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Träfflista för sökning "WFRF:(Khan Sofia) srt2:(2007-2009)"

Sökning: WFRF:(Khan Sofia) > (2007-2009)

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1.
  • Khan, Sofia, et al. (författare)
  • Evaluation of accuracy and applicability of protein models: retrospective analysis of biological and biomedical predictions.
  • 2009
  • Ingår i: In Silico Biology. - IOS Press. - 1386-6338. ; 9:5, s. 307-331
  • Tidskriftsartikel (refereegranskat)abstract
    • In order to study protein function and activity structural data is required. Since experimental structures are available for just a small fraction of all known protein sequences, computational methods such as protein modelling can provide useful information. Over the last few decades we have predicted, with homology modelling methods, the structures for numerous proteins. In this study we assess the structural quality and validity of the biological and medical interpretations and predictions made based on the models. All the models had correct scaffolding and were ranked at least as correct or good by numerical evaluators even though the sequence identity with the template was as low as 8%. The biological explanations made based on models were well in line with experimental structures and other experimental studies. Retrospective analysis of homology models indicates the power of protein modelling when made carefully from sequence alignment to model building and refinement. Modelling can be applied to studying and predicting different kinds of biological phenomena and according to our results it can be done so with success.
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2.
  • Khan, Sofia, et al. (författare)
  • Spectrum of disease-causing mutations in protein secondary structures.
  • 2007
  • Ingår i: BMC Structural Biology. - BioMed Central (BMC). - 1471-2237. ; 7, s. 56-56
  • Tidskriftsartikel (refereegranskat)abstract
    • Most genetic disorders are linked to missense mutations as even minor changes in the size or properties of an amino acid can alter or prevent the function of the protein. Further, the effect of a mutation is also dependent on the sequence and structure context of the alteration.
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3.
  • Liu, Wennuan, et al. (författare)
  • Copy number analysis indicates monoclonal origin of lethal metastatic prostate cancer.
  • 2009
  • Ingår i: Nature Medicine. - Nature Publishing Group. - 1546-170X. ; 15:5, s. 559-565
  • Tidskriftsartikel (refereegranskat)abstract
    • Many studies have shown that primary prostate cancers are multifocal and are composed of multiple genetically distinct cancer cell clones. Whether or not multiclonal primary prostate cancers typically give rise to multiclonal or monoclonal prostate cancer metastases is largely unknown, although studies at single chromosomal loci are consistent with the latter case. Here we show through a high-resolution genome-wide single nucleotide polymorphism and copy number survey that most, if not all, metastatic prostate cancers have monoclonal origins and maintain a unique signature copy number pattern of the parent cancer cell while also accumulating a variable number of separate subclonally sustained changes. We find no relationship between anatomic site of metastasis and genomic copy number change pattern. Taken together with past animal and cytogenetic studies of metastasis and recent single-locus genetic data in prostate and other metastatic cancers, these data indicate that despite common genomic heterogeneity in primary cancers, most metastatic cancers arise from a single precursor cancer cell. This study establishes that genomic archeology of multiple anatomically separate metastatic cancers in individuals can be used to define the salient genomic features of a parent cancer clone of proven lethal metastatic phenotype.
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4.
  • Pärssinen, Jenita, et al. (författare)
  • Identification of differentially expressed genes after PPM1D silencing in breast cancer.
  • 2008
  • Ingår i: Cancer Letters. - Elsevier. - 1872-7980. ; 259:1, s. 61-70
  • Tidskriftsartikel (refereegranskat)abstract
    • Amplification and overexpression of PPM1D (protein phosphatase magnesium-dependent 1 delta) has been observed in various cancer cell lines and primary tumors and has also been associated with cancers of poor prognosis. In addition to the negative feedback regulation of p38-p53 signaling, PPM1D inhibits other tumor suppressor activities and is involved in the control of DNA damage and repair pathways. To elucidate the functional significance of PPM1D in breast cancer, we employed RNA interference to downregulate PPM1D expression in BT-474, MCF7, and ZR-75-1 breast cancer cell lines and then investigated the effects of PPM1D silencing on global gene expression patterns and signaling pathways using oligonucleotide microarrays. We identified 1798 differentially expressed (at least a two-fold change) gene elements with functions related to key cellular processes, such as regulation of cell cycle, assembly of various intracellular structures and components, and regulation of signaling pathways and metabolic cascades. For instance, genes involved in apoptosis (NR4A1, RAB25, PLK1), formation of nucleosome structure (HIST1H2AC, HIST1H2BF, HIST1H2BO, HIST1H1D), and hormone related activities (NR4A1, ESR1, STC1) were among the differentially expressed genes. Overall, our findings suggest that PPM1D contributes to breast cancer associated phenotypic characteristics by directly or indirectly affecting several important cellular signaling pathways.
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