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26 results on '"Kalinina, Juliya"'

1. Supplemental Tables 2-6 from Selective Detection of the D-enantiomer of 2-Hydroxyglutarate in the CSF of Glioma Patients with Mutated Isocitrate Dehydrogenase

Author

Kalinina, Juliya, primary, Ahn, Jun, primary, Devi, Narra S., primary, Wang, Liya, primary, Li, Yuancheng, primary, Olson, Jeffrey J., primary, Glantz, Michael, primary, Smith, Thomas, primary, Kim, Ella L., primary, Giese, Alf, primary, Jensen, Randy L., primary, Chen, Clark C., primary, Carter, Bob S., primary, Mao, Hui, primary, He, Miao, primary, and Van Meir, Erwin G., primary

Published
2023
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2. Suppl. Table 1 from Selective Detection of the D-enantiomer of 2-Hydroxyglutarate in the CSF of Glioma Patients with Mutated Isocitrate Dehydrogenase

Author

Kalinina, Juliya, primary, Ahn, Jun, primary, Devi, Narra S., primary, Wang, Liya, primary, Li, Yuancheng, primary, Olson, Jeffrey J., primary, Glantz, Michael, primary, Smith, Thomas, primary, Kim, Ella L., primary, Giese, Alf, primary, Jensen, Randy L., primary, Chen, Clark C., primary, Carter, Bob S., primary, Mao, Hui, primary, He, Miao, primary, and Van Meir, Erwin G., primary

Published
2023
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3. supplemental figures from Selective Detection of the D-enantiomer of 2-Hydroxyglutarate in the CSF of Glioma Patients with Mutated Isocitrate Dehydrogenase

Author

Kalinina, Juliya, primary, Ahn, Jun, primary, Devi, Narra S., primary, Wang, Liya, primary, Li, Yuancheng, primary, Olson, Jeffrey J., primary, Glantz, Michael, primary, Smith, Thomas, primary, Kim, Ella L., primary, Giese, Alf, primary, Jensen, Randy L., primary, Chen, Clark C., primary, Carter, Bob S., primary, Mao, Hui, primary, He, Miao, primary, and Van Meir, Erwin G., primary

Published
2023
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10. Selective Detection of the D-enantiomer of 2-Hydroxyglutarate in the CSF of Glioma Patients with Mutated Isocitrate Dehydrogenase

Author

Kalinina, Juliya, primary, Ahn, Jun, additional, Devi, Narra S., additional, Wang, Liya, additional, Li, Yuancheng, additional, Olson, Jeffrey J., additional, Glantz, Michael, additional, Smith, Thomas, additional, Kim, Ella L., additional, Giese, Alf, additional, Jensen, Randy L., additional, Chen, Clark C., additional, Carter, Bob S., additional, Mao, Hui, additional, He, Miao, additional, and Van Meir, Erwin G., additional

Published
2016
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12. F5-02-04: Cerebrospinal fluid amyloid oligomers measured in a subset of the aibl and optima age-matched healthy control and Alzheimer's cohorts

Author

Savage, Mary J., primary, Kalinina, Juliya, additional, Holder, Dan, additional, Stromswold, Julie, additional, Egan, Michael, additional, Laterza, Omar, additional, Emancipator, Kenneth, additional, Darby, David G., additional, Li, Qiao-Xin, additional, Wilcock, Gordon, additional, Smith, David, additional, and Masters, Colin L., additional

Published
2015
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16. miR-21 in the Extracellular Vesicles (EVs) of Cerebrospinal Fluid (CSF): A Platform for Glioblastoma Biomarker Development

Author

Akers, Johnny C., primary, Ramakrishnan, Valya, additional, Kim, Ryan, additional, Skog, Johan, additional, Nakano, Ichiro, additional, Pingle, Sandeep, additional, Kalinina, Juliya, additional, Hua, Wei, additional, Kesari, Santosh, additional, Mao, Ying, additional, Breakefield, Xandra O., additional, Hochberg, Fred H., additional, Van Meir, Erwin G., additional, Carter, Bob S., additional, and Chen, Clark C., additional

Published
2013
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18. Homodimerization Controls the Fibroblast Growth Factor 9 Subfamily's Receptor Binding and Heparan Sulfate-Dependent Diffusion in the Extracellular Matrix

Author

Kalinina, Juliya, primary, Byron, Sara A., additional, Makarenkova, Helen P., additional, Olsen, Shaun K., additional, Eliseenkova, Anna V., additional, Larochelle, William J., additional, Dhanabal, Mohanraj, additional, Blais, Steven, additional, Ornitz, David M., additional, Day, Loren A., additional, Neubert, Thomas A., additional, Pollock, Pamela M., additional, and Mohammadi, Moosa, additional

Published
2009
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20. Molecular Insights into the Klotho-Dependent, Endocrine Mode of Action of Fibroblast Growth Factor 19 Subfamily Members

Author

Goetz, Regina, primary, Beenken, Andrew, additional, Ibrahimi, Omar A., additional, Kalinina, Juliya, additional, Olsen, Shaun K., additional, Eliseenkova, Anna V., additional, Xu, ChongFeng, additional, Neubert, Thomas A., additional, Zhang, Fuming, additional, Linhardt, Robert J., additional, Yu, Xijie, additional, White, Kenneth E., additional, Inagaki, Takeshi, additional, Kliewer, Steven A., additional, Yamamoto, Masaya, additional, Kurosu, Hiroshi, additional, Ogawa, Yasushi, additional, Kuro-o, Makoto, additional, Lanske, Beate, additional, Razzaque, Mohammed S., additional, and Mohammadi, Moosa, additional

Published
2007
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22. A Sensitive Aβ Oligomer Assay Discriminates Alzheimer's and Aged Control Cerebrospinal Fluid.

Author

Savage, Mary J., Kalinina, Juliya, Wolfe, Abigail, Tugusheva, Katherine, Korn, Rachel, Cash-Mason, Tanesha, Maxwell, Jill W., Hatcher, Nathan G., Haugabook, Sharie J., Guoxin Wu, Howell, Bonnie J., Renger, John J., Shughrue, Paul J., and McCampbell, Alexander

Subjects
*OLIGOMERIZATION, *MICROBIOLOGICAL assay, *ALZHEIMER'S disease, *CEREBROSPINAL fluid examination, *BRAIN abnormalities
Abstract

Ahallmark of Alzheimer's disease (AD) brain is the amyloidβ (Aβ) plaque, which is comprised of Aβ peptides. Multiple lines of evidence suggest that Aβ oligomers are more toxic than other peptide forms. We sought to develop a robust assay to quantify oligomers from CSF. Antibody 19.3 was compared in one-site and competitive ELISAs for oligomer binding specificity. A two-site ELISA for oligomers was developed using 19.3 coupled to a sensitive, bead-based fluorescent platform able to detect single photons of emitted light. The two-site ELISA wasβ2500>selective for Aβ oligomers over Aβ monomers with a limit of detection~0.09 pg/ml in human CSF. The lower limit of reliable quantification of the assay was 0.18 pg/ml and the antibody pairs recognized Aβ multimers comprised of either synthetic standards, or endogenous oligomers isolated from confirmed human AD and healthy control brain. Using the assay, a significant 3- to 5-fold increase in Aβ oligomers in human AD CSF compared with comparably aged controls was demonstrated. The increase was seen in three separatehumancohorts, totaling 63ADand 54 controls. CSF oligomers ranged between 0.1 and 10 pg/ml.Aβ oligomer levels did not strongly associate with age or gender, but had an inverse correlation withMMSEscore. The C statistic for theAβ oligomer ROC curve was 0.86, with 80% sensitivity and 88% specificity to detect AD, suggesting reasonable discriminatory power for theADstate and the potential for utility as a diagnostic marker. [ABSTRACT FROM AUTHOR]

Published
2014
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26. Somatic FGF9 mutations in colorectal and endometrial carcinomas associated with membranous beta-catenin.

Author

Abdel-Rahman WM, Kalinina J, Shoman S, Eissa S, Ollikainen M, Elomaa O, Eliseenkova AV, Bützow R, Mohammadi M, and Peltomäki P

Subjects
Base Sequence, Cell Line, Tumor, DNA, Neoplasm genetics, Female, Fibroblast Growth Factor 9 chemistry, Fibroblast Growth Factor 9 metabolism, Humans, Ligands, Loss of Heterozygosity, MAP Kinase Signaling System, Male, Membrane Proteins genetics, Membrane Proteins metabolism, Models, Molecular, Ovarian Neoplasms genetics, Ovarian Neoplasms metabolism, Protein Conformation, Wnt Proteins metabolism, beta Catenin genetics, Colorectal Neoplasms genetics, Colorectal Neoplasms metabolism, Endometrial Neoplasms genetics, Endometrial Neoplasms metabolism, Fibroblast Growth Factor 9 genetics, Mutation, beta Catenin metabolism
Abstract

We previously described striking molecular features including high frequency of membranous beta-catenin in subsets of familial colon cancers with as yet unknown predisposition. We hypothesized that such tumors might carry mutations in Wnt/beta-catenin target genes. Fibroblast growth factor 9 (FGF9) was an attractive target, as it maps to a common area of loss of heterozygosity (LOH) in colorectal carcinomas on 13q12.11. Here, we report, for the first time, the occurrence of FGF9 mutations in human cancers. We found a total of six distinct FGF9 mutations including one frameshift, four missense, and one nonsense, in 10 (six colorectal and four endometrial) out of 203 tumors and cell lines. The frameshift mutation was detected in five different tumors. Mapping of these mutations onto the crystal structure of FGF9 predicted that they should all lead to loss of function albeit through variable mechanisms. The p.R173K mutation should diminish ligand affinity for heparin/heparan sulfate, the p.V192M, p.D203G, and p.L188YfsX18 (FGF9(Delta205-208)) mutations should negatively impact ligand's interaction with receptor, while p.G84E and p.E142X (FGF9(Delta142-208)) mutations should interfere with ligand folding. Consistent with these structural predictions, the p.V192M, p.D203G, and p.L188YfsX18 (FGF9(Delta205-208)) mutations impaired the ability of ligand to activate mitogen-activated protein kinase (MAPK) cascade in cultured cells expressing FGF receptors. LOH was observed in seven out of nine FGF9 mutant tumors, supporting the predicted loss of function. Interestingly, eight out of 10 (80%) of the FGF9 mutant tumors showed normal membranous beta-catenin expression and the absence of mutation in the beta-catenin gene (CTNNB1). These data suggest that FGF9 plays a role in colorectal and endometrial carcinogenesis.

Published
2008
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