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)



Gene Review

Prkci  -  protein kinase C, iota

Mus musculus

Synonyms: 2310021H13Rik, AI427505, Atypical protein kinase C-lambda/iota, PKClambda, Pkci, ...
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.

High impact information on Prkci

  • In spite of the loss of adherens junctions in the neuroepithelium of conditional aPKClambda knockout mice, neurons were produced at a normal rate [1].
  • In conditional aPKClambda knockout mice, neuroepithelial cells of the neocortical region lost aPKClambda protein at embryonic day 15 and demonstrated a loss of adherens junctions, retraction of apical processes and impaired interkinetic nuclear migration that resulted in disordered neuroepithelial tissue architecture [1].
  • These persistent spot-like AJs in aPKClambda-expressing cells contain all TJ membrane proteins and PAR-3, indicating that aPKC kinase activity is not required for their translocation to these premature junctional complexes but is indispensable for their further differentiation into belt-like AJs and TJs [2].
  • Immunofluorescence analysis revealed that PAR-3 and aPKClambda translocate to cell-cell contact regions later than the formation of the primordial spot-like adherens junctions (AJs) containing E-cadherin and ZO-1 [2].
  • Consistently, the expression of a dominant-negative mutant of aPKClambda (aPKClambdakn) in wound healing cells does not inhibit the formation of the spot-like AJs; rather, it blocks their development into belt-like AJs [2].

Anatomical context of Prkci

  • These results indicate that the expression of aPKClambda in differentiating photoreceptors is required for total retinal lamination [3].

Other interactions of Prkci


Analytical, diagnostic and therapeutic context of Prkci

  • To elucidate the functions of aPKClambda, one out of two aPKC members, in mouse neocortical neurogenesis, a Nestin-Cre mediated conditional gene targeting system was employed [1].


  1. Inactivation of aPKC{lambda} results in the loss of adherens junctions in neuroepithelial cells without affecting neurogenesis in mouse neocortex. Imai, F., Hirai, S., Akimoto, K., Koyama, H., Miyata, T., Ogawa, M., Noguchi, S., Sasaoka, T., Noda, T., Ohno, S. Development (2006) [Pubmed]
  2. aPKC kinase activity is required for the asymmetric differentiation of the premature junctional complex during epithelial cell polarization. Suzuki, A., Ishiyama, C., Hashiba, K., Shimizu, M., Ebnet, K., Ohno, S. J. Cell. Sci. (2002) [Pubmed]
  3. Function of atypical protein kinase C lambda in differentiating photoreceptors is required for proper lamination of mouse retina. Koike, C., Nishida, A., Akimoto, K., Nakaya, M.A., Noda, T., Ohno, S., Furukawa, T. J. Neurosci. (2005) [Pubmed]
WikiGenes - Universities