Search Results - (Author, Cooperation:J. Kere)

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  1. 1
    A. R. Forrest ; H. Kawaji ; M. Rehli ; J. K. Baillie ; M. J. de Hoon ; V. Haberle ; T. Lassmann ; I. V. Kulakovskiy ; M. Lizio ; M. Itoh ; R. Andersson ; C. J. Mungall ; T. F. Meehan ; S. Schmeier ; N. Bertin ; M. Jorgensen ; E. Dimont ; E. Arner ; C. Schmidl ; U. Schaefer ; Y. A. Medvedeva ; C. Plessy ; M. Vitezic ; J. Severin ; C. Semple ; Y. Ishizu ; R. S. Young ; M. Francescatto ; I. Alam ; D. Albanese ; G. M. Altschuler ; T. Arakawa ; J. A. Archer ; P. Arner ; M. Babina ; S. Rennie ; P. J. Balwierz ; A. G. Beckhouse ; S. Pradhan-Bhatt ; J. A. Blake ; A. Blumenthal ; B. Bodega ; A. Bonetti ; J. Briggs ; F. Brombacher ; A. M. Burroughs ; A. Califano ; C. V. Cannistraci ; D. Carbajo ; Y. Chen ; M. Chierici ; Y. Ciani ; H. C. Clevers ; E. Dalla ; C. A. Davis ; M. Detmar ; A. D. Diehl ; T. Dohi ; F. Drablos ; A. S. Edge ; M. Edinger ; K. Ekwall ; M. Endoh ; H. Enomoto ; M. Fagiolini ; L. Fairbairn ; H. Fang ; M. C. Farach-Carson ; G. J. Faulkner ; A. V. Favorov ; M. E. Fisher ; M. C. Frith ; R. Fujita ; S. Fukuda ; C. Furlanello ; M. Furino ; J. Furusawa ; T. B. Geijtenbeek ; A. P. Gibson ; T. Gingeras ; D. Goldowitz ; J. Gough ; S. Guhl ; R. Guler ; S. Gustincich ; T. J. Ha ; M. Hamaguchi ; M. Hara ; M. Harbers ; J. Harshbarger ; A. Hasegawa ; Y. Hasegawa ; T. Hashimoto ; M. Herlyn ; K. J. Hitchens ; S. J. Ho Sui ; O. M. Hofmann ; I. Hoof ; F. Hori ; L. Huminiecki ; K. Iida ; T. Ikawa ; B. R. Jankovic ; H. Jia ; A. Joshi ; G. Jurman ; B. Kaczkowski ; C. Kai ; K. Kaida ; A. Kaiho ; K. Kajiyama ; M. Kanamori-Katayama ; A. S. Kasianov ; T. Kasukawa ; S. Katayama ; S. Kato ; S. Kawaguchi ; H. Kawamoto ; Y. I. Kawamura ; T. Kawashima ; J. S. Kempfle ; T. J. Kenna ; J. Kere ; L. M. Khachigian ; T. Kitamura ; S. P. Klinken ; A. J. Knox ; M. Kojima ; S. Kojima ; N. Kondo ; H. Koseki ; S. Koyasu ; S. Krampitz ; A. Kubosaki ; A. T. Kwon ; J. F. Laros ; W. Lee ; A. Lennartsson ; K. Li ; B. Lilje ; L. Lipovich ; A. Mackay-Sim ; R. Manabe ; J. C. Mar ; B. Marchand ; A. Mathelier ; N. Mejhert ; A. Meynert ; Y. Mizuno ; D. A. de Lima Morais ; H. Morikawa ; M. Morimoto ; K. Moro ; E. Motakis ; H. Motohashi ; C. L. Mummery ; M. Murata ; S. Nagao-Sato ; Y. Nakachi ; F. Nakahara ; T. Nakamura ; Y. Nakamura ; K. Nakazato ; E. van Nimwegen ; N. Ninomiya ; H. Nishiyori ; S. Noma ; T. Noazaki ; S. Ogishima ; N. Ohkura ; H. Ohimiya ; H. Ohno ; M. Ohshima ; M. Okada-Hatakeyama ; Y. Okazaki ; V. Orlando ; D. A. Ovchinnikov ; A. Pain ; R. Passier ; M. Patrikakis ; H. Persson ; S. Piazza ; J. G. Prendergast ; O. J. Rackham ; J. A. Ramilowski ; M. Rashid ; T. Ravasi ; P. Rizzu ; M. Roncador ; S. Roy ; M. B. Rye ; E. Saijyo ; A. Sajantila ; A. Saka ; S. Sakaguchi ; M. Sakai ; H. Sato ; S. Savvi ; A. Saxena ; C. Schneider ; E. A. Schultes ; G. G. Schulze-Tanzil ; A. Schwegmann ; T. Sengstag ; G. Sheng ; H. Shimoji ; Y. Shimoni ; J. W. Shin ; C. Simon ; D. Sugiyama ; T. Sugiyama ; M. Suzuki ; N. Suzuki ; R. K. Swoboda ; P. A. t Hoen ; M. Tagami ; N. Takahashi ; J. Takai ; H. Tanaka ; H. Tatsukawa ; Z. Tatum ; M. Thompson ; H. Toyodo ; T. Toyoda ; E. Valen ; M. van de Wetering ; L. M. van den Berg ; R. Verado ; D. Vijayan ; I. E. Vorontsov ; W. W. Wasserman ; S. Watanabe ; C. A. Wells ; L. N. Winteringham ; E. Wolvetang ; E. J. Wood ; Y. Yamaguchi ; M. Yamamoto ; M. Yoneda ; Y. Yonekura ; S. Yoshida ; S. E. Zabierowski ; P. G. Zhang ; X. Zhao ; S. Zucchelli ; K. M. Summers ; H. Suzuki ; C. O. Daub ; J. Kawai ; P. Heutink ; W. Hide ; T. C. Freeman ; B. Lenhard ; V. B. Bajic ; M. S. Taylor ; V. J. Makeev ; A. Sandelin ; D. A. Hume ; P. Carninci ; Y. Hayashizaki
    Nature Publishing Group (NPG)
    Published 2014
    Staff View
    Publication Date:
    2014-03-29
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Animals ; *Atlases as Topic ; Cell Line ; Cells, Cultured ; Cluster Analysis ; Conserved Sequence/genetics ; Gene Expression Regulation/genetics ; Gene Regulatory Networks/genetics ; Genes, Essential/genetics ; Genome/genetics ; Humans ; Mice ; *Molecular Sequence Annotation ; Open Reading Frames/genetics ; Organ Specificity ; Promoter Regions, Genetic/*genetics ; RNA, Messenger/analysis/genetics ; Transcription Factors/metabolism ; Transcription Initiation Site ; Transcription, Genetic/genetics ; Transcriptome/*genetics
    Published by:
    http://www.nature.com/

    Latest Papers from Table of Contents or Articles in Press
  2. 2
    VAALAMO, M. ; WECKROTH, M. ; PUOLAKKAINEN, P. ; KERE, J. ; SAARINEN, P. ; LAUHARANTA, J. ; SAARIALHO-KERE, U.K.

    Oxford, UK : Blackwell Publishing Ltd
    Published 1996
    Staff View
    ISSN:
    1365-2133
    Source:
    Blackwell Publishing Journal Backfiles 1879-2005
    Topics:
    Medicine
    Notes:
    Summary The present study was carried out to characterize the patterns of expression of matrix metalloproteinases or their tissue inhibitor (TIMP-1) in normally healing, acute vs. chronic, skin wounds. In situ hybridization was performed to localize collagenase, stromelysin-1, stromelysin-2, matrilysin, urokinase plasminogen activator (uPA) and TIMP-1 mRNAs in 14 chronic venous ulcers and 10 normally healing wounds, representing different time points after wounding. Surgical wounds, made in piglets harvested at several time points, were studied as controls. Collagenase, stromelysin-1 and -2, as well as uPa, were expressed in keratinocytes in both acute and chronic wounds, while epithelial TIMP-1 mRNA was not detected in any chronic wound biopsies studied. However, TIMP-1 was expressed at the epithelial edges of both acute human and pig wounds. Our results suggest that the balance between metalloenzymes and their inhibitor TIMP-1, is disturbed, in poorly healing wounds.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1046/j.1365-2133.1996.d01-932.x

    Articles: DFG German National Licenses
  3. 3
    Melén, E. ; Kere, J. ; Pershagen, G. ; Svartengren, M. ; Wickman, M.

    Oxford, UK : Blackwell Science Ltd
    Published 2004
    Staff View
    ISSN:
    1365-2222
    Source:
    Blackwell Publishing Journal Backfiles 1879-2005
    Topics:
    Medicine
    Notes:
    Background Boys have been reported to be more susceptible to childhood wheezing, whereas girls are more susceptible later in life. This difference might be related to both genetic and environmental factors.Objective To investigate the influence of male sex and parental allergic disease on the development of childhood wheezing.Methods Infants (n=4089) born in Stockholm were recruited in a prospective study, BAMSE. Data on parental allergic diseases were obtained from questionnaires answered at the children's birth and on symptoms of wheezing at 1, 2 and 4 years of age. Sensitization to inhalant allergens and lung function was investigated at the age of 4 years.Results Children were classified as having recurrent, transient (n=266), early-onset persistent (n=319) and late-onset wheezing (n=195). Boys were over-represented in all groups of wheezing (odds ratio, OR=1.4–1.5) and both maternal and paternal allergic disease was of importance for the wheezing outcomes. A dominating influence from maternal allergic disease was only seen in children with persistent wheezing. An interaction exceeding additivity was found between male sex and parental allergic disease, particularly in children with persistent wheezing (OR=2.9 and 95% confidence interval, CI 95% 2.1–4.0 for boys with any parental history vs. OR=1.4, CI 95% 1.0–2.1 for girls). Interaction between male sex and parental allergic disease was also observed in children who wheezed at the age of 4 years and were sensitized to inhalant allergens.Conclusion Our data suggest an interaction between male sex and parental allergic disease in childhood wheezing, which may represent a sex-specific genetic influence.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1111/j.1365-2222.2004.01957.x

    Articles: DFG German National Licenses
  4. 4
    Ylikoski, E. ; Kinos, R. ; Sirkkanen, N. ; Pykäläinen, M. ; Savolainen, J. ; Laitinen, L. A. ; Kere, J. ; Laitinen, T. ; Lahesmaa, R.

    Oxford, UK : Blackwell Science Ltd
    Published 2004
    Staff View
    ISSN:
    1365-2222
    Source:
    Blackwell Publishing Journal Backfiles 1879-2005
    Topics:
    Medicine
    Notes:
    Objective T-box expressed in T cells (T-bet) is a transcription factor regulating the commitment of T helper (Th) cells by driving the cells into the Th1 direction. Abnormal Th1/Th2 balance may lead to complex disorders like asthma or autoimmune diseases. Recent studies have suggested that T-bet might be a candidate gene for asthma. This led us to screen 23 Finnish individuals for single-nucleotide polymorphisms (SNPs) in the T-bet locus and study the association between the SNPs and high serum IgE level and asthma.Methods We screened all six exons, adjacent intronic areas and 2 kb of the 5′-flanking region from 23 individuals utilizing WAVE™ technology. To explore whether T-bet is associated in serum IgE regulation or asthma we genotyped the SNPs in a Finnish asthmatic founder population. The association analyses were made using haplotype pattern mining.Results Fifteen novel SNPs were found in the T-bet gene. Within the Finnish asthmatic founder population, there was no association between T-bet SNPs and high serum IgE level or asthma.〈section xml:id="abs1-2"〉〈title type="main"〉Conclusions The genetic variability in the T-bet gene does not play a role in the pathogenesis of human asthma. Our results provide a novel panel of SNPs in T-bet and will help determine whether the SNPs have a functional role in other T cell-mediated diseases.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1111/j.1365-2222.2004.01995.x

    Articles: DFG German National Licenses
  5. 5
    Montonen, O. ; Ezer, S. ; Laurikkala, J. ; Karjalainen-Lindsberg, M.-L. ; Thesleff, I. ; Kere, J. ; Saarialho-Kere, U.

    Oxford, UK : Blackwell Publishing Ltd
    Published 1998
    Staff View
    ISSN:
    1600-0625
    Source:
    Blackwell Publishing Journal Backfiles 1879-2005
    Topics:
    Medicine
    Notes:
    Abstract: X-linked anhidrotic ectodermal dysplasia (EDA) is characterized by defects in the development of hair, teeth, and sweat glands. We have recently cloned the gene for EDA by positional cloning. The EDA gene encodes a transmembrane protein with a putative role in epithelial-mesenchymal interactions. Since EDA could play a role in cell-cell or cell-matrix adhesion, acantholytic skin diseases and several types of non-invasive and invasive skin cancers were studied using in situ hybridization. Because of the observation that the promoter region of the EDA gene contains a binding site for LEF-1, which is involved in the signaling through E-cadherin/beta catenin complex, we compared the expression of EDA with immunolocalization for E-cadherin (E-CD). EDA expression during hair growth cycle, in benign adnexal tumors, and neuroectodermderived nevus cells was also examined. Our findings indicate that EDA expression is less abundant in malignant tumors, including basal and squamous cell carcinomas and melanoma, and in acantholytic keratinocytes compared to normal epidermis. The reduction in expression also coincides with diminished E-CD staining in all malignant cell types and in acantholytic cells. Our results suggest that EDA protein functions in the regulation of epithelial cell contacts and that it may be associated with the E-CD signaling pathway.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1111/j.1600-0625.1998.tb00319.x

    Articles: DFG German National Licenses
  6. 6
    Virolainen, E. ; Niemi, K-M. ; Gånemo, A. ; Kere, J. ; Vahlquist, A. ; Saarialho-Kere, U.

    Oxford, UK : Blackwell Science Ltd
    Published 2001
    Staff View
    ISSN:
    1365-2133
    Source:
    Blackwell Publishing Journal Backfiles 1879-2005
    Topics:
    Medicine
    Notes:
    Congenital ichthyoses are a group of heterogeneous disorders of cornification. Autosomal recessive congenital ichthyosis (ARCI) can be clinically subdivided into congenital ichthyosiform erythroderma and lamellar ichthyosis. Ultrastructurally, ARCI is classified into four groups: ichthyosis congenita (IC) types I–IV. The genetic background of the ARCI disorders is heterogeneous, but only one disease gene, transglutaminase 1, has been detected so far. We describe six patients with severe congenital ichthyosis from six different Scandinavian families. They could not be classified ultrastructurally into the four IC groups because of atypical findings of electron microscopy. These included abnormal lamellar bodies, alterations in keratohyalin, remnant organelles and lipid inclusions in the upper epidermal cells, which resembled the ultrastructural findings of harlequin ichthyosis (HI), although the HI phenotype was not present at birth. Some clinical features, such as thick scales, erythroderma, alopecia and ectropion were common to all patients. Ichthyosis was usually accentuated in the scalp and four patients had clumped fingers and toes. None of the patients carried the transglutaminase 1 mutation. We conclude that ultrastructural findings resembling those detected in previous HI cases (type 1 and 2) can also be found in patients who do not have classic clinical features of that rare ichthyosis. This may be due to lack of specificity of ultrastructural markers for HI or to its clinical heterogeneity.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1111/j.1365-2133.2001.04401.x

    Articles: DFG German National Licenses
  7. 7
    Staff View
    ISSN:
    0888-7543
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1016/0888-7543(92)90183-S

    Articles: DFG German National Licenses
  8. 8
    Staff View
    ISSN:
    0888-7543
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1016/0888-7543(92)90182-R

    Articles: DFG German National Licenses
  9. 9
    Staff View
    ISSN:
    0888-7543
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1016/S0888-7543(05)80212-5

    Articles: DFG German National Licenses
  10. 10
    Staff View
    ISSN:
    0888-7543
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1016/0888-7543(87)90109-1

    Articles: DFG German National Licenses
  11. 11
    Staff View
    ISSN:
    0888-7543
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1016/0888-7543(91)90001-U

    Articles: DFG German National Licenses
  12. 12
    Staff View
    ISSN:
    0014-5793
    Keywords:
    DNA-test ; Familial amyloid polyneuropathy ; Finnish hereditary amyloidosis ; Gelsolin gene ; Oligonucleotide hybridization ; Point mutation
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Chemistry and Pharmacology
    Physics
    Type of Medium:
    Electronic Resource
    URL:
    http://linkinghub.elsevier.com/retrieve/pii/0014-5793(90)80510-P

    Articles: DFG German National Licenses
  13. 13
    Staff View
    ISSN:
    0888-7543
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1016/S0888-7543(05)80212-5

    Articles: DFG German National Licenses
  14. 14
    Staff View
    ISSN:
    0888-7543
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1006/geno.1993.1189

    Articles: DFG German National Licenses
  15. 15
    Partanen, J. ; Kere, J. ; Wessberg, S. ; Koskimies, S.

    Amsterdam : Elsevier
    Staff View
    ISSN:
    0888-7543
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1016/0888-7543(89)90067-0

    Articles: DFG German National Licenses
  16. 16
    Chen, E.Y. ; Schlessinger, D. ; Kere, J.

    Amsterdam : Elsevier
    Staff View
    ISSN:
    0888-7543
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1006/geno.1993.1385

    Articles: DFG German National Licenses
  17. 17
    Staff View
    ISSN:
    0888-7543
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1016/0888-7543(87)90052-8

    Articles: DFG German National Licenses
  18. 18
    Staff View
    ISSN:
    0165-4608
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    http://linkinghub.elsevier.com/retrieve/pii/0165-4608(89)90659-6

    Articles: DFG German National Licenses
  19. 19
    Staff View
    ISSN:
    0942-0940
    Keywords:
    Keywords: Haemangioblastoma; von Hippel-Lindau disease; surgery; survival.
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Summary ¶ The aim was to assess the frequency of von Hippel-Lindau disease (VHL) and the long-term prognosis of VHL and non-VHL patients among 110 consecutive patients with haemangioblastoma (HB) of the CNS treated between 1953 and 1993 at one neurosurgical unit.  To reveal VHL manifestations we performed a detailed clinical and radiological examination (neuraxis and abdomen) (61/110), VHL-gene mutation analysis (40/110), and collection of all available clinical, imaging, operative and autopsy data from the hospitals involved. All patients were followed-up with a median of 14 years (excluding 14 operative deaths), and no patient was lost to follow-up. Altogether 49 patients died during the follow-up.  In the 14 VHL patients (13%), HB(s) of the CNS were detected at a median age of 33 years, retinal HB(s) at 39 years, and renal cell carcinoma (RCC) at 43 years. The frequency of VHL in patients operated on for HB(s) was 29% before the age of 25 years, 19% between 25 and 45 years, and only 2% after 45 years. HB patients not meeting the VHL criteria had internal organ cysts in 14%. One non-VHL patient (4%) had two adjacent HBs in the same cyst wall. The growth rates of non-VHL and VHL-related HBs were similar as indicated by the median time to recurrence and the proliferation indices (MIB-1). Recurrence of the HB in patients whose primary operation was considered radical developed in four of the 10 VHL patients at a median of 19 years, and in nine of the 74 non-VHL patients at a median of 11 years. The median length of life of all VHL and non-VHL patients was 46 and 63 years, respectively. In VHL, RCC and HBs were equal causes of death.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/s007010050412

    Articles: DFG German National Licenses
  20. 20
    Staff View
    ISSN:
    1432-1203
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Biology
    Medicine
    Notes:
    Summary We report a rare allele detected using pMP6d-9, a probe very closely linked to cystic fibrosis (CF), on digestion with MspI. This allele has been found in normal and CF chromosomes, and therefore cannot be related to the mutation causing the disease.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF00285181

    Articles: DFG German National Licenses