The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Granulocyte macrophage colony-stimulating factor and interleukin-3 regulate chemokine and chemokine receptor expression in bone marrow macrophages.

The beta-chemokine macrophage inflammatory protein-1 alpha (MIP-1alpha) and its associated receptors are involved in the regulation of pro-inflammatory and haemopoietic processes. This study was designed to investigate regulation of expression MIP-1alpha and its receptors by other haemopoietic cytokines. Murine bone marrow macrophages (BMM) were treated with or without GM-CSF or IL-3 and expression of MIP-1alpha, other chemokines and their receptors examined by Northern blotting. Receptor levels were also examined using Scatchard analysis and functional tests. Treatment of BMM with GM-CSF revealed a striking increase in MIP-1alpha mRNA levels, relative to untreated cells with a corresponding increase in MIP-1alpha protein. A similar increase in mRNA levels was found when BMM were treated with IL-3. An increase in the expression of three other beta-chemokines namely MIP-1beta, MCP-1 and MCP-3, was also found following treatment with GM-CSF or IL-3. We have additionally examined the expression of the known beta-chemokine receptors in BMM and observed an increase in CCR1 mRNA levels following treatment with GM-CSF and IL-3, but no change was seen in the level of CCR5 expression. The increase in CCR1 expression was reflected in an increase in the number of cell surface receptors for MIP-1alpha on the GM-CSF treated BMM and in an enhanced response of the GM-CSF treated BMM to CCR1 ligands. These data suggest that GM-CSF and IL-3 may be involved in mechanisms regulating expression levels of MIP-1alpha and its receptors.[1]

References

 
WikiGenes - Universities