNA expression pattern

More reference expression data

Orthologs
Human Mouse
Entrez 23560 69237
Ensembl ENSG00000107937 n/a
Uniprot Q9BZE4 n/a
Refseq NM_012341 (mRNA)
NP_036473 (protein)
NM_027000 (mRNA)
NP_081276 (protein)
Location Chr 10: 1.02 - 1.06 Mb n/a
Pubmed search [1] [2]

GTP binding protein 4, also known as GTPBP4, is a human gene.[1]

GTP-binding proteins are GTPases and function as molecular switches that can flip between two states: active, when GTP is bound, and inactive, when GDP is bound. 'Active' in this context usually means that the molecule acts as a signal to trigger other events in the cell. When an extracellular ligand binds to a G-protein-linked receptor, the receptor changes its conformation and switches on the trimeric G proteins that associate with it by causing them to eject their GDP and replace it with GTP. The switch is turned off when the G protein hydrolyzes its own bound GTP, converting it back to GDP. But before that occurs, the active protein has an opportunity to diffuse away from the receptor and deliver its message for a prolonged period to its downstream target.[1]

[edit] References

[edit] Further reading

  • Maruyama K, Sugano S (1994). "Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides.". Gene 138 (1-2): 171–4. PMID 8125298. 
  • Suzuki Y, Yoshitomo-Nakagawa K, Maruyama K, et al. (1997). "Construction and characterization of a full length-enriched and a 5'-end-enriched cDNA library.". Gene 200 (1-2): 149–56. PMID 9373149. 
  • Laping NJ, Olson BA, Zhu Y (2001). "Identification of a novel nuclear guanosine triphosphate-binding protein differentially expressed in renal disease.". J. Am. Soc. Nephrol. 12 (5): 883–90. PMID 11316846. 
  • Scherl A, Couté Y, Déon C, et al. (2003). "Functional proteomic analysis of human nucleolus.". Mol. Biol. Cell 13 (11): 4100–9. doi:10.1091/mbc.E02-05-0271. PMID 12429849. 
  • Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMID 12477932. 
  • Ota T, Suzuki Y, Nishikawa T, et al. (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs.". Nat. Genet. 36 (1): 40–5. doi:10.1038/ng1285. PMID 14702039. 
  • Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMID 15489334. 
  • Olsen JV, Blagoev B, Gnad F, et al. (2006). "Global, in vivo, and site-specific phosphorylation dynamics in signaling networks.". Cell 127 (3): 635–48. doi:10.1016/j.cell.2006.09.026. PMID 17081983. 
  • Lee H, Kim D, Dan HC, et al. (2007). "Identification and characterization of putative tumor suppressor NGB, a GTP-binding protein that interacts with the neurofibromatosis 2 protein.". Mol. Cell. Biol. 27 (6): 2103–19. doi:10.1128/MCB.00572-06. PMID 17210637. 
  • Ewing RM, Chu P, Elisma F, et al. (2007). "Large-scale mapping of human protein-protein interactions by mass spectrometry.". Mol. Syst. Biol. 3: 89. doi:10.1038/msb4100134. PMID 17353931.