Library

X
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
    JunB does not inhibit the induction of c-Jun during the retinoic acid induced differentiation of F9 cells (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 193 (1992), S. 193-198 
    Details
    ISSN: 0002-9106
    Keywords: AP-1 ; Embryonial Carcinoma ; Intermediate Filament ; Keratin ; Laminin ; Plasminogen activator ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: JunB, a member of the jun gene family of transcription factors, is distinguished from c-Jun by its differential activity on certain arrangements of promoter regulatory elements and the ability of JunB to inhibit the action of cJun in both transforming and trans-activating assays. We have tested the potential negative regulatory role of JunB during the retinoic acid induced differentiation of F9 murine embryonal carcinoma cells. Constitutive expression of high levels of JunB in F9 cells failed to inhibit the differentiation dependent induction of c-Jun or the coincident expression of differentiation markers keratin 8 and 18, tissue plasminogen activator, and laminin Bl. Among these marker genes, keratin 18, has been shown to contain an AP-1 binding site, TGA(C/G)TCA, which is essential for high level, differentiation dependent expression and which is transactivated by Jun and Fos proteins. These results suggest that JunB does not play a major negative or positive regulatory role during the retinoic acid induced differentiation of F9 cells.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1001930211
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Parent-specific expression of a human keratin 18/β-galactosidase fusion gene in transgenic mice (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 195 (1992), S. 100-112 
    Details
    ISSN: 0002-9106
    Keywords: Genomic imprinting ; LacZ reporter gene ; Cytokeratins ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Insertion of a human keratin 18 (K18)-bacterial β-galactosidase (LacZ) fusion gene into mice has led to a unique transgenic line in which expression of the transgene is subject to unusual germ line-specific, genomic imprinting effects. Fetal expression of the LacZ reporter gene depends on the gender of the transmitting parent, with appropriate expression in liver after maternal inheritance, and ectopic expression in retina and mesodermal tissues after paternal inheritance. This tissue-specific imprinting pattern is superimposed upon a basic expression pattern which is unaffected by parental inheritance. Insertion of the transgene has led to a recessive-lethal phenotype, with no parent-of-origin effects on viability, suggesting that the transgene has not inserted into an imprinted region of the genome. HpaII and HhaI methylation sensitive restriction sites within the bacterial LacZ reporter gene are completely methylated when activity of the maternally inherited transgene is detected in the fetal liver, and not methylated when the paternally inherited transgene is silent. Thus DNA methylation of LacZ is correlated with maternal inheritance and may be implicated in the genomic imprinting mechanism as others have suggested. However, in contrast to the commonly found correlation of expression and low DNA methylation, the LacZ gene was expressed in fetal liver when fully methylated. This result may imply the existence of negative regulatory activities that recognize the unmethylated LacZ gene. © 1992 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1001950204
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...