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Gene Review

HNRNPC  -  heterogeneous nuclear ribonucleoprotein C...

Homo sapiens

Synonyms: C1, C2, HNRNP, HNRPC, Heterogeneous nuclear ribonucleoproteins C1/C2, ...
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Disease relevance of HNRPC

  • We have also shown that in a glutathione S-transferase (GST) pull-down assay, GST/hnRNP C1 binds to poliovirus polypeptide 3CD, a precursor to the viral RNA-dependent RNA polymerase, 3D(pol), as well as to P2 and P3, precursors to the nonstructural proteins [1].
  • Studies using a recombinant acidic C-terminal domain of hnRNP-C overexpressed in Escherichia coli demonstrate that protein kinase CK2 phosphorylates hnRNP-C1/C2 at S247, while protein kinase A and several protein kinase C isoforms fail to phosphorylate the isolated domain [2].
  • The syndrome of acquired angioedema and C1-inhibitor deficiency is associated with B-cell lymphoproliferative disease [3].
  • Occipital neuralgia and C1-C2 arthrosis [4].
  • Mean levels of the classical components C1, C4, and C2 in bacteremic patients in whom shock subsequently developed did not differ significantly (p greater than 0.05) from those of patients with uncomplicated bacteremia [5].

Psychiatry related information on HNRPC

  • Head trauma and vigorous physical activity were followed by delayed-onset posterior circulation stroke in a 5-year-old boy with odontoid aplasia and C1-C2 subluxation [6].
  • A COOH-terminal fragment of PrPc, designated C1, is abundant in normal and CJD brains as well as in human neuroblastoma cells [7].
  • Among the co-twins of 69 monozygotic probands there were found 46 with manic-depressive disorders, and a further 14 had presented other psychoses or marked affective personality disorders or had committed suicide, yielding a proband rate of strict concordance, C1 = 0-67 and of broad, partial concordance, C2 = 0-87 [8].
  • These results, together with the previously established properties of C1 and C2, suggest that the early stages of contour-specific processing in the visual cortex have relatively short response latencies and durations and are uninfluenced by the subsequent presentation of metacontrast masking stimuli [9].
  • We have therefore determined the influence of the common polymorphisms in TF, C1 and C2, in dementia [10].

High impact information on HNRPC

  • We screened factor B (BF) and complement component 2 (C2) genes, located in the major histocompatibility complex class III region, for genetic variation in two independent cohorts comprising approximately 900 individuals with AMD and approximately 400 matched controls [11].
  • It is characterized by accelerated consumption of C1q and C1 inhibitor in vivo and by low levels of serum C2 and C4 [3].
  • These results suggest that an interaction between the idiotype of monoclonal immunoglobulins and antiidiotypic antibodies causes increased consumption of C1q and C1 inhibitor in patients with acquired angioedema and C1-inhibitor deficiency [3].
  • The early components of human complement (C1, C4, and C2) plus certain serum euglobulins will kill pathogenic strains of Shigella sonnei [12].
  • New structural and biochemical analyses of C1, C2, PH, FYVE, FERM and other domains have led to an unprecedented amount of information on the molecular interactions of these signaling proteins with regulatory lipids [13].

Chemical compound and disease context of HNRPC

  • Furthermore, we demonstrated that poliovirus positive-strand and negative-strand RNA present in cytoplasmic extracts prepared from infected HeLa cells coimmunoprecipitated with hnRNP C1/C2 [1].
  • Formation of an RNP complex with poliovirus RNA was severely impaired by substitution of a lysine, highly conserved among vertebrates, with glutamine in the RNA recognition motif (RRM) of recombinant hnRNP C1, suggesting that the binding is mediated by the RRM in the protein [1].
  • Other complement components were normal during remission of lupus, but C1, C4, C2, and C3 levels fell during exacerbations [14].
  • During a 72-h period after hospital admission significant decreases in C1, C4, and C3 occurred in six patients with recent chest pain but no evidence of acute myocardial infarction [15].
  • Intergroup trial 0153 (Southwest Oncology Group trial 9415) was developed to compare the efficacy of continuous-infusion FU (CIFU) plus levamisole to FU/LV plus levamisole in the adjuvant treatment of high-risk Dukes' B2 and C1 or C2 colon cancer [16].

Biological context of HNRPC

  • Two of those were identified as the heterogeneous ribonucleoproteins C1 and C2, whereas the third, a 38-kDa, poly(U) binding protein (p38), remained unidentified [17].
  • Cisplatin-resistant sublines, LNCaP/C1, LNCaP/ C2, and LNCaP/C3 cells, were 6.3-, 9.1-, and 22.3-fold more resistant to cisplatin than LNCaP cells, respectively, and this resistance was paralleled with reduced induction of apoptosis [18].
  • The C2 USE, however, also increases the affinity of general polyadenylation factors independently for the C2 poly(A) signal as detected by enhanced binding of cleavage-stimulaton factor (CstF) [19].
  • A role for hnRNP C1/C2 and Unr in internal initiation of translation during mitosis [20].
  • We have isolated cDNAs for the major heterogeneous nuclear ribonucleoprotein (hnRNP) A2, B1, and C2 proteins and determined their nucleotide and deduced amino acid sequences [21].

Anatomical context of HNRPC

  • The internal ribosome entry site-mediated translation of antiapoptotic protein XIAP is modulated by the heterogeneous nuclear ribonucleoproteins C1 and C2 [22].
  • HeLa cell mRNA that was hybrid-selected with the cDNA clone (1.1 kilobases long) was translated in vitro and yielded both the C1 and C2 proteins (41 and 43 kDa, respectively) [23].
  • Rapid phosphorylation of heterogeneous nuclear ribonucleoprotein C1/C2 in response to physiologic levels of hydrogen peroxide in human endothelial cells [24].
  • Membrane recruitment of these peripheral proteins is mediated by a growing number of modular membrane-targeting domains, including C1, C2, PH, FYVE, PX, ENTH, ANTH, BAR, FERM, and tubby domains, that recognize specific lipid molecules in the membranes [25].
  • Incorporation of DAF into the cell membranes was temperature dependent, took place on pronase- or trypsin-treated erythrocytes, and did not depend on prior deposition of antibody, C1 or C4 [26].

Associations of HNRPC with chemical compounds

  • CEAP clinical class for limbs was C1: 15%, C2: 81%, C3: 0.5%, C4: 2%, C5: 0.2%, C6: 0.4% [27].
  • The CEAP clinical stage was C0:182 limbs, C1: 241, C2: 22, C3: 0, C4: 11, C5: 2, C6:1 [27].
  • By the use of complement- and Ig-deficient mice it was found that C1q, C4, C2, and plasma Ig were all required for this spontaneous C3 activation, with the alternative complement pathway further amplifying C3 fragment generation [28].
  • Exposure of normal human sera to isolated human heart mitochondria at 37 degrees C resulted in the consumption of C1, C4, C2, and C3 without significant consumption of the terminal components of the complement system (C6 through C9) [15].
  • In 63 cases (98.4%), intense leucine naphthylamidase (LNAase) activity was found histochemically in the cytoplasm of nearly all cancer cells except type C-2 [29].

Other interactions of HNRPC


Analytical, diagnostic and therapeutic context of HNRPC

  • Radial double immunodiffusion experiments using antiserum to C1q, C1r, and C1s on HFf-treated serum demonstrated the dissociation of the C1 trimolecular complex, with concomitant reduction of C1r antigenicity that is indicative of C1 activation [34].
  • Moreover, simple incubation of human plasma with dialyzer cellophane causes conversion of C3 and factor B, accompanied by depletion of total hemolytic complement and C3 but sparing of hemolytic C1 [35].
  • Membranes in brain tissues other than myelin (heavy membrane fraction obtained on sucrose density gradient centrifugation) were unable to activate C1 [36].
  • In situ hybridizations with N1- and C1-specific probes demonstrated that N1 cassette splicing occurs in most neurons but that C1 splicing is heterogeneous and is restricted to a subset of neuronal types in the electrosensory system [37].
  • Three of the seven patients in whom mobilization was poor after G1 had > or =2x10(6) CD34(+) cells/kg with two leukaphereses after C2 [38].


  1. Functional interaction of heterogeneous nuclear ribonucleoprotein C with poliovirus RNA synthesis initiation complexes. Brunner, J.E., Nguyen, J.H., Roehl, H.H., Ho, T.V., Swiderek, K.M., Semler, B.L. J. Virol. (2005) [Pubmed]
  2. Basal and hydrogen peroxide stimulated sites of phosphorylation in heterogeneous nuclear ribonucleoprotein C1/C2. Stone, J.R., Maki, J.L., Collins, T. Biochemistry (2003) [Pubmed]
  3. Acquired C1-inhibitor deficiency associated with antiidiotypic antibody to monoclonal immunoglobulins. Geha, R.S., Quinti, I., Austen, K.F., Cicardi, M., Sheffer, A., Rosen, F.S. N. Engl. J. Med. (1985) [Pubmed]
  4. Occipital neuralgia and C1-C2 arthrosis. Ehni, G., Benner, B. N. Engl. J. Med. (1984) [Pubmed]
  5. Activation of the properdin pathway of complement in patients with gram-negative of bacteremia. Fearon, D.T., Ruddy, S., Schur, P.H., McCabe, W.R. N. Engl. J. Med. (1975) [Pubmed]
  6. Congenital odontoid aplasia and posterior circulation stroke in childhood. Phillips, P.C., Lorentsen, K.J., Shropshire, L.C., Ahn, H.S. Ann. Neurol. (1988) [Pubmed]
  7. Truncated forms of the human prion protein in normal brain and in prion diseases. Chen, S.G., Teplow, D.B., Parchi, P., Teller, J.K., Gambetti, P., Autilio-Gambetti, L. J. Biol. Chem. (1995) [Pubmed]
  8. A Danish twin study of manic-depressive disorders. Bertelsen, A., Harvald, B., Hauge, M. The British journal of psychiatry : the journal of mental science. (1977) [Pubmed]
  9. A visual evoked potential study of metacontrast masking. Jeffreys, D.A., Musselwhite, M.J. Vision Res. (1986) [Pubmed]
  10. Transferrin gene polymorphism in Alzheimer's disease and dementia with Lewy bodies in humans. Hussain, R.I., Ballard, C.G., Edwardson, J.A., Morris, C.M. Neurosci. Lett. (2002) [Pubmed]
  11. Variation in factor B (BF) and complement component 2 (C2) genes is associated with age-related macular degeneration. Gold, B., Merriam, J.E., Zernant, J., Hancox, L.S., Taiber, A.J., Gehrs, K., Cramer, K., Neel, J., Bergeron, J., Barile, G.R., Smith, R.T., Hageman, G.S., Dean, M., Allikmets, R., Chang, S., Yannuzzi, L.A., Merriam, J.C., Barbazetto, I., Lerner, L.E., Russell, S., Hoballah, J., Hageman, J., Stockman, H. Nat. Genet. (2006) [Pubmed]
  12. Complement-mediated bactericidal system: evidence for a new pathway of complement action. Moreau, S.C., Skarnes, R.C. Science (1975) [Pubmed]
  13. Subcellular targeting by membrane lipids. Hurley, J.H., Meyer, T. Curr. Opin. Cell Biol. (2001) [Pubmed]
  14. Hereditary deficiency of the fifth component of complement in man. I. Clinical, immunochemical, and family studies. Rosenfeld, S.I., Kelly, M.E., Leddy, J.P. J. Clin. Invest. (1976) [Pubmed]
  15. Consumption of classical complement components by heart subcellular membranes in vitro and in patients after acute myocardial infarction. Pinckard, R.N., Olson, M.S., Giclas, P.C., Terry, R., Boyer, J.T., O'Rourke, R.A. J. Clin. Invest. (1975) [Pubmed]
  16. Phase III Southwest Oncology Group 9415/Intergroup 0153 randomized trial of fluorouracil, leucovorin, and levamisole versus fluorouracil continuous infusion and levamisole for adjuvant treatment of stage III and high-risk stage II colon cancer. Poplin, E.A., Benedetti, J.K., Estes, N.C., Haller, D.G., Mayer, R.J., Goldberg, R.M., Weiss, G.R., Rivkin, S.E., Macdonald, J.S. J. Clin. Oncol. (2005) [Pubmed]
  17. The inhibitory activity of the AU-rich RNA element in the human papillomavirus type 1 late 3' untranslated region correlates with its affinity for the elav-like HuR protein. Sokolowski, M., Furneaux, H., Schwartz, S. J. Virol. (1999) [Pubmed]
  18. Expression of the inhibitors of apoptosis proteins in cisplatin-resistant prostate cancer cells. Nomura, T., Yamasaki, M., Nomura, Y., Mimata, H. Oncol. Rep. (2005) [Pubmed]
  19. The upstream sequence element of the C2 complement poly(A) signal activates mRNA 3' end formation by two distinct mechanisms. Moreira, A., Takagaki, Y., Brackenridge, S., Wollerton, M., Manley, J.L., Proudfoot, N.J. Genes Dev. (1998) [Pubmed]
  20. A role for hnRNP C1/C2 and Unr in internal initiation of translation during mitosis. Schepens, B., Tinton, S.A., Bruynooghe, Y., Parthoens, E., Haegman, M., Beyaert, R., Cornelis, S. EMBO J. (2007) [Pubmed]
  21. Primary structures of the heterogeneous nuclear ribonucleoprotein A2, B1, and C2 proteins: a diversity of RNA binding proteins is generated by small peptide inserts. Burd, C.G., Swanson, M.S., Görlach, M., Dreyfuss, G. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  22. The internal ribosome entry site-mediated translation of antiapoptotic protein XIAP is modulated by the heterogeneous nuclear ribonucleoproteins C1 and C2. Holcík, M., Gordon, B.W., Korneluk, R.G. Mol. Cell. Biol. (2003) [Pubmed]
  23. Molecular cloning of cDNA for the nuclear ribonucleoprotein particle C proteins: a conserved gene family. Nakagawa, T.Y., Swanson, M.S., Wold, B.J., Dreyfuss, G. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  24. Rapid phosphorylation of heterogeneous nuclear ribonucleoprotein C1/C2 in response to physiologic levels of hydrogen peroxide in human endothelial cells. Stone, J.R., Collins, T. J. Biol. Chem. (2002) [Pubmed]
  25. Membrane-protein interactions in cell signaling and membrane trafficking. Cho, W., Stahelin, R.V. Annual review of biophysics and biomolecular structure. (2005) [Pubmed]
  26. Inhibition of complement activation on the surface of cells after incorporation of decay-accelerating factor (DAF) into their membranes. Medof, M.E., Kinoshita, T., Nussenzweig, V. J. Exp. Med. (1984) [Pubmed]
  27. Chronic venous disease treated by ultrasound guided foam sclerotherapy. Smith, P.C. European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery. (2006) [Pubmed]
  28. Continual low-level activation of the classical complement pathway. Manderson, A.P., Pickering, M.C., Botto, M., Walport, M.J., Parish, C.R. J. Exp. Med. (2001) [Pubmed]
  29. Cytoplasmic leucine naphthylamidase activity expressed in signet-ring cell carcinoma of the stomach. Kubota, K., Yamada, S., Ito, M., Nakamura, W., Nagayo, T. J. Natl. Cancer Inst. (1977) [Pubmed]
  30. Heterogeneous nuclear ribonucleoprotein C binds exclusively to the functionally important UUUUU-motifs in the human papillomavirus type-1 AU-rich inhibitory element. Sokolowski, M., Schwartz, S. Virus Res. (2001) [Pubmed]
  31. Cell type-specific proteins which interact with the 5' nontranslated region of hepatitis A virus RNA. Chang, K.H., Brown, E.A., Lemon, S.M. J. Virol. (1993) [Pubmed]
  32. Regulation of urokinase receptor mRNA stability by hnRNP C in lung epithelial cells. Shetty, S. Mol. Cell. Biochem. (2005) [Pubmed]
  33. Heterogeneous nuclear ribonucleoprotein C1/C2, MeCP1, and SWI/SNF form a chromatin remodeling complex at the beta-globin locus control region. Mahajan, M.C., Narlikar, G.J., Boyapaty, G., Kingston, R.E., Weissman, S.M. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  34. Activation of the classical pathway of complement by Hageman factor fragment. Ghebrehiwet, B., Silverberg, M., Kaplan, A.P. J. Exp. Med. (1981) [Pubmed]
  35. Hemodialysis leukopenia. Pulmonary vascular leukostasis resulting from complement activation by dialyzer cellophane membranes. Craddock, P.R., Fehr, J., Dalmasso, A.P., Brighan, K.L., Jacob, H.S. J. Clin. Invest. (1977) [Pubmed]
  36. Complement activation by isolated myelin: activation of the classical pathway in the absence of myelin-specific antibodies. Vanguri, P., Koski, C.L., Silverman, B., Shin, M.L. Proc. Natl. Acad. Sci. U.S.A. (1982) [Pubmed]
  37. Alternative RNA splicing of the NMDA receptor NR1 mRNA in the neurons of the teleost electrosensory system. Bottai, D., Maler, L., Dunn, R.J. J. Neurosci. (1998) [Pubmed]
  38. Randomized cross-over trial of progenitor-cell mobilization: high-dose cyclophosphamide plus granulocyte colony-stimulating factor (G-CSF) versus granulocyte-macrophage colony-stimulating factor plus G-CSF. Koç, O.N., Gerson, S.L., Cooper, B.W., Laughlin, M., Meyerson, H., Kutteh, L., Fox, R.M., Szekely, E.M., Tainer, N., Lazarus, H.M. J. Clin. Oncol. (2000) [Pubmed]
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