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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Retroviridae

 
 
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Disease relevance of Retroviridae

 

Psychiatry related information on Retroviridae

 

High impact information on Retroviridae

  • To determine whether Rb functions in these processes in a cell-autonomous manner, we used a replication-incompetent retrovirus encoding Cre recombinase to inactivate the Rb1(lox) allele in individual retinal progenitor cells in vivo [9].
  • A natural allele of Nxf1 suppresses retrovirus insertional mutations [10].
  • Insertional mutagenesis by the latent retrovirus was synergistic with loss of Cdkn2a expression, as indicated by a marked acceleration in the development of both myeloid and lymphoid tumors [11].
  • An ex vivo approach to gene therapy for familial hypercholesterolaemia (FH) has been developed in which the recipient is transplanted with autologous hepatocytes that are genetically corrected with recombinant retroviruses carrying the LDL receptor [12].
  • Using a retrovirus construct modified to express BCR-ABL and MYC genes simultaneously, we show that dominant negative MYC suppressed transformation of primary mouse bone marrow pre-B cells by BCR-ABL [13].
 

Chemical compound and disease context of Retroviridae

 

Biological context of Retroviridae

 

Anatomical context of Retroviridae

 

Gene context of Retroviridae

  • When placed under the control of a retrovirus LTR, the clone was transcribed at levels comparable to that observed in cells transformed by SSV DNA [29].
  • Fibroblast cells overexpressing the LYAR cDNA from a retrovirus vector, though not phenotypically transformed in vitro, had increased ability to form tumors in nu/nu mice [30].
  • In addition, using a self-inactivating retrovirus luciferase reporter construct we showed that TGF-beta1 induces Smad4, which then binds to and activates the IL-10 promoter [31].
  • A retrovirus encoding polyoma middle T antigen has been used to infect a murine hemopoietic cell line (FDC-P1) dependent on either granulocyte-macrophage colony-stimulating factor (GM-CSF) or multipotential colony-stimulating factor (Multi-CSF) [32].
  • Infection of TF-1 cells with a retrovirus containing a normal murine EpoR was able to restore both Epo-induced STAT5 activity and cellular proliferation [33].
 

Analytical, diagnostic and therapeutic context of Retroviridae

References

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