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)
 

Editor

Share

Personal info

View

Links

  • Homologues
  • NCBI Gene
  • NCBI SNP
  • iHOP resource
  • SNPedia

Table of contents

About

Terms

 

Gene Review: 

tax-2  -  Protein TAX-2

Caenorhabditis elegans

 
 
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.
 

Psychiatry related information on tax-2

 

High impact information on tax-2

  • We show that mutations in tax-2 or tax-4 disrupt social feeding, and that tax-4 is required in several neurons for social feeding, including one or more of AQR, PQR and URX [2].
  • Some sensory neurons display axon outgrowth defects in tax-2 mutants [1].
  • TAX-2 and TAX-4 have been proposed to form a transduction channel for chemosensation and thermosensation, and tax-2 activity is required in the adult stage for normal chemotaxis to NaCl and odorants [3].
 

Biological context of tax-2

  • Several classes of mutants (dyf, daf-3, tax-4, and tax-2) that are defective in dauer formation at lower temperatures reverse their phenotypes at 27 degrees and form dauers constitutively [4].
 

Anatomical context of tax-2

  • The tax-2 and tax-4 genes of C. elegans encode two subunits of a cyclic nucleotide-gated channel that is required for chemosensation, thermosensation and normal axon outgrowth of some sensory neurons [3].
 

Associations of tax-2 with chemical compounds

  • NPR-1 activity in AQR, PQR and URX neurons seems to suppress social feeding by antagonizing signalling through a cyclic GMP-gated ion channel encoded by tax-2 and tax-4 [2].
 

Other interactions of tax-2

  • Here we show that, in tax-2 and tax-4 mutants, young larvae have superficially normal axons, but axon outgrowth resumes in inappropriate regions in late larval stages [3].

References

  1. A putative cyclic nucleotide-gated channel is required for sensory development and function in C. elegans. Coburn, C.M., Bargmann, C.I. Neuron (1996) [Pubmed]
  2. Antagonistic pathways in neurons exposed to body fluid regulate social feeding in Caenorhabditis elegans. Coates, J.C., de Bono, M. Nature (2002) [Pubmed]
  3. A cyclic nucleotide-gated channel inhibits sensory axon outgrowth in larval and adult Caenorhabditis elegans: a distinct pathway for maintenance of sensory axon structure. Coburn, C.M., Mori, I., Ohshima, Y., Bargmann, C.I. Development (1998) [Pubmed]
  4. Dauer formation induced by high temperatures in Caenorhabditis elegans. Ailion, M., Thomas, J.H. Genetics (2000) [Pubmed]
Contributions to this collaborative article are from individual authors of WikiGenes or mined by the WikiGenes Data Mining Engine from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
 
WikiGenes - Universities