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Gene Review

Wnt1  -  wingless-type MMTV integration site family...

Rattus norvegicus

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Disease relevance of Wnt1

  • Ectopic expression of Wnt1 converts the PC12 neural crest-derived rat pheochromocytoma cell line from a round phenotype that express chromaffin markers to flat adherent cells (termed PC12/Wnt1) that do not express them [1].
  • The Wnt-1 inhibitory effect was not reversed by several other PKC inhibitors, by phorbol ester-induced down-regulation of PKC, or by pertussis toxin, which is known to inhibit another Wnt signaling pathway, the Wnt/Ca(2+) pathway [2].
  • Because expression of the Wnt-1 protooncogene results in induction of the glial-type glutamate transporter GLAST in PC12 neuron-like cells, we have evaluated the effect of Wnt-1-induced signaling on glutamate transporter expression in rat C6 glioma cells [3].

High impact information on Wnt1


Chemical compound and disease context of Wnt1


Biological context of Wnt1

  • These results demonstrate that the expression of some Wnt genes changes in PC12 cells upon conversion to the flat phenotype, and suggest that Wnt1 may modulate expression of several other Wnt genes in these cells [1].
  • Clonal lines exhibit elevated cytosolic and nuclear beta-cateninS37A and Tcf transcriptional activation, comparable to that elicited by Wnt-1 expression [7].
  • As ectopic expression of beta-cateninS37A only partially mimics Wnt-1 effects on Rat-1 cells, we conclude that Wnt-1 signaling elicits biochemical events that act in addition to beta-catenin/Tcf signaling to promote cell growth [7].
  • Here, we report that cells expressing Wnt-1 were resistant to cancer therapy-mediated apoptosis [4].
  • The Wnt-1 proto-oncogene regulates MAP kinase activation by multiple growth factors in PC12 cells [8].

Anatomical context of Wnt1

  • Differential expression of Wnt genes in normal and flat variants of PC12 cells, a cell line responsive to ectopic Wnt1 expression [1].
  • Beta-catenin/Tcf activation partially mimics the transforming activity of Wnt-1 in Rat-1 fibroblasts [7].
  • Wnt-1 and Wnt-3a exhibit redundancy in neural crest development [2].
  • However, both Wnt-1 or Wnt-3a inhibit nerve growth factor (NGF)-induced neurite outgrowth [2].
  • These data imply that the ability of embryonic spinal cord to act as an inducer of nephrogenesis may result from its production of Wnt-1 protein and suggest that a member of the Wnt gene family may be a mediator of renal epithelial morphogenesis in vivo [9].

Associations of Wnt1 with chemical compounds

  • The inhibition is reversed by the protein kinase C (PKC) inhibitor, bisindolylmaleimide-I, but it did not reverse Wnt-1-induced activation of the canonical Wnt pathway [2].
  • In spite of absent Wnt-1 expression, they retained their flat cell morphology, glutamate/aspartate transporter activity, increased neu mRNA levels and lack of both norepinephrine transporter activity and nerve growth factor-induced differentiation [10].
  • In this report we demonstrate that Wnt-1, a gene that encodes a secreted glycoprotein expressed in embryonic spinal cord, is capable of conferring nephron-inducing activity to fibroblast cell lines [9].
  • Wnt-1-expressing C6 cells may thus represent a novel in vitro system for studying GLT-1 transporter expression at the transcriptional and/or posttranscriptional levels [3].
  • The effect of Wnt-1 in activating NF-kappaB can be mimicked by inhibition of glycogen synthase kinase-3beta (GSK-3beta) with lithium or with a dominant negative GSK-3beta [11].

Regulatory relationships of Wnt1

  • We suggest that one or both of the GLT-1 RNA species induced by Wnt-1 either fail to be translated or yield abnormal translation products that are quickly degraded [3].
  • Wnt-1/PC12 cells also proliferate more rapidly and express increased levels of cyclin D1 [12].

Other interactions of Wnt1


  1. Differential expression of Wnt genes in normal and flat variants of PC12 cells, a cell line responsive to ectopic Wnt1 expression. Erdreich-Epstein, A., Shackleford, G.M. Growth Factors (1998) [Pubmed]
  2. Inhibition by Wnt-1 or Wnt-3a of nerve growth factor-induced differentiation of PC12 cells is reversed by bisindolylmaleimide-I but not by several other PKC inhibitors. Chou, A.H., Howard, B.D. Oncogene (2002) [Pubmed]
  3. Wnt signaling induces GLT-1 expression in rat C6 glioma cells. Palos, T.P., Zheng, S., Howard, B.D. J. Neurochem. (1999) [Pubmed]
  4. Wnt-1 signaling inhibits apoptosis by activating beta-catenin/T cell factor-mediated transcription. Chen, S., Guttridge, D.C., You, Z., Zhang, Z., Fribley, A., Mayo, M.W., Kitajewski, J., Wang, C.Y. J. Cell Biol. (2001) [Pubmed]
  5. Wnt-1 induces growth, cytosolic beta-catenin, and Tcf/Lef transcriptional activation in Rat-1 fibroblasts. Young, C.S., Kitamura, M., Hardy, S., Kitajewski, J. Mol. Cell. Biol. (1998) [Pubmed]
  6. Wnt-1 has multiple effects on the expression of glutamate transporters. Jimenez, A.L., Chou, A.H., Khadadadi, O., Palos, T.P., Howard, B.D. Neurochem. Int. (2003) [Pubmed]
  7. Beta-catenin/Tcf activation partially mimics the transforming activity of Wnt-1 in Rat-1 fibroblasts. Young, C.S., Masckauchan, T.N., Kitajewski, J. Differentiation (2003) [Pubmed]
  8. The Wnt-1 proto-oncogene regulates MAP kinase activation by multiple growth factors in PC12 cells. Pan, M.G., Wang, Y.H., Hirsch, D.D., Labudda, K., Stork, P.J. Oncogene (1995) [Pubmed]
  9. Induction of kidney epithelial morphogenesis by cells expressing Wnt-1. Herzlinger, D., Qiao, J., Cohen, D., Ramakrishna, N., Brown, A.M. Dev. Biol. (1994) [Pubmed]
  10. The induction of ret by Wnt-1 in PC12 cells is atypically dependent on continual Wnt-1 expression. Zheng, S., Ramachandran, B., Haigh, J.R., Palos, T.P., Steger, K., Howard, B.D. Oncogene (1996) [Pubmed]
  11. Wnt-1 dependent activation of the survival factor NF-kappaB in PC12 cells. Bournat, J.C., Brown, A.M., Soler, A.P. J. Neurosci. Res. (2000) [Pubmed]
  12. Altered expression of helix-loop-helix transcriptional regulators and cyclin D1 in Wnt-1-transformed PC12 cells. Issack, P.S., Ziff, E.B. Cell Growth Differ. (1998) [Pubmed]
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