Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Genetics 35 (2001), S. 209-241 
    ISSN: 0066-4197
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology
    Notes: Abstract The development of cancer requires multiple genetic alterations perturbing distinct cellular pathways. In human cancers, these alterations often arise owing to mutations in tumor-suppressor genes whose normal function is to either inhibit the proliferation, apoptosis, or differentiation of cells, or maintain their genomic integrity. Mouse models for tumor suppressors frequently provide definitive evidence for the antitumorigenic functions of these genes. In addition, animal models permit the identification of previously unsuspected roles of these genes in development and differentiation. The availability of null and tissue-specific mouse mutants for tumor-suppressor genes has greatly facilitated our understanding of the mechanisms leading to cancer. In this review, we describe mouse models for tumor-suppressor genes.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 169 (1999), S. 0 
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: Apoptosis, or programed cell death (PCD), is che subject of much current investigative interest. Developing embryos and many adult organ systems require che tight coupling of cellular proliferation and PCD Co ensure proper organogenesis and optimal tissue function. Over the past decade, our knowledge of the genetic basis underlying the execution of apoptosis in mammals has progressed enormously, thanks largely to groundbreaking studies performed in the nematode Caenorhabditis elegans. In contrast, the components of the signaling apparatus that links che various death stimuli and the receptors they stimulate to the execution mechanism remain relatively unknown, it is only in the past 4 years that studies of signal transduction via members of the tumor necrosis factor (TNF) receptor superfamily have identified a plethora of novel, signaling proteins, including molecules that are directly involved in apoptosis signaling, and others that regulate che induction of cell death. This two-part review focuses on the biology of apoptosis and signaling through members of the TNF receptor superfamily as revealed by the study of gene-targeted “knockout” mice. These genetic mutant animals are invaluable tools not only for confirming or refuting a proposed function of a particular gene in an in vivo setting, but also for uncovering novel functions for a gene that were not anticipated from conventional in vitro experiments. In the field of apoptosis, as for many other areas of biomedical research, knockout mice and cell lines can be used as models for studying human disease, with the ultimate goal of developing therapeutic strategies.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Programmed cell death is a fundamental requirement for embryogenesis, organ metamorphosis and tissue homeostasis. In mammals, release of mitochondrial cytochrome c leads to the cytosolic assembly of the apoptosome—a caspase activation complex involving Apaf1 and caspase-9 that induces ...
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] SAPKs/JNKs are activated by the phosphorylation of tyrosine and threonine residues, which is catalysed by the dual-specificity kinase Sekl (MKK4 or JNKK)7"9. To examine the function of the Sekl-regulated stress signalling pathway, we generated mouse ES cell lines lacking sekl expression by using ...
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature genetics 16 (1997), S. 298-302 
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] To determine whether the effect of the Brcal5–6 mutation could be mitigated by altering p53 levels, the Brcal5–6 mutation was introduced into a p53 null background11. From double heterozygote Brcal5–6−/−: p53+/− intercrosses, no Brcal5–6+/−: ...
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    ISSN: 1573-9368
    Keywords: homologous recombination ; inducible nitric oxide synthase ; embryonic stem cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Gene targeting by double homologous recombination in murine embryonic stem (ES) cells is a powerful tool used to study the cellular consequences of specific genetic mutations. A typical targeting construct consists of a neomycin phosphotransferase (neo) gene flanked by genomic DNA fragments that are homologous to sequences in the target chromosomal locus. Homologous DNA fragments are typically cloned from a murine genomic DNA library. Here we describe an alternative approach whereby the inducible nitric oxide synthase (NOS2) gene locus is partially mapped and homologous DNA sequences obtained using a long-range PCR method. A 7 kb NOS2 amplicon is used to construct a targeting vector where theneo gene is flanked by PCR-derived homologous DNA sequences. The vector also includes a thymidine kinase (tk) negative-selectable marker gene. Following transfection into ES cells, the PCR-based targeting vector undergoes efficient homologous recombination into the NOS2 locus. Thus, PCR-based gene targeting can be a valuable alternative to the conventional cloning approach. It expedites the acquisition of homologous genomic DNA sequences and simplifies the construction of targeting plasmids by making use of defined cloning sites. This approach should result in substantial time and cost savings for appropriate homologous recombination projects.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of mammary gland biology and neoplasia 3 (1998), S. 431-445 
    ISSN: 1573-7039
    Keywords: BRCA1 ; BRCA2 ; PROLIFERATION ; TROPHOBLAST ; GASTRULATION ; CANCER
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In humans, the inheritance of mutations in thebreast cancer susceptibility genes BRCA1 and BRCA2increases the risk of developing breast and ovariancancer. To study their biological function and to create animal models for these cancer susceptibilitygenes, several strains of mice mutated in the homologousgenes Brca1 and Brca2 have been generated by genetargeting. Analyses of these “knock-out” mouse mutants have provided invaluableknowledge about the function of these genes. Brca1 andBrca2 null mutants are similar in phenotype: mutationsin both genes result in embryonic lethality and thedeveloping embryos show signs of a cellular proliferationdefect associated with activation of the p53 pathway.The significance of this activation, as well as the roleof these cancer susceptibility genes in DNA damage repair, is discussed.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...