27 results on '"S.M. Zakian"'
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2. Generation of an induced pluripotent stem cell line, ICGi028-A, by reprogramming peripheral blood mononuclear cells of a patient suffering from hypertrophic cardiomyopathy and carrying a heterozygous p.E510Q mutation in HADHA
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E.V. Dementyeva, Yu.V. Vyatkin, A.M. Chernyavsky, and S.M. Zakian
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Biology (General) ,QH301-705.5 - Abstract
Hypertrophic cardiomyopathy (HCM) is a frequent cardiovascular pathology caused by a huge number of mutations in sarcomere-associated proteins. This genetic diversity leads to differences in pathogenetic mechanisms and hampers HCM therapy. Cardiomyocytes derived from patient-specific induced pluripotent stem cells give new opportunities for studying underlying HCM mechanisms. We generated an iPSC line from peripheral blood mononuclear cells of an HCM patient with a heterozygous p.E510Q mutation in HADHA using non-integrating episomal vectors. The iPSC line showed typical morphology, expression of pluripotency markers, capacity to be differentiated into derivatives of three germ layers, and presence of the patient-specific mutation.
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- 2021
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3. Generation of an induced pluripotent stem cell line, ICGi029-A, by reprogramming peripheral blood mononuclear cells of a patient suffering from hypertrophic cardiomyopathy and carrying a heterozygous p.N515del mutation in MYBPC3
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E.V. Dementyeva, S.V. Pavlova, A.M. Chernyavsky, and S.M. Zakian
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Biology (General) ,QH301-705.5 - Abstract
Hypertrophic cardiomyopathy (HCM) is a common cardiovascular disease. However, effective methods of its therapy have not been developed so far. To date patient-specific induced pluripotent stem cell-derived cardiomyocytes are supposed to be a useful tool for studying HCM molecular mechanisms and to help find new approaches to HCM therapy. Using non-integrating episomal vectors, we generated an iPSC line from peripheral blood mononuclear cells of an HCM patient carrying a heterozygous p.N515del mutation in MYBPC3. The iPSC line expressed pluripotency markers, gave rise to derivatives of three germ layers during spontaneous differentiation, had normal karyotype, and retained the patient-specific mutation.
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- 2021
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4. Generation of induced pluripotent stem cell lines ICGi021-A and ICGi022-A from peripheral blood mononuclear cells of two healthy individuals from Siberian population
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A.A. Malakhova, E.V. Grigor'eva, S.V. Pavlova, T.B. Malankhanova, K.R. Valetdinova, Y.V. Vyatkin, E.A. Khabarova, J.A. Rzaev, S.M. Zakian, and S.P. Medvedev
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Biology (General) ,QH301-705.5 - Abstract
ICGi021-A and ICGi022-A iPSC lines were obtained by reprogramming PBMCs of two healthy women of the Siberian population using episomal non-integrating vectors expressing Yamanaka factors. iPSC lines expressed pluripotency markers, had a normal karyotype and demonstrated the ability to differentiate into derivatives of the three germ layers. Clinical exome sequencing data of the original biosamples of the donors are available in the NCBI SRA database. The generated cell lines are useful as “healthy” control in biomedical studies.
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- 2020
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5. Generation of a spinal muscular atrophy type III patient-specific induced pluripotent stem cell line ICGi003-A
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V.S. Ovechkina, M.A. Maretina, A.A. Egorova, V.S. Baranov, A.V. Kiselev, S.M. Zakian, and K.R. Valetdinova
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Biology (General) ,QH301-705.5 - Abstract
Spinal muscular atrophy (SMA) is a genetic disease, which characterized by the degeneration of motor neurons in the spinal cord and further striated muscle atrophy. The research of the processes in diseased neurons is complicated due to the impossibility of obtaining them safely from patients. Thus, we generated SMA type III induced pluripotent stem cell lines via using non-integrated episomal plasmid vectors. The resulting cell line expresses the major pluripotency markers and can differentiate in vitro into derivatives of three germ layers. The iPSC line can be used for further studies by providing in vitro the relevant cell types.
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- 2020
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6. Generation of three Duchenne muscular dystrophy patient-derived induced pluripotent stem cell (iPSC) lines ICGi002-A, ICGi002-B and ICGi002-C
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K.R. Valetdinova, M.A. Maretina, Y.V. Vyatkin, M.P. Perepelkina, A.A. Egorova, V.S. Baranov, A.V. Kiselev, P.M. Gershovich, and S.M. Zakian
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Biology (General) ,QH301-705.5 - Abstract
Duchenne muscular dystrophy (DMD) is a severe and rapidly progressive hereditary muscular disease with X-linked recessive inheritance, occurring mainly in males. A complete loss of dystrophin resulted from out-of-frame deletion mutations in the DMD gene leads to Duchenne muscular dystrophy. DMD induced pluripotent stem cells (iPSCs) are a suitable cell model to study muscle development and disease mechanisms underlying muscular dystrophy and to screen novel compounds with potential therapeutic effects. We generated iPSCs from a DMD patient using non-integrating episomal plasmid vectors. The obtained iPSC lines showed ESC-like morphology, expression pluripotency markers, displayed a normal karyotype and possessed trilineage differentiation potential.
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- 2020
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7. Generation of two induced pluripotent stem cell lines from peripheral blood mononuclear cells of a patient with Wilson’s disease
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A.A. Malakhova, E.V. Grigor'eva, O.Yu. Vasilyeva, D.I. Zhigalina, N.A. Skryabin, A.A. Sivtcev, N.A. Kolesnikov, A.O. Bueverov, I.N. Lebedev, P.O. Bogomolov, and S.M. Zakian
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Biology (General) ,QH301-705.5 - Abstract
Wilson’s disease is an inherited disorder associated with copper accumulation in the liver, brain and other vital organs. Wilson’s disease is caused by mutations in the ATP7B gene. Over 300 mutations of ATP7B have been described. Despite the disease is autosomal recessive, the patient whose PBMCs were reprogrammed in the study harbours heterozygous mutation c.3207C > A (p.H1069Q). Detailed analysis of the ATP7B complete gene sequencing data has not revealed other known disease associated mutation. The generated iPSC lines maintained the original genotype, expressed pluripotency markers, had normal karyotype and demonstrated the ability to differentiate into derivatives of the three germ layers.
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- 2020
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8. Generation of two clonal iPSC lines, ICGi019-A and ICGi019-B, by reprogramming peripheral blood mononuclear cells of a patient suffering from hypertrophic cardiomyopathy and carrying a heterozygous p.M659I mutation in MYH7
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E.V. Dementyeva, V.R. Kovalenko, M.K. Zhiven, E.I. Ustyantseva, E.I. Kretov, Yu.V. Vyatkin, and S.M. Zakian
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Biology (General) ,QH301-705.5 - Abstract
Hypertrophic cardiomyopathy (HCM) is one of the most frequent cardiovascular diseases but no methods to prevent its progression have been developed. Cardiomyocytes derived from patient-specific induced pluripotent stem cells can become a platform to study pathogenesis of the disease and to search for more effective therapy methods. We generated two iPSC lines from peripheral blood mononuclear cells of an HCM patient with heterozygous p.M659I mutation in MYH7 using episomal vectors. The iPSC lines expressed pluripotency markers, demonstrated ability to spontaneously differentiate into derivatives of three germ layers, and retained the mutation.
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- 2020
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9. Generation of induced pluripotent stem cell line ICGi018-A from peripheral blood mononuclear cells of a patient with Huntington's disease
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A.A. Malakhova, E.V. Grigor'eva, T.B. Malankhanova, S.V. Pavlova, K.R. Valetdinova, N.Yu. Abramycheva, A.S. Vetchinova, S.N. Illarioshkin, and S.M. Zakian
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Biology (General) ,QH301-705.5 - Abstract
Huntington's disease (HD) is an autosomal dominant neurodegenerative disease caused by CAG repeat expansion in the HTT gene. HD patient-specific induced pluripotent stem cells (iPSCs) represent an excellent model for the disease study. We generated iPSC line from blood mononuclear cells of HD patient with 38 CAG repeats in the HTT exon 1 using integration free episomal plasmids expressing Yamanaka factors. The iPSC line retained the disease causing mutation and expressed pluripotency markers. It also displayed a normal karyotype and the ability to differentiate into derivatives of three germ layers.
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- 2020
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10. Generation of an induced pluripotent stem cell line, ICGi014-A, by reprogramming peripheral blood mononuclear cells from a patient with homozygous D90A mutation in SOD1 causing Amyotrophic lateral sclerosis
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E.I. Ustyantseva, S.P. Medvedev, A.S. Vetchinova, S.N. Illarioshkin, S.V. Leonov, and S.M. Zakian
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Biology (General) ,QH301-705.5 - Abstract
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by death of motor neurons. To date, neither etiology nor pathogenesis of ALS are known, which leads to the absence of an effective treatment strategy. ALS patient-specific induced pluripotent stem cells (iPSCs) represent an excellent tool for the disease study. We obtained iPSCs line from peripheral blood mononuclear cells of the patient with homozygous Asp90Ala mutation in the SOD1 gene using non-integrating episomal vectors. The iPSCs line retained pathological genotype and expressed pluripotency markers. It also displayed a normal karyotype and the ability to differentiate into derivatives of three germ layers.
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- 2020
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11. Generation of two iPSC lines, (ICGi015-A and ICGi015-B), by reprogramming peripheral blood mononuclear cells from a patient with Parkinson's disease
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D.V. Sharipova, V.R. Kovalenko, E.M. Bairamova, V.A. Vartanova, E.V. Grigor'eva, Y.V. Vyatkin, E.A. Khabarova, D.A. Rzaev, S.M. Zakian, and S.P. Medvedev
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Biology (General) ,QH301-705.5 - Abstract
Studying Parkinson's disease (PD), one of the most common neurodegenerative disorders worldwide, requires different model systems, including patient-specific induced pluripotent stem cell lines. With the help of non-integrating episomal vectors the iPSC lines ICGi015-A and ICGi015-B were generated from blood mononuclear cells of PD patient, carrying three SNPs, associated with PD development. The obtained iPSC lines express pluripotency markers and demonstrate the ability to in vitro differentiate into the three germ layers. These cell lines may be useful for studying molecular mechanisms of PD and for drug screening.
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- 2019
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12. Generation of two iPSC lines (ICGi008-A and ICGi008-B) from skin fibroblasts of a patient with early-onset Alzheimer's disease caused by London familial APP mutation (V717I)
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E.V. Grigor'eva, T.B. Malankhanova, E.I. Ustyantseva, J.M. Minina, O.E. Redina, V.V. Morozov, A.I. Shevela, S.M. Zakian, and S.P. Medvedev
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Biology (General) ,QH301-705.5 - Abstract
The induced pluripotent stem cell (iPSC) lines ICGi008-A and ICGi008-B were generated from dermal fibroblasts using episomal vectors expressing pluripotency factors. Dermal fibroblasts were obtained from a 55 year old male Сaucasian familial Alzheimer's disease (AD) patient carrying heterozygous V717I mutation in the APP gene. The generated iPSC lines maintained the original APP genotype, expressed pluripotency markers, exhibited a normal karyotype and retained the ability to differentiate into cell types of the three germ layers. The iPSC lines will be useful for the study of the AD molecular and cellular mechanisms and drug screening.
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- 2019
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13. Generation of two spinal muscular atrophy (SMA) type I patient-derived induced pluripotent stem cell (iPSC) lines and two SMA type II patient-derived iPSC lines
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K.R. Valetdinova, M.A. Maretina, M.L. Kuranova, E.V. Grigor'eva, Y.M. Minina, E.A. Kizilova, A.V. Kiselev, S.P. Medvedev, V.S. Baranov, and S.M. Zakian
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Biology (General) ,QH301-705.5 - Abstract
Spinal muscular atrophy (SMA) is a neuromuscular disease caused by deletion or mutation in SMN1 gene. SMA human induced pluripotent stem cells (iPSCs) represent a useful and valid model for the study of the disorder, as they provide in vitro the target cells. We generated iPSCs from a SMA type I patient and SMA type II patient by using non-integrating episomal plasmid vectors. The resulting iPSCs are episomal-free, express pluripotency markers, display a normal karyotype, retain the mutation (homozygous deletion of SMN1) and are able to differentiate into the three germ layers.
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- 2019
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14. Generation of induced pluripotent stem cell line, ICGi007-A, by reprogramming peripheral blood mononuclear cells from a patient with Huntington's disease
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E.V. Grigor'eva, T.B. Malankhanova, A. Surumbayeva, J.M. Minina, V.V. Morozov, N. Yu Abramycheva, S.N. Illarioshkin, A.A. Malakhova, and S.M. Zakian
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Biology (General) ,QH301-705.5 - Abstract
Huntington's disease (HD) is an autosomal dominant neurodegenerative disease caused by mutation in the HTT gene encoding HTT protein. The mutant protein leads to the neuronal death through dysregulation of multiple cellular processes. HD human induced pluripotent stem cells (iPSCs) represent a useful and valid model for the disease study. iPSC line from HD patient with 47 CAG repeats in HTT was generated from blood mononuclear cells by non-integrating episomal vectors. The iPSC line retained the mutation, expressed pluripotency markers, had a normal karyotype and displayed in vitro differentiation to the three germ layers.Resource table.Unlabelled TableUnique stem cell lines identifierICGi007-AAlternative name(s) of stem cell line47Q-3LfInstitutionFederal Research Center Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, Novosibirsk, RussiaContact information of distributorElena V. Grigor'evaevlena@bionet.nsc.ruType of cell linesiPSCOriginHumanAdditional origin infoAge: 27Sex: FEthnicity: CaucasianCell SourcePeripheral blood mononuclear cellsClonalityClonalMethod of reprogrammingTransgene free episomal plasmid vectorsGenetic ModificationYESType of ModificationHereditaryAssociated diseaseHuntington's diseaseGene/locusHTT/4p16.3Method of modificationN/AName of transgene or resistanceN/AInducible/constitutive systemN/ADate archived/stock dateDecember 2017Cell line repository/bankhttps://hpscreg.eu/cell-line/ICGi007-AEthical approvalThe generation of iPSC line from cells donated by patient with informed consent was reviewed and approved by “Center of New Medical Technology in Akademgorodok” (protocol No. 21)
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- 2019
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15. Applying Patient-Specific Induced Pluripotent Stem Cells to Create a Model of Hypertrophic Cardiomyopathy
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E.V. Dementyeva, S.M. Zakian, M M Slotvitsky, Dmitry Shtokalo, E. A. Pokushalov, V.R. Kovalenko, E.I. Kretov, Sergey P. Medvedev, and Yu.V. Vyatkin
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Adult ,Male ,Cellular differentiation ,Induced Pluripotent Stem Cells ,Cardiomyopathy ,Disease ,medicine.disease_cause ,Models, Biological ,Biochemistry ,Pathogenesis ,03 medical and health sciences ,Directed differentiation ,medicine ,Humans ,Induced pluripotent stem cell ,Cells, Cultured ,0303 health sciences ,Mutation ,business.industry ,030302 biochemistry & molecular biology ,Hypertrophic cardiomyopathy ,Cell Differentiation ,General Medicine ,Cardiomyopathy, Hypertrophic ,medicine.disease ,Cancer research ,Calcium ,business - Abstract
Generation of patient-specific induced pluripotent stem cells (iPSCs) and their subsequent differentiation into cardiomyocytes opened new opportunities for studying pathogenesis of inherited cardiovascular diseases. One of these diseases is hypertrophic cardiomyopathy (HCM) for which no efficient therapy methods have been developed so far. In this study, the approach based on patient-specific iPSCs was applied to create a model of the disease. Genetic analysis of a hypertrophic cardiomyopathy patient revealed R326Q mutation in the MYBPC3 gene. iPSCs of the patient were generated and characterized. The cells were differentiated into cardiomyocytes together with the control iPSCs from a healthy donor. The patient's iPSC-derived cardiomyocytes exhibited early HCM features, such as abnormal calcium handling and increased intracellular calcium concentration. Therefore, cardiomyocytes obtained by directed differentiation of iPSCs from the HCM patient can be used as a model system to study HCM pathogenesis.
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- 2019
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16. Identification of specific gene methylation patterns during motor neuron differentiation from spinal muscular atrophy patient-derived iPSC
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M.A. Maretina, K.R. Valetdinova, N.A. Tsyganova, A.A. Egorova, V.S. Ovechkina, H.B. Schiöth, S.M. Zakian, V.S. Baranov, and A.V. Kiselev
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Motor Neurons ,PAX6 Transcription Factor ,Neurogenesis ,GTPase-Activating Proteins ,Induced Pluripotent Stem Cells ,Gene Expression Regulation, Developmental ,Cell Differentiation ,General Medicine ,DNA Methylation ,Survival of Motor Neuron 1 Protein ,Muscular Atrophy, Spinal ,Survival of Motor Neuron 2 Protein ,Genetics ,Humans ,Cells, Cultured - Abstract
Spinal muscular atrophy is a progressive motor neuron disorder caused by deletions or point mutations in the SMN1 gene. It is not known why motor neurons are particularly sensitive to a decrease in SMN protein levels and what factors besides SMN2 underlie the high clinical heterogeneity of the disease. Here we studied the methylation patterns of genes on sequential stages of motor neuron differentiation from induced pluripotent stem cells derived from the patients with SMA type I and II. The genes involved in the regulation of pluripotency, neural differentiation as well as those associated with spinal muscular atrophy development were included. The results show that the PAX6, HB9, CHAT, ARHGAP22, and SMN2 genes are differently methylated in cells derived from SMA patients compared to the cells of healthy individuals. This study clarifies the specificities of the disease pathogenesis and extends the knowledge of pathways involved in the SMA progression.
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- 2020
17. Diverse developmental strategies of X chromosome dosage compensation in eutherian mammals
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Irina S. Zakharova, E.V. Dementyeva, Alexander I. Shevchenko, and S.M. Zakian
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Male ,Pluripotent Stem Cells ,Embryology ,X Chromosome ,Rodentia ,Biology ,X-inactivation ,Epigenesis, Genetic ,Genomic Imprinting ,03 medical and health sciences ,Downregulation and upregulation ,X Chromosome Inactivation ,Animals ,Gene silencing ,Gene Silencing ,Epigenetics ,X chromosome ,030304 developmental biology ,Genetics ,0303 health sciences ,Dosage compensation ,Up-Regulation ,Female ,RNA, Long Noncoding ,XIST ,Genomic imprinting ,Developmental Biology - Abstract
In eutherian mammals, dosage compensation arose to balance X-linked gene expression between sexes and relatively to autosomal gene expression in the evolution of sex chromosomes. Dosage compensation occurs in early mammalian development and comprises X chromosome upregulation and inactivation that are tightly coordinated epigenetic processes. Despite a uniform principle of dosage compensation, mechanisms of X chromosome inactivation and upregulation demonstrate a significant variability depending on sex, developmental stage, cell type, individual, and mammalian species. The review focuses on relationships between X chromosome inactivation and upregulation in mammalian early development.
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- 2019
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18. Generation of two iPSC lines (ICGi008-A and ICGi008-B) from skin fibroblasts of a patient with early-onset Alzheimer's disease caused by London familial APP mutation (V717I)
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V.V. Morozov, J.M. Minina, E.I. Ustyantseva, T.B. Malankhanova, S.M. Zakian, A.I. Shevela, E.V. Grigor'eva, Sergey P. Medvedev, and O.E. Redina
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Genetic Markers ,Male ,0301 basic medicine ,Heterozygote ,Cell type ,Induced Pluripotent Stem Cells ,Karyotype ,Germ layer ,medicine.disease_cause ,Cell Line ,Amyloid beta-Protein Precursor ,03 medical and health sciences ,0302 clinical medicine ,Alzheimer Disease ,Genotype ,Amyloid precursor protein ,medicine ,Humans ,Early-onset Alzheimer's disease ,Induced pluripotent stem cell ,lcsh:QH301-705.5 ,Skin ,Mutation ,biology ,Cell Differentiation ,Cell Biology ,General Medicine ,Fibroblasts ,Middle Aged ,medicine.disease ,030104 developmental biology ,lcsh:Biology (General) ,biology.protein ,Cancer research ,030217 neurology & neurosurgery ,Developmental Biology - Abstract
The induced pluripotent stem cell (iPSC) lines ICGi008-A and ICGi008-B were generated from dermal fibroblasts using episomal vectors expressing pluripotency factors. Dermal fibroblasts were obtained from a 55 year old male Сaucasian familial Alzheimer's disease (AD) patient carrying heterozygous V717I mutation in the APP gene. The generated iPSC lines maintained the original APP genotype, expressed pluripotency markers, exhibited a normal karyotype and retained the ability to differentiate into cell types of the three germ layers. The iPSC lines will be useful for the study of the AD molecular and cellular mechanisms and drug screening.
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- 2019
19. Contents, Vol. 76, 1997
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D. Birnbaum, N.Z. Parsa, C. Flores, A.G. Shilov, B. Sèle, U. Claussen, M. Gastaldi, J. Zimmer, B. Andréo, A.F. Markham, D.T. Bonthron, H.S. Tenenhouse, H. Lovec, O.I. Olopade, R. Hernandez, D. Adrian, S. Rousseaux, A. Frady, N.B. Rubtsov, M. Goldfarb, J.M. Trent, K.J. Gratton, B.G. Beatty, P. Eydoux, N. Tommerup, M. Schmid, D.R. Lohmann, J. Benet, S.K. Bohlander, N.V. Rubtsova, A. Girardet, P. Mühlig, T.P. Moynihan, D. Stephan, R. Hliscs, M.H. Dreyling, Y. Zhu, J. Torresani, J. Navarro, J.P. Grillasca, X.-Y. Zhang, N.T. Bech-Hansen, W. Jiang, M. Dean, H.H. Quek, G.J. Pappanicolaou, B. Wainwright, J.P. Charlieu, H. Hartung, S.M. Zakian, M.A. Peters, J.L. Coate, M.B. Qumsiyeh, C. Wicking, P. Bray-Ward, S. Taviaux, J. Wirth, G. Valle, M. Ehrlich, T. Muraro, R.A. Gravel, N.J. Lench, F. Yang, R. Zimbello, J.A. Peppers, E. Chevret, I. Garkavtsev, B. Horsthemke, F. Coulier, C. Pressman, X.X. Zhang, T.B. Nesterova, A-S. Verdier, A.A. Isaenko, S. Mori, S. Levanat, K. Riabowol, A. Sahota, G. Lefort, D. Demetrick, M-G. Matté, P.C.M. O’Brien, E.H. Hoffman, J.L VandeBerg, V.T.K. Chow, J. Cozzi, R. Planells, J. Wienberg, I. Parra, H. Satoh, K. Sperling, K. Buiting, K.L. Stoddart, A. León-Del-Rio, J. Weissenbach, A.E. Bale, M.R. Gailani, H.-J. Lüdecke, J.A. Tischfield, N.V. Vorobieva, P.S. Meltzer, G. Scherer, M-G. Mattéi, B. Windle, E.J. Taparowsky, A. Chidambaram, G. Lanfranch, H. Leffers, J.P. Leek, A.S. Hewson, R. Toftgard, E. Back, N. Tiso, M.L. Kennedy, G.A. Danieli, M. Varela, M.R. Martorell, T. Wagner, R. Anwar, P.K. Gupta, C. Shao, F. Pellestor, K.M. Boycott, E.H. McConkey, C. Márquez, J.C. Myers, B.J. Moore, I. Nanda, M. Monteil, J. Egozcue, N.M. Matveeva, P.K. Kennedy, M.A. Ferguson-Smith, B. Roland, and R. Pelletier
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Botany ,Genetics ,Zoology ,Biology ,Molecular Biology ,Genetics (clinical) - Published
- 1997
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20. Contents, Vol. 65, 1994
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R. Tupler, N.G. Laing, H.J. Eyre, M.A. Garrido-Ramos, N.A. Mazurok, S.J. Goss, D. Francis, A. Vandenberghe, S.M. Zakian, L. Kedes, E. Le Guern, M. Gugenheim, C. Bonnebouche, S.A. Lane, P.F.R. Little, M. Cortinovis, C. Meredith, D.A. Miller, E.I. Yantsen, D.F. Callen, E.Kh. Ginsburg, C.H. van Os, G. Melmer, R. Gouider, L. Tiepolo, F. Sturtz, M. Lafage-Pochitaloff, A. Plet, Y. Agid, R. Lozano, B. Chérif-Zahar, Angela Maria Vianna-Morgante, C. Ruiz Rejón, P. Bouche, M Janson, E. Dainotti, I. Siedlaczck, N.M. Matveeva, J.-M. Blanchard, D.O. Weghuis, A. Mincheva, N. Ravisé, J.T. Epplen, David W. Hale, O.J. Miller, T.M. Fink, M. Jamilena, I. Salvignol, A. Brice, A. Geurts van Kessel, P. Maraschio, P.M.T. Deen, B. Wieringa, G. Chazot, S. Tardieu, L.L. Deaven, P. Calvas, I. Todorov, T.B. Nesterova, J. Imbert, C. Cerdan, Q.-Q. Cai, Anne Lise Børresen, Peter Lichter, J.A.M. Graves, P.-M. Gonnaud, D. Depétris, R.A. Sturm, J.L. Cassady, S.D. Wilton, M. Ruiz Rejón, P.A. Akkari, A. Blancher, O. Riess, M.-G. Mattéi, Carla Rosenberg, A.G. Shilov, D.I. Francis, M. Nordeskjöld, D. Werner, and S. Kredtke
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Botany ,Genetics ,Zoology ,Biology ,Molecular Biology ,Genetics (clinical) - Published
- 1994
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21. Title Page / Table of Contents / Abstracts
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A. Kumamoto, Rosalyn Slater, A. Geurts van Kessel, J.W. Wessels, B.M. Cattanach, E.J. Dreef, R.E. Kibbelaar, G. Otulakowski, Charles E. Schwartz, S. Parikh, G.J. den Ottolander, J. George, I. Hansmann, U. Francke, G.M. Greig, H. Nakai, M.G. Byers, F. Yang, S. Boularand, Roger E. Stevenson, N.S.-F. Ma, J. Hayakawa, L.-C. Tsui, D.W. Threadgill, S. Kubota, D.H. Ledbetter, J. Spencer, I.A. Noordermeer, D.B. Farber, T.B. Nesterova, J.E. Womack, C.A. Kozak, L. Shi, C. Collet, M.C. Phelan, M. Vercruyssen, W.E. Fibbe, J. Mallet, H.F. Willard, E.P. Evans, C. Hanson, R.G. Taylor, N.B. Rubtsov, L.T. Williams, Andries Westerveld, R.G. Lafreniere, S. Navankasattusas, C. Szpirer, C.-L. Hsieh, C. Rasberry, E. Solomon, M.A. Abruzzo, M. Rivière, D.S. Gerhard, J.A. Escobedo, S.I. Radjabli, S.W. Scherer, D. Sheer, I.V. Nikitina, R.H. Brakenhoff, J.A. Miller, T.A. Jones, K.I. Kivirikko, T.J.M. Hulsebos, R.R. Mclnnes, T. Koizumi, M.C. Darmon, A. Goddard, P. Stanislovitis, S.P. Craig, N.J. Nowak, V.E. Powers, M.C. Simmler, S.M. Zakian, Y. Nakai, A.C.B. Peters, M. Kimura, J. Szpirer, M. Danciger, L. Dandolo, M. Westerman, M. van der Ploeg, L. Pajunen, E.P.J. Arnoldus, A.K. Raap, G.C. Beverstock, S. Schnittger, M. Katsuki, V.G. Matveeva, T. Shinohara, J. García-Heras, S.C. Bock, T.B. Shows, K. Klinger, A.P. Jackson, H. van Kamp, Franki Speleman, D.S. Gallagher, P.M. Kluin, A. Kuwano, T. Kajii, H.A. Taylor, B. Redeker, P. Van Oostveldt, T. Pihlajaniemi, JG Leroy, G.N. Hendy, Marcel M.A.M. Mannens, I.W. Craig, P. Avner, T. Abe, B.H. Robinson, V.L. Singer, P. Parham, E.K. Bijlsma, G. Levan, S. Kohno, S.J. Sadler, and V.V.N.G. Rao
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Genetics ,Library science ,Table of contents ,Biology ,Title page ,Molecular Biology ,Genetics (clinical) - Published
- 1991
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22. Contents, Vol. 56, 1991
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G. Levan, S.P. Craig, I.W. Craig, I.V. Nikitina, N.J. Nowak, T. Pihlajaniemi, C.A. Kozak, M.C. Simmler, H.A. Taylor, C. Collet, G.N. Hendy, C.-L. Hsieh, P. Van Oostveldt, R.G. Taylor, J.A. Miller, M.C. Darmon, A.C.B. Peters, J.W. Wessels, E. Solomon, M.A. Abruzzo, T. Abe, S.M. Zakian, M. Kimura, Y. Nakai, D. Sheer, B.M. Cattanach, Rosalyn Slater, Franki Speleman, P.M. Kluin, A. Kuwano, M. Westerman, S. Kohno, S.J. Sadler, N.S.-F. Ma, D.S. Gallagher, V.E. Powers, T.B. Shows, J. George, M. Van der Ploeg, K. Klinger, G.M. Greig, G. Otulakowski, M.C. Phelan, V.L. Singer, J. Szpirer, A.K. Raap, A. Geurts van Kessel, W.E. Fibbe, V.V.N.G. Rao, M. Vercruyssen, E.P. Evans, E.P.J. Arnoldus, E.J. Dreef, L.-C. Tsui, P. Parham, I. Hansmann, S. Parikh, L. Shi, L.T. Williams, R.E. Kibbelaar, J. Hayakawa, T. Kajii, M. Rivière, T. Shinohara, D.S. Gerhard, E.K. Bijlsma, M.G. Byers, A.P. Jackson, S.W. Scherer, S. Boularand, F. Yang, J. Mallet, J.A. Escobedo, Andries Westerveld, H.F. Willard, Roger E. Stevenson, R.R. Mclnnes, P. Stanislovitis, H. van Kamp, D.W. Threadgill, T. Koizumi, T.B. Nesterova, J.E. Womack, N.B. Rubtsov, T.A. Jones, T.J.M. Hulsebos, M. Danciger, S. Kubota, M. Katsuki, D.H. Ledbetter, S. Navankasattusas, C. Szpirer, V.G. Matveeva, S.I. Radjabli, L. Pajunen, R.H. Brakenhoff, J. García-Heras, G.C. Beverstock, S.C. Bock, Charles E. Schwartz, L. Dandolo, S. Schnittger, I.A. Noordermeer, C. Hanson, B.H. Robinson, A. Kumamoto, D.B. Farber, C. Rasberry, B. Redeker, K.I. Kivirikko, G.J. den Ottolander, H. Nakai, JG Leroy, Marcel M.A.M. Mannens, P. Avner, U. Francke, J. Spencer, R.G. Lafreniere, and A. Goddard
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Botany ,Genetics ,Zoology ,Biology ,Molecular Biology ,Genetics (clinical) - Published
- 1991
- Full Text
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23. Contents Vol. 99, 2002
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H. Suzuki, R. Kunita, J.-N. Volff, R. Willemsen, A. von der Wense, S.B.A. Fonteles, A. Wolf, K. Saso, K. Sekiya, S.M. Gartler, I. Miura, S. Christin-Maitre, M. Ito, T. Tada, J.T. Lee, C.B. Moysés, D.J. Penman, W. Feichtinger, J. Bernardino-Sgherri, K. Sasaki, Y. Matsuda, S. Jakubiczka, C. Steinlein, M. Matsumura, A. Gal, W. Werner, S. Yamaguchi, D.K. Griffin, Y. Hasegawa, A.I. Shevchenko, A. Fernández Badillo, C.J. Brown, M. Fellous, M. Kuro-o, K. Kutsche, Y. Sabbagh, S. Kirsch, C.E. Schwartz, N. Brockdorff, G.A. Rappold, M. Ogata, T.V. Karamysheva, D.J. Paull, S.-S. Tan, P.G. Johnston, L.V. Pereira, J. Manzanilla Pupo, J.-Y. Lee, T. Ogata, A. Kuroiwa, D. Flagiello, P. Meinecke, K.D. Tsuchiya, L.L. Hall, M.F.Z. Daniel-Silva, T. Namikawa, A.D. Riggs, J.S. Masabanda, R. Campos-Ramos, H. Hameister, Julie Cocquet, C.E. Lopes, K. Abe, P. Muschke, F. Vialard, O.V. Anopriyenko, N.A. Mazurok, M. Schmid, S. Shetty, S. Mizuno, M. Tsudzuki, I. Yoshida, R. Visbal García, T. Kida, H.S. Tenenhouse, T. Hori, J.M.A. Turner, O. Nakabayashi, T. Sado, M. Harata, M. Gomez, E. Heard, O. Bartsch, Y. Fujinuki, H. Kiyosawa, M. Yoshino, Z. Webster, D. Zarkower, P. Wieacker, M. Teranishi, M. Alexiou, G.N. Filippova, C. Ikebe, Paul S. Burgoyne, M. Yamazaki, N. Arai, M. Monk, K. Tanaka, N.B. Rubtsov, S. Kim, Y. Watanabe, C. Gauthier, Y. Itoh, T.B. Nesterova, Y. Fukushima, L.F. de Almeida-Toledo, T. Nakamura, T. Yokomine, M. Adams, T. Kubota, P.J. Kirby, M. Schartl, H. Kimura, B.A. Oostra, I. Nanda, R. Wimmer, N. Okamoto, Y. Arakawa, N. Nakatsuji, E. Li, G.E. Herman, S. Sutou, Y. Goto, W. Schempp, S.C. Harvey, C. Nishida-Umehara, I.B. Van den Veyver, A. Akama, M.-L. Caparros, M. Krawczak, D.W. Burt, N. Takagi, H. Ohashi, Daniel Vaiman, R. Feil, I. Wieland, H.M. El-Hodiri, Y. Kuroda, H. Sasaki, S.M. Zakian, M. Tada, K. Akaba, M. Guggiari, L. Gerlach, L.-J. Ayling, M.N. Klöckner, F. Foresti, L.R. Vasques, B. Dutrillaux, T. Haaf, M. Okabe, R.E. Stevenson, J. Gécz, R.S. Hansen, S. Kohno, O.A. Ojarikre, T. Igarashi, N.V. Rubtsova, M. Sugimoto, M. Hemberger, S. Hatano, Y. Izumisawa, J.C. Chow, J.A.M. Graves, Reiner A. Veitia, J.B. Lawrence, Y. Ogawa, C.M. Watson, C.M. Disteche, A. Weber, K. Muroya, A. Ogawa, N.R. Bromage, B.R. Migeon, H. Ohtani, K. Wakui, Y. Ichikawa, J. Chaumeil, and I. Okamoto
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Botany ,Genetics ,Zoology ,Biology ,Molecular Biology ,Genetics (clinical) - Published
- 2002
- Full Text
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24. Subject Index Vol. 99, 2002
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K. Abe, S. Yamaguchi, H. Ohashi, J.M.A. Turner, M. Tsudzuki, D.K. Griffin, M. Tada, K. Tanaka, M. Hemberger, Y. Fujinuki, C.J. Brown, Y. Watanabe, A. Weber, M. Fellous, S. Hatano, Y. Izumisawa, A. Gal, R. Wimmer, J.C. Chow, K. Muroya, J.A.M. Graves, Reiner A. Veitia, R.E. Stevenson, A.D. Riggs, J. Gécz, R.S. Hansen, Y. Arakawa, N. Arai, T. Sado, Y. Hasegawa, L.-J. Ayling, Y. Itoh, M. Adams, T. Kubota, C.M. Disteche, L.V. Pereira, N. Okamoto, M. Yoshino, I. Nanda, L.F. de Almeida-Toledo, K. Saso, T. Yokomine, J.-N. Volff, F. Foresti, M. Schartl, K. Akaba, M. Ogata, D.J. Paull, S.-S. Tan, J. Manzanilla Pupo, Y. Fukushima, D. Zarkower, M.N. Klöckner, C.E. Schwartz, N. Brockdorff, O.A. Ojarikre, N. Nakatsuji, S. Sutou, G.N. Filippova, N.B. Rubtsov, J.B. Lawrence, Y. Sabbagh, S. Kim, C. Gauthier, J.T. Lee, H. Sasaki, N.R. Bromage, S. Kirsch, C.B. Moysés, M. Ito, L.L. Hall, P.J. Kirby, Y. Goto, C. Nishida-Umehara, T. Tada, D.J. Penman, Y. Ogawa, J.S. Masabanda, I. Wieland, B.A. Oostra, S.M. Gartler, M.F.Z. Daniel-Silva, T. Namikawa, Julie Cocquet, M. Guggiari, L. Gerlach, F. Vialard, C. Ikebe, Z. Webster, S.C. Harvey, A. Fernández Badillo, H.M. El-Hodiri, H. Hameister, P. Wieacker, G.E. Herman, T. Ogata, O.V. Anopriyenko, M. Monk, T. Igarashi, N.V. Rubtsova, M. Sugimoto, W. Feichtinger, J. Bernardino-Sgherri, M. Matsumura, R. Willemsen, S. Mizuno, D. Flagiello, Y. Kuroda, J.-Y. Lee, R. Visbal García, R. Feil, S. Jakubiczka, S.M. Zakian, N.A. Mazurok, S. Shetty, R. Kunita, N. Takagi, Daniel Vaiman, A. von der Wense, A. Akama, H.S. Tenenhouse, M. Alexiou, H. Suzuki, T. Hori, T. Kida, G.A. Rappold, B. Dutrillaux, L.R. Vasques, W. Werner, T.B. Nesterova, A.I. Shevchenko, E. Li, W. Schempp, T. Haaf, M. Okabe, M. Kuro-o, S. Kohno, S.B.A. Fonteles, A. Wolf, I. Miura, I.B. Van den Veyver, M. Krawczak, M. Harata, K. Sekiya, M. Gomez, E. Heard, T.V. Karamysheva, S. Christin-Maitre, A. Kuroiwa, C.E. Lopes, K. Kutsche, P. Muschke, M. Schmid, I. Yoshida, O. Nakabayashi, O. Bartsch, K. Sasaki, Y. Matsuda, P.G. Johnston, C. Steinlein, Y. Ichikawa, J. Chaumeil, I. Okamoto, B.R. Migeon, H. Ohtani, K. Wakui, C.M. Watson, A. Ogawa, H. Kiyosawa, M. Teranishi, Paul S. Burgoyne, M. Yamazaki, P. Meinecke, K.D. Tsuchiya, R. Campos-Ramos, T. Nakamura, H. Kimura, M.-L. Caparros, and D.W. Burt
- Subjects
Index (economics) ,Statistics ,Genetics ,Subject (documents) ,Biology ,Molecular Biology ,Genetics (clinical) - Published
- 2002
- Full Text
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25. Subject Index, Vol. 76, 1997
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M.R. Martorell, J.M. Trent, D. Stephan, M. Dean, M.B. Qumsiyeh, H. Lovec, T. Muraro, B. Horsthemke, J.L VandeBerg, J. Wirth, C. Shao, A.G. Shilov, A. Girardet, B. Sèle, J. Torresani, U. Claussen, N.B. Rubtsov, F. Coulier, S.M. Zakian, S. Taviaux, N.T. Bech-Hansen, M.H. Dreyling, M.A. Ferguson-Smith, P.S. Meltzer, O.I. Olopade, P. Eydoux, J. Benet, S. Levanat, G. Scherer, X.X. Zhang, M. Goldfarb, M-G. Mattéi, N. Tommerup, J.A. Peppers, B. Windle, T.P. Moynihan, N.V. Rubtsova, W. Jiang, X.-Y. Zhang, M. Schmid, H. Leffers, H.S. Tenenhouse, T.B. Nesterova, M. Ehrlich, P.K. Gupta, P. Mühlig, H.H. Quek, C. Wicking, Y. Zhu, D. Adrian, J.P. Grillasca, G. Lefort, E. Back, H.-J. Lüdecke, J. Zimmer, N.V. Vorobieva, N. Tiso, I. Nanda, M. Monteil, J.L. Coate, R. Zimbello, I. Garkavtsev, C. Pressman, J.P. Leek, A.S. Hewson, I. Parra, S. Rousseaux, J.P. Charlieu, R. Hernandez, A.E. Bale, E.H. Hoffman, B. Andréo, A.F. Markham, V.T.K. Chow, E.J. Taparowsky, K.L. Stoddart, M.L. Kennedy, A-S. Verdier, A. Sahota, G.J. Pappanicolaou, B. Wainwright, H. Satoh, K. Buiting, S.K. Bohlander, P.C.M. O’Brien, A. Frady, M.A. Peters, M.R. Gailani, T. Wagner, D.T. Bonthron, A. León-Del-Rio, F. Yang, A. Chidambaram, G. Lanfranch, H. Hartung, K.J. Gratton, B.G. Beatty, P. Bray-Ward, D. Demetrick, M-G. Matté, J.A. Tischfield, D.R. Lohmann, R.A. Gravel, G. Valle, A.A. Isaenko, S. Mori, J. Wienberg, J. Navarro, R. Hliscs, D. Birnbaum, N.Z. Parsa, C. Flores, M. Gastaldi, J. Egozcue, N.M. Matveeva, P.K. Kennedy, B. Roland, R. Pelletier, C. Márquez, J.C. Myers, B.J. Moore, G.A. Danieli, F. Pellestor, N.J. Lench, K. Riabowol, K. Sperling, J. Weissenbach, M. Varela, R. Toftgard, R. Anwar, E. Chevret, J. Cozzi, R. Planells, K.M. Boycott, and E.H. McConkey
- Subjects
Index (economics) ,Statistics ,Genetics ,Subject (documents) ,Biology ,Molecular Biology ,Genetics (clinical) - Published
- 1997
- Full Text
- View/download PDF
26. Subject Index Vol. 56, 1991
- Author
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L. Dandolo, D.S. Gallagher, P.M. Kluin, A. Kuwano, B.H. Robinson, G. Otulakowski, S.P. Craig, N.J. Nowak, G. Levan, M. Van der Ploeg, M.A. Abruzzo, A.C.B. Peters, P. Stanislovitis, Charles E. Schwartz, M.C. Simmler, L.-C. Tsui, D.W. Threadgill, C.A. Kozak, D. Sheer, A. Kumamoto, M.C. Darmon, A.K. Raap, I.V. Nikitina, S.M. Zakian, S. Kubota, M. Kimura, D.H. Ledbetter, A. Goddard, S. Kohno, S.J. Sadler, T. Kajii, D.S. Gerhard, D.B. Farber, S.W. Scherer, JG Leroy, R.R. Mclnnes, Marcel M.A.M. Mannens, C. Rasberry, C. Hanson, M. Vercruyssen, T. Koizumi, J. Mallet, Rosalyn Slater, P. Avner, U. Francke, M. Rivière, N.B. Rubtsov, V.L. Singer, K.I. Kivirikko, E.K. Bijlsma, P. Parham, T.B. Nesterova, J.E. Womack, J. Spencer, M.C. Phelan, B. Redeker, S. Navankasattusas, G.N. Hendy, V.V.N.G. Rao, R.G. Lafreniere, J.W. Wessels, Y. Nakai, C. Szpirer, B.M. Cattanach, R.G. Taylor, Andries Westerveld, M. Westerman, I. Hansmann, J. George, E. Solomon, G.J. den Ottolander, S. Boularand, V.E. Powers, Roger E. Stevenson, H. Nakai, T. Abe, G.M. Greig, M. Danciger, N.S.-F. Ma, L. Pajunen, J. Hayakawa, G.C. Beverstock, C.-L. Hsieh, J.A. Miller, S. Schnittger, H.F. Willard, S.I. Radjabli, R.H. Brakenhoff, A. Geurts van Kessel, E.J. Dreef, S. Parikh, L. Shi, A.P. Jackson, H. van Kamp, T.B. Shows, K. Klinger, I.A. Noordermeer, C. Collet, M. Katsuki, V.G. Matveeva, J. García-Heras, S.C. Bock, T. Pihlajaniemi, R.E. Kibbelaar, M.G. Byers, F. Yang, H.A. Taylor, P. Van Oostveldt, J. Szpirer, E.P.J. Arnoldus, I.W. Craig, W.E. Fibbe, E.P. Evans, Franki Speleman, T. Shinohara, L.T. Williams, J.A. Escobedo, T.A. Jones, and T.J.M. Hulsebos
- Subjects
Index (economics) ,Statistics ,Genetics ,Subject (documents) ,Biology ,Molecular Biology ,Genetics (clinical) - Published
- 1991
- Full Text
- View/download PDF
27. Subject Index Vol. 65, 1994
- Author
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R. Tupler, S.D. Wilton, G. Melmer, P.A. Akkari, I. Todorov, J.L. Cassady, D. Werner, M.A. Garrido-Ramos, N.A. Mazurok, D.A. Miller, L.L. Deaven, P.F.R. Little, M. Cortinovis, Y. Agid, P. Bouche, A. Blancher, O. Riess, N. Ravisé, J.-M. Blanchard, D.O. Weghuis, D. Francis, A. Plet, E.I. Yantsen, P.M.T. Deen, D.F. Callen, T.M. Fink, C. Meredith, P. Calvas, M Janson, M. Lafage-Pochitaloff, Angela Maria Vianna-Morgante, S. Kredtke, A. Geurts van Kessel, C.H. van Os, N.M. Matveeva, G. Chazot, M.-G. Mattéi, P.-M. Gonnaud, E.Kh. Ginsburg, Carla Rosenberg, N.G. Laing, S.M. Zakian, A. Mincheva, O.J. Miller, S.A. Lane, L. Tiepolo, M. Jamilena, David W. Hale, H.J. Eyre, M. Gugenheim, B. Chérif-Zahar, C. Bonnebouche, I. Siedlaczck, S.J. Goss, L. Kedes, A. Vandenberghe, B. Wieringa, E. Le Guern, A. Brice, C. Cerdan, S. Tardieu, D.I. Francis, R.A. Sturm, R. Lozano, F. Sturtz, E. Dainotti, M. Nordeskjöld, C. Ruiz Rejón, Q.-Q. Cai, Anne Lise Børresen, J.T. Epplen, I. Salvignol, P. Maraschio, R. Gouider, A.G. Shilov, M. Ruiz Rejón, J. Imbert, Peter Lichter, T.B. Nesterova, J.A.M. Graves, and D. Depétris
- Subjects
Index (economics) ,Statistics ,Genetics ,Subject (documents) ,Biology ,Molecular Biology ,Genetics (clinical) - Published
- 1994
- Full Text
- View/download PDF
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