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Gene Review

FCP1  -  F-cell production 1

Homo sapiens

Synonyms: FCP, FCPX, HBFQTL3
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Disease relevance of FCP1


High impact information on FCP1

  • We show that CCFDN is caused by a single-nucleotide substitution in an antisense Alu element in intron 6 of CTDP1 (encoding the protein phosphatase FCP1, an essential component of the eukaryotic transcription machinery), resulting in a rare mechanism of aberrant splicing and an Alu insertion in the processed mRNA [6].
  • Stimulation of F-cell production in patients with sickle-cell anemia treated with cytarabine or hydroxyurea [7].
  • Treatments that increased F-cell production also increased the patient's hematocrit and caused only minor, transient decreases in white cells [7].
  • Fcp1 and Scp1 belong to a family of Mg(2+)-dependent phosphoserine (P.Ser)/phosphothreonine (P.Thr)-specific phosphatases [8].
  • Fcp1 plays a major role in the regulation of CTD phosphorylation and, hence, critically influences the function of Pol II throughout the transcription cycle [9].

Chemical compound and disease context of FCP1


Biological context of FCP1

  • Multiple regression analysis, including all variables, showed that the FCP locus is the strongest predictor, accounting for 40% of Hb F variation. beta-Globin haplotypes, alpha-globin genes, and age accounted for less than 10% of the variation [1].
  • The variation within each FCP phenotype is modulated by factors associated with the three common beta-globin haplotypes and other as yet unidentified factor(s) [1].
  • Linkage analysis using polymorphic restriction sites along the X chromosome in eight SS and one AA family localized the F-cell production (FCP) locus to Xp22.2, with a maximum lod score (logarithm of odds of linkage v independent assortment) of 4.6 at a recombination fraction of 0.04 [11].
  • Accordingly, the specificity of FCP1 is sufficiently broad to dephosphorylate RNAP IIO at any point in the transcription cycle irrespective of the site of serine phosphorylation within the consensus repeat [12].
  • Transcription activation by targeted recruitment of the RNA polymerase II CTD phosphatase FCP1 [13].

Anatomical context of FCP1

  • F-cell production as determined by F reticulocyte levels in SS females was also higher than in SS males (17% +/- 10% v 13% +/- 8%) [11].
  • As an alternative method to assess FCP1 specificity, RNAP IIO isozymes were prepared in vitro by the phosphorylation of purified calf thymus RNAP IIA with specific CTD kinases and used as substrates for FCP1 [12].
  • We set out to purify an FCP1 kinase from HeLa cells and identified casein kinase 2, which, surprisingly, displayed a negative effect on FCP1-associated activities [14].
  • In cultured cells treated with CTD kinase inhibitors, the dephosphorylation of RNAPII on serine 2 was inhibited by 45% by preincubation with okadaic acid, which inhibits phosphatases of PPP family, including PP1 but not FCP1 [15].
  • To identify FCP1-associated proteins, we constructed a human cell line expressing epitope-tagged FCP1 [16].

Associations of FCP1 with chemical compounds


Physical interactions of FCP1

  • In addition, we demonstrate that the C-terminus region of FCP1 suffices for efficient binding in vivo to the RAP74 subunit of TFIIF and is also required for the exclusive nuclear localization of the protein [13].

Regulatory relationships of FCP1


Other interactions of FCP1


Analytical, diagnostic and therapeutic context of FCP1

  • SETTING: Cases and controls were identified from a population-based sample of men and women combining all of the 5 cross-sectional surveys conducted from 1979 to 1990 of the Stanford Five-City Project (FCP) [26].
  • The purpose of the present study was to determine whether positron emission tomography (PET) studies in monkeys with the dopamine (DA) D2 receptor ligand [18F]fluoroclebopride (FCP) would be significantly influenced by anesthetic induction with isoflurane (approximately 5.0%) compared to induction with 10 mg/kg ketamine [27].
  • In the control group the formazan cell percentage (FCP) was 73.8 +/- 1.6% (range 63% to 83%) [28].
  • The decreased percentage of FCP per year in LADA patients were correlated with GAD-Ab index, body mass index (BMI) and age at onset (r(s)=0.408, -0.301 and -0.523 respectively, P<0.05) [29].
  • METHODS: Silastic models of a Taylor patch, a Miller cuff and a femoro-crural patch prosthesis (FCPP) were attached to a circuit driven by a Berlin Heart, providing a pulsatile flow with an amplitude of 450 to 25 ml/min (mean 200 ml/min) [30].


  1. An analysis of fetal hemoglobin variation in sickle cell disease: the relative contributions of the X-linked factor, beta-globin haplotypes, alpha-globin gene number, gender, and age. Chang, Y.C., Smith, K.D., Moore, R.D., Serjeant, G.R., Dover, G.J. Blood (1995) [Pubmed]
  2. Inhibition of Tat transactivation by the RNA polymerase II CTD-phosphatase FCP1. Licciardo, P., Napolitano, G., Majello, B., Lania, L. AIDS (2001) [Pubmed]
  3. Why are hemoglobin F levels increased in HbE/beta thalassemia? Rees, D.C., Porter, J.B., Clegg, J.B., Weatherall, D.J. Blood (1999) [Pubmed]
  4. Microscopic method for assaying F cell production: illustrative changes during infancy and in aplastic anemia. Dover, G.J., Boyer, S.H., Bell, W.R. Blood (1978) [Pubmed]
  5. Ultrastructural analysis of pancreatic carcinogenesis. II. Establishment and morphology of a transplantable hamster pancreatic adenocarcinoma, FCP. Flaks, A., Moore, M.A., Flaks, B. Carcinogenesis (1980) [Pubmed]
  6. Partial deficiency of the C-terminal-domain phosphatase of RNA polymerase II is associated with congenital cataracts facial dysmorphism neuropathy syndrome. Varon, R., Gooding, R., Steglich, C., Marns, L., Tang, H., Angelicheva, D., Yong, K.K., Ambrugger, P., Reinhold, A., Morar, B., Baas, F., Kwa, M., Tournev, I., Guerguelcheva, V., Kremensky, I., Lochmüller, H., Müllner-Eidenböck, A., Merlini, L., Neumann, L., Bürger, J., Walter, M., Swoboda, K., Thomas, P.K., von Moers, A., Risch, N., Kalaydjieva, L. Nat. Genet. (2003) [Pubmed]
  7. Stimulation of F-cell production in patients with sickle-cell anemia treated with cytarabine or hydroxyurea. Veith, R., Galanello, R., Papayannopoulou, T., Stamatoyannopoulos, G. N. Engl. J. Med. (1985) [Pubmed]
  8. Determinants for Dephosphorylation of the RNA Polymerase II C-Terminal Domain by Scp1. Zhang, Y., Kim, Y., Genoud, N., Gao, J., Kelly, J.W., Pfaff, S.L., Gill, G.N., Dixon, J.E., Noel, J.P. Mol. Cell (2006) [Pubmed]
  9. Fcp1 directly recognizes the C-terminal domain (CTD) and interacts with a site on RNA polymerase II distinct from the CTD. Suh, M.H., Ye, P., Zhang, M., Hausmann, S., Shuman, S., Gnatt, A.L., Fu, J. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  10. Fasting plasma C-peptide levels in health and impaired glucose tolerance: relations to blood glucose and relative body weight. Birgerstam, G., Malmquist, J. Scand. J. Clin. Lab. Invest. (1985) [Pubmed]
  11. Fetal hemoglobin levels in sickle cell disease and normal individuals are partially controlled by an X-linked gene located at Xp22.2. Dover, G.J., Smith, K.D., Chang, Y.C., Purvis, S., Mays, A., Meyers, D.A., Sheils, C., Serjeant, G. Blood (1992) [Pubmed]
  12. TFIIF-associating carboxyl-terminal domain phosphatase dephosphorylates phosphoserines 2 and 5 of RNA polymerase II. Lin, P.S., Dubois, M.F., Dahmus, M.E. J. Biol. Chem. (2002) [Pubmed]
  13. Transcription activation by targeted recruitment of the RNA polymerase II CTD phosphatase FCP1. Licciardo, P., Ruggiero, L., Lania, L., Majello, B. Nucleic Acids Res. (2001) [Pubmed]
  14. The C-terminal domain phosphatase and transcription elongation activities of FCP1 are regulated by phosphorylation. Friedl, E.M., Lane, W.S., Erdjument-Bromage, H., Tempst, P., Reinberg, D. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  15. Protein phosphatase-1 dephosphorylates the C-terminal domain of RNA polymerase-II. Washington, K., Ammosova, T., Beullens, M., Jerebtsova, M., Kumar, A., Bollen, M., Nekhai, S. J. Biol. Chem. (2002) [Pubmed]
  16. The FCP1 phosphatase interacts with RNA polymerase II and with MEP50 a component of the methylosome complex involved in the assembly of snRNP. Licciardo, P., Amente, S., Ruggiero, L., Monti, M., Pucci, P., Lania, L., Majello, B. Nucleic Acids Res. (2003) [Pubmed]
  17. Enhanced binding of RNAP II CTD phosphatase FCP1 to RAP74 following CK2 phosphorylation. Abbott, K.L., Renfrow, M.B., Chalmers, M.J., Nguyen, B.D., Marshall, A.G., Legault, P., Omichinski, J.G. Biochemistry (2005) [Pubmed]
  18. Hydroxyurea induction of hemoglobin F production in sickle cell disease: relationship between cytotoxicity and F cell production. Dover, G.J., Humphries, R.K., Moore, J.G., Ley, T.J., Young, N.S., Charache, S., Nienhuis, A.W. Blood (1986) [Pubmed]
  19. Induction of fetal hemoglobin production in subjects with sickle cell anemia by oral sodium phenylbutyrate. Dover, G.J., Brusilow, S., Charache, S. Blood (1994) [Pubmed]
  20. Diatom fucoxanthin chlorophyll a/c-binding protein (FCP) and land plant light-harvesting proteins use a similar pathway for thylakoid membrane Insertion. Lang, M., Kroth, P.G. J. Biol. Chem. (2001) [Pubmed]
  21. Induction of fetal hemoglobin by cell-cycle-specific drugs and recombinant erythropoietin. Stamatoyannopoulos, G., Veith, R., al-Khatti, A., Papayannopoulou, T. The American journal of pediatric hematology/oncology. (1990) [Pubmed]
  22. Dephosphorylation of RNA polymerase II by CTD-phosphatase FCP1 is inhibited by phospho-CTD associating proteins. Palancade, B., Marshall, N.F., Tremeau-Bravard, A., Bensaude, O., Dahmus, M.E., Dubois, M.F. J. Mol. Biol. (2004) [Pubmed]
  23. Two siblings with unusually mild homozygous beta-thalassemia: a didactic example of the effect of a nonallelic modifier gene of the expressivity of a monogenic disorder. Prchal, J., Stamatoyannopoulos, G. Am. J. Med. Genet. (1981) [Pubmed]
  24. Human CD34(+) and CD34(+)CD38(-) hematopoietic progenitors in sickle cell disease differ phenotypically and functionally from normal and suggest distinct subpopulations that generate F cells. Luck, L., Zeng, L., Hiti, A.L., Weinberg, K.I., Malik, P. Exp. Hematol. (2004) [Pubmed]
  25. Trimidox-mediated morphological changes during erythroid differentiation is associated with the stimulation of hemoglobin and F-cell production in human K562 cells. Iyamu, E.W., Adunyah, S.E., Elford, H.L., Fasold, H., Turner, E.A. Biochem. Biophys. Res. Commun. (1998) [Pubmed]
  26. Association of small low-density lipoprotein particles with the incidence of coronary artery disease in men and women. Gardner, C.D., Fortmann, S.P., Krauss, R.M. JAMA (1996) [Pubmed]
  27. PET imaging of dopamine D2 receptors with [18F]fluoroclebopride in monkeys: effects of isoflurane- and ketamine-induced anesthesia. Nader, M.A., Grant, K.A., Gage, H.D., Ehrenkaufer, R.L., Kaplan, J.R., Mach, R.H. Neuropsychopharmacology (1999) [Pubmed]
  28. Endotoxin stimulated nitroblue-tetrazolium (NBT)-test in patients with hypoparathyroidism, pseudohypoparathyroidism and other forms of hypocalcemia. Andler, W., Stolecke, H., Funk, R., Hierholzer, E. Eur. J. Pediatr. (1978) [Pubmed]
  29. Six-year follow-up of pancreatic beta cell function in adults with latent autoimmune diabetes. Yang, L., Zhou, Z.G., Huang, G., Ouyang, L.L., Li, X., Yan, X. World J. Gastroenterol. (2005) [Pubmed]
  30. Flow pattern and shear stress distribution of distal end-to-side anastomoses. A comparison of the instantaneous velocity fields obtained by particle image velocimetry. Heise, M., Schmidt, S., Krüger, U., Rückert, R., Rösler, S., Neuhaus, P., Settmacher, U. Journal of biomechanics. (2004) [Pubmed]
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