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)
 

Links

 

Gene Review

DDX11  -  DEAD/H (Asp-Glu-Ala-Asp/His) box helicase 11

Homo sapiens

Synonyms: CHL1, CHL1-related protein 1, CHLR1, ChlR1, DEAD/H box protein 11, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of DDX11

  • Two of them, CHL1 and fls485, are located within or close to the uveal melanoma susceptibility locus UVM2 at 3p25 [1].
 

High impact information on DDX11

  • Human hCHLR expression is not extinguished during hemin-induced differentiation of the same cell line, which produces erythrocyte-like cells that continue to proliferate [2].
  • Prevention of neuronal cell death by neural adhesion molecules L1 and CHL1 [3].
  • The results demonstrate that the neural adhesion molecule L1 and its relative CHL1 are potential neuronal survival factors for neurons of the central nervous system [3].
  • The yeast Chl1 gene encodes a putative helicase that appears to be essential for normal chromosome transmission [4].
  • In addition, a comparison of the hCHLR gene sequences with available databases indicates that a large portion of these genes, including exons encoding two functional domains of the carboxyl-terminal region of these proteins, has been duplicated as part of a larger human telomeric repeat sequence found on many human chromosomes [4].
 

Chemical compound and disease context of DDX11

  • We investigated the expression and the subcellular localization of gp100 in lung tissue from patients with LAM and in human melanoma cell lines (Malme-3M, A2058, and CHL-1), and the relationship between this expression and cellular proliferation [5].
 

Biological context of DDX11

  • Chl1 and Ctf4 are required for damage-induced recombinations [6].
  • Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion [6].
 

Associations of DDX11 with chemical compounds

  • The levels of Chl1 and Ctf4 associated with chromatin increased considerably after exposure of the cells to MMS and phleomycin [6].
 

Analytical, diagnostic and therapeutic context of DDX11

References

  1. Tumor classification based on gene expression profiling shows that uveal melanomas with and without monosomy 3 represent two distinct entities. Tschentscher, F., Hüsing, J., Hölter, T., Kruse, E., Dresen, I.G., Jöckel, K.H., Anastassiou, G., Schilling, H., Bornfeld, N., Horsthemke, B., Lohmann, D.R., Zeschnigk, M. Cancer Res. (2003) [Pubmed]
  2. Characterization of putative human homologues of the yeast chromosome transmission fidelity gene, CHL1. Amann, J., Kidd, V.J., Lahti, J.M. J. Biol. Chem. (1997) [Pubmed]
  3. Prevention of neuronal cell death by neural adhesion molecules L1 and CHL1. Chen, S., Mantei, N., Dong, L., Schachner, M. J. Neurobiol. (1999) [Pubmed]
  4. Localization of chi1-related helicase genes to human chromosome regions 12p11 and 12p13: similarity between parts of these genes and conserved human telomeric-associated DNA. Amann, J., Valentine, M., Kidd, V.J., Lahti, J.M. Genomics (1996) [Pubmed]
  5. Markers of cell proliferation and expression of melanosomal antigen in lymphangioleiomyomatosis. Matsumoto, Y., Horiba, K., Usuki, J., Chu, S.C., Ferrans, V.J., Moss, J. Am. J. Respir. Cell Mol. Biol. (1999) [Pubmed]
  6. Chl1 and Ctf4 are required for damage-induced recombinations. Ogiwara, H., Ui, A., Lai, M.S., Enomoto, T., Seki, M. Biochem. Biophys. Res. Commun. (2007) [Pubmed]
 
WikiGenes - Universities