| 1611. |
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| 1612. |
- Zabarovska, V, et al.
(författare)
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CIS--cloning of identical sequences between two complex genomes
- 2000
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Ingår i: Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology. - : Springer Science and Business Media LLC. - 0967-3849. ; 8:1, s. 77-84
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Tidskriftsartikel (refereegranskat)
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| 1613. |
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| 1614. |
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| 1615. |
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| 1616. |
- Zayats, T, et al.
(författare)
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Exome chip analyses in adult attention deficit hyperactivity disorder
- 2016
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Ingår i: Translational Psychiatry. - : Nature Publishing Group. - 2158-3188 .- 2158-3188. ; 6:10
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Tidskriftsartikel (refereegranskat)abstract
- Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable childhood-onset neuropsychiatric condition, often persisting into adulthood. The genetic architecture of ADHD, particularly in adults, is largely unknown. We performed an exome-wide scan of adult ADHD using the Illumina Human Exome Bead Chip, which interrogates over 250 000 common and rare variants. Participants were recruited by the International Multicenter persistent ADHD CollaboraTion (IMpACT). Statistical analyses were divided into 3 steps: (1) gene-level analysis of rare variants (minor allele frequency (MAF)<1%); (2) single marker association tests of common variants (MAF⩾1%), with replication of the top signals; and (3) pathway analyses. In total, 9365 individuals (1846 cases and 7519 controls) were examined. Replication of the most associated common variants was attempted in 9847 individuals (2077 cases and 7770 controls) using fixed-effects inverse variance meta-analysis. With a Bonferroni-corrected significance level of 1.82E-06, our analyses of rare coding variants revealed four study-wide significant loci: 6q22.1 locus (P=4.46E-08), where NT5DC1 and COL10A1 reside; the SEC23IP locus (P=6.47E-07); the PSD locus (P=7.58E-08) and ZCCHC4 locus (P=1.79E-06). No genome-wide significant association was observed among the common variants. The strongest signal was noted at rs9325032 in PPP2R2B (odds ratio=0.81, P=1.61E-05). Taken together, our data add to the growing evidence of general signal transduction molecules (NT5DC1, PSD, SEC23IP and ZCCHC4) having an important role in the etiology of ADHD. Although the biological implications of these findings need to be further explored, they highlight the possible role of cellular communication as a potential core component in the development of both adult and childhood forms of ADHD.
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| 1617. |
- Zetterberg, H, et al.
(författare)
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The Epstein-Barr virus ZEBRA protein activates transcription from the early lytic F promoter by binding to a promoter-proximal AP-1-like site
- 2002
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Ingår i: The Journal of general virology. - : Microbiology Society. - 0022-1317 .- 1465-2099. ; 83:Pt 8, s. 2007-2014
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Tidskriftsartikel (refereegranskat)abstract
- The ZEBRA protein encoded by the Epstein–Barr virus (EBV) genome activates a switch from the latent to the lytic gene expression programme of the virus. ZEBRA, a member of the basic leucine zipper family of DNA-binding proteins, is a transcriptional activator capable of inducing expression from several virus lytic cycle promoters by binding to activator protein 1 (AP-1)-like sites. The Epstein–Barr virus BamHI F promoter, Fp, was for some time believed to initiate EBNA1-specific transcription in EBV-transformed latent cells. More recent data, however, show that Fp is an early lytic promoter and that the dominant EBNA1 gene promoter in latent cells is Qp, located about 200 bp downstream of Fp. In the present investigation we confirm that Fp displays the characteristics of a lytic promoter. Fp is downregulated in latently EBV-infected cells, both in the endogenous virus genome and in reporter plasmids that carry Fp regulatory sequences upstream of position −136 and down to +10 relative to the Fp transcription start site (+1), and is activated on induction of the virus lytic cycle. We show that the repression of Fp in latent stages of infection can be abolished by ZEBRA, and demonstrate that ZEBRA activates Fp through a direct interaction with an AP-1-like site at position −52/−46 in the promoter-proximal Fp region.
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| 1618. |
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| 1619. |
- Zoback, Mary Lou, et al.
(författare)
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Global patterns of tectonic stress
- 1989
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 341:6240, s. 291-298
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Forskningsöversikt (refereegranskat)abstract
- Regional patterns of present-day tectonic stress can be used to evaluate the forces acting on the lithosphere and to investigate intraplate seismicity. Most intraplate regions are characterized by a compressional stress regime; extension is limited almost entirely to thermally uplifted regions. In several plates the maximum horizontal stress is subparallel to the direction of absolute plate motion, suggesting that the forces driving the plates also dominate the stress distribution in the plate interior.
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| 1620. |
- Östman, Arne, et al.
(författare)
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PDGF receptors as targets in tumor treatment
- 2007
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Ingår i: Advances in Cancer Research. - San Diego : Academic Press. - 0065-230X .- 2162-5557. - 9780120066971 ; 97, s. 247-274
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Forskningsöversikt (refereegranskat)abstract
- Signaling through platelet-derived growth factor (PDGF) receptors contributes to multiple tumor-associated processes. The recent introduction of clinically useful PDGF inhibitors have the last years validated PDGF receptors in malignant and stromal cells as relevant cancer drug targets. Mutational activation of PDGF receptor signaling in malignant cells has been described in some rare tumor types such as dermatofibrosarcoma protuberans, a subset of GISTs, and some hematologic malignancies. Furthermore, expression of PDGF receptors on pericytes is a common characteristic of solid tumors. The clinical efficacy of novel multikinase inhibitors, such as sunitimb and sorafemb, most likely involves targeting of PDGF receptor-dependent pericytes. Preclinical studies suggest that targeting of stromal PDGF receptors might also constitute a novel strategy to enhance tumor drug uptake. Finally, recent studies have implied both pro- and antimetastatic effects of PDGF receptors on malignant and stromal cells. The studies on the roles of PDGF receptors in cancer signaling are thus presently in a dynamic phase where collaborations between oncologists, pathologists, and tumor biologists are predicted to be highly productive.
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