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KRT83  -  keratin 83

Homo sapiens

 
 
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Disease relevance of KRT83

  • Bindings of the parental HB3 parasite strain to HMEC-1 and HUVEC were higher than that to HBEC-51 and C32 melanoma cells [1].
 

High impact information on KRT83

  • Cells parasitized by the chloroquine-sensitive HB3 clone and the chloroquine-resistant Dd2 clone of P falciparum were equally susceptible to MC540-sensitized photolysis [2].
  • A sequence-ready map was constructed for an 1100-kb gene-rich interval flanked by the markers HB3 and DXS1039, from which six novel ESTs/STSs were isolated, thus increasing the number of markers used in this interval to thirty [3].
  • Homology modeling revealed an unusual structure of the Hb 3 binding site of inositol hexakisphoshate [4].
  • Although cuticular differentiation proceeded without the expression of further type II hair keratins, cortex cells simultaneously expressed hHb1, hHb3, and hHb6 at an advanced stage of differentiation [5].
  • In this study, we have used a genetic cross between the strains HB3 and 3D7 to study inheritance of sensitivity to the structurally unrelated drugs mefloquine and artemisinin, and to several other antimalarials [6].
 

Biological context of KRT83

  • To analyze the degree of dependence on glycophorin B for invasion by P. falciparum through the trypsin-resistant pathway, we have studied the invasion phenotypes of five parasite strains, 3D7, HB3, Dd2, 7G8, and Indochina I, on trypsin-treated normal and glycophorin B-deficient erythrocytes [7].
  • An apparent crossover between the 3D7 and the HB3 parent chromosomes accounts for a chromosome of intermediate size in clone XP5 [8].
  • A clone encoding the aspartic proteinase (PFAPD) from Plasmodium falciparum strain HB3 was obtained during the course of a project designed to sequence and identify the protein coding regions of the parasite's genome [9].
  • One P. ovale and the P. vivax FeSOD genes presented the same nucleotide sequence as that of the P. falciparum strain HB3 whereas the second P. ovale and the P. malariae genes exhibited two punctual mutations [10].
 

Anatomical context of KRT83

  • Four strains, 3D7, HB3, Dd2, and Indochina I, invaded trypsin-treated erythrocytes, while invasion by the 7G8 strain was reduced by 90% [7].
  • We observed significant acidification of lysosomes containing PfCRT HB3 and Dd2, with Dd2 acidifying significantly more than HB3 [11].
 

Associations of KRT83 with chemical compounds

  • The inhibition constants for pyrimethamine increased from 0.19 +/- 0.08 nM (3D7) to 2.0 +/- 0.3 nM (HB3) to 8.9 +/- 0.8 nM (7G8) [12].
  • The Km value for dihydrofolate was altered 13-fold comparing the sensitive clone 3D7 (3.2 +/- 0.6 microM) with the resistant clone HB3 (42.6 +/- 1.6 microM), with the Km for the resistant clone 7G8 falling in between (11.9 +/- 1.2 microM) [12].
  • We also compared the processing of exogenous folic acid, folinic acid and p-aminobenzoic acid (pABA) in metabolic labelling studies of HB3 and Dd2 [13].
  • In clinical use, GST-HB3 could accurately measure therapeutic heparin levels in plasma (0.2 to 2U/ml) [14].
  • In the accompanying paper (Ursos, L. et al., following paper this issue) we describe how pH(vac) is affected by exposure to chloroquine and verapamil for HB3 versus Dd2 [15].
 

Analytical, diagnostic and therapeutic context of KRT83

  • 6. We suggest the similarity between the hematin pH titration midpoint and the measured value of HB3 pH(vac) is not coincidental, and that decreased pH(vac) for Dd2 titrates limited initial drug target (i.e. soluble heme) to lower concentration [15].
  • In this paper, we measure both short term (i.e. initial perfusion conditions) and longer-term effects of CQ and VPL for living, intraerythrocytic CQS (HB3) and CQR (Dd2) malarial parasites under constant perfusion with physiologically relevant buffers [16].
  • Regular intrauterine transfusions were performed to manage the severe fetal anemia (Hb 3 g/dL) [17].

References

  1. Plasmodium falciparum: involvement of additional receptors in the cytoadherence of infected erythrocytes to microvascular endothelial cells. Xiao, L., Yang, C., Dorovini-Zis, K., Tandon, N.N., Ades, E.W., Lal, A.A., Udhayakumar, V. Exp. Parasitol. (1996) [Pubmed]
  2. Merocyanine 540-sensitized photoinactivation of human erythrocytes parasitized by Plasmodium falciparum. Smith, O.M., Dolan, S.A., Dvorak, J.A., Wellems, T.E., Sieber, F. Blood (1992) [Pubmed]
  3. Long-range map of a 3.5-Mb region in Xp11.23-22 with a sequence-ready map from a 1.1-Mb gene-rich interval. Schindelhauer, D., Hellebrand, H., Grimm, L., Bader, I., Meitinger, T., Wehnert, M., Ross, M., Meindl, A. Genome Res. (1996) [Pubmed]
  4. The functionally distinct hemoglobins of the Arctic spotted wolffish Anarhichas minor. Verde, C., Carratore, V., Riccio, A., Tamburrini, M., Parisi, E., Di Prisco, G. J. Biol. Chem. (2002) [Pubmed]
  5. The catalog of human hair keratins. II. Expression of the six type II members in the hair follicle and the combined catalog of human type I and II keratins. Langbein, L., Rogers, M.A., Winter, H., Praetzel, S., Schweizer, J. J. Biol. Chem. (2001) [Pubmed]
  6. Increased sensitivity to the antimalarials mefloquine and artemisinin is conferred by mutations in the pfmdr1 gene of Plasmodium falciparum. Duraisingh, M.T., Roper, C., Walliker, D., Warhurst, D.C. Mol. Microbiol. (2000) [Pubmed]
  7. Plasmodium falciparum is able to invade erythrocytes through a trypsin-resistant pathway independent of glycophorin B. Gaur, D., Storry, J.R., Reid, M.E., Barnwell, J.W., Miller, L.H. Infect. Immun. (2003) [Pubmed]
  8. Long-range restriction maps of Plasmodium falciparum chromosomes: crossingover and size variation among geographically distant isolates. Sinnis, P., Wellems, T.E. Genomics (1988) [Pubmed]
  9. Sequence, expression and modeled structure of an aspartic proteinase from the human malaria parasite Plasmodium falciparum. Dame, J.B., Reddy, G.R., Yowell, C.A., Dunn, B.M., Kay, J., Berry, C. Mol. Biochem. Parasitol. (1994) [Pubmed]
  10. Cloning and characterization of iron-containing superoxide dismutase from the human malaria species Plasmodium ovale, P. malariae and P. vivax. Baert, C.B., Deloron, P., Viscogliosi, E., Delgado-Viscogliosi, P., Camus, D., Dive, D. Parasitol. Res. (1999) [Pubmed]
  11. Chloroquine-resistant isoforms of the Plasmodium falciparum chloroquine resistance transporter acidify lysosomal pH in HEK293 cells more than chloroquine-sensitive isoforms. Reeves, D.C., Liebelt, D.A., Lakshmanan, V., Roepe, P.D., Fidock, D.A., Akabas, M.H. Mol. Biochem. Parasitol. (2006) [Pubmed]
  12. Kinetic and molecular properties of the dihydrofolate reductase from pyrimethamine-sensitive and pyrimethamine-resistant clones of the human malaria parasite Plasmodium falciparum. Chen, G.X., Mueller, C., Wendlinger, M., Zolg, J.W. Mol. Pharmacol. (1987) [Pubmed]
  13. Genetic and metabolic analysis of folate salvage in the human malaria parasite Plasmodium falciparum. Wang, P., Nirmalan, N., Wang, Q., Sims, P.F., Hyde, J.E. Mol. Biochem. Parasitol. (2004) [Pubmed]
  14. A selective protein sensor for heparin detection. Cai, S., Dufner-Beattie, J.L., Prestwich, G.D. Anal. Biochem. (2004) [Pubmed]
  15. Digestive vacuolar pH of intact intraerythrocytic P. falciparum either sensitive or resistant to chloroquine. Dzekunov, S.M., Ursos, L.M., Roepe, P.D. Mol. Biochem. Parasitol. (2000) [Pubmed]
  16. The effects of chloroquine and verapamil on digestive vacuolar pH of P. falciparum either sensitive or resistant to chloroquine. Ursos, L.M., Dzekunov, S.M., Roepe, P.D. Mol. Biochem. Parasitol. (2000) [Pubmed]
  17. Use of recombinant erythropoietin for the management of severe hemolytic disease of the newborn of a K0 phenotype mother. Manoura, A., Korakaki, E., Hatzidaki, E., Saitakis, E., Maraka, S., Papamastoraki, I., Matalliotakis, E., Foundouli, K., Giannakopoulou, C. Pediatric hematology and oncology (2007) [Pubmed]
 
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