Literature DB >> 9422779

Structure, expression, and properties of an atypical protein kinase C (PKC3) from Caenorhabditis elegans. PKC3 is required for the normal progression of embryogenesis and viability of the organism.

S L Wu1, J Staudinger, E N Olson, C S Rubin.   

Abstract

Little is known about differential expression, functions, regulation, and targeting of "atypical" protein kinase C (aPKC) isoenzymes in vivo. We have cloned and characterized a novel cDNA that encodes a Caenorhabditis elegans aPKC (PKC3) composed of 597 amino acids. In post-embryonic animals, a 647-base pair segment of promoter/enhancer DNA directs transcription of the 3.6-kilobase pair pkc-3 gene and coordinates accumulation of PKC3 protein in approximately 85 muscle, epithelial, and hypodermal cells. These cells are incorporated into tissues involved in feeding, digestion, excretion, and reproduction. Mammalian aPKCs promote mitogenesis and survival of cultured cells. In contrast, C. elegans PKC3 accumulates in non-dividing, terminally differentiated cells that will not undergo apoptosis. Thus, aPKCs may control cell functions that are independent of cell cycle progression and programmed cell death. PKC3 is also expressed during embryogenesis. Ablation of PKC3 function by microinjection of antisense RNA into oocytes yields disorganized, developmentally arrested embryos. Thus, PKC3 is essential for viability. PKC3 is enriched in particulate fractions of disrupted embryos and larvae. Immunofluorescence microscopy revealed that PKC3 accumulates near cortical actin cytoskeleton/plasma membrane at the apical surface of intestinal cells and in embryonic cells. A candidate anchoring/targeting protein, which binds PKC3 in vitro, has been identified.

Entities:  

Mesh:

Substances:

Year:  1998        PMID: 9422779     DOI: 10.1074/jbc.273.2.1130

Source DB:  PubMed          Journal:  J Biol Chem        ISSN: 0021-9258            Impact factor:   5.157


  9 in total

Review 1.  Regulation of the ABC kinases by phosphorylation: protein kinase C as a paradigm.

Authors:  Alexandra C Newton
Journal:  Biochem J       Date:  2003-03-01       Impact factor: 3.857

Review 2.  The extended protein kinase C superfamily.

Authors:  H Mellor; P J Parker
Journal:  Biochem J       Date:  1998-06-01       Impact factor: 3.857

3.  Bazooka and atypical protein kinase C are required to regulate oocyte differentiation in the Drosophila ovary.

Authors:  D N Cox; S A Seyfried; L Y Jan; Y N Jan
Journal:  Proc Natl Acad Sci U S A       Date:  2001-12-04       Impact factor: 11.205

4.  DLG-1 is a MAGUK similar to SAP97 and is required for adherens junction formation.

Authors:  B L Firestein; C Rongo
Journal:  Mol Biol Cell       Date:  2001-11       Impact factor: 4.138

5.  Binding to PKC-3, but not to PAR-3 or to a conventional PDZ domain ligand, is required for PAR-6 function in C. elegans.

Authors:  Jin Li; Heon Kim; Donato G Aceto; Jeffrey Hung; Shinya Aono; Kenneth J Kemphues
Journal:  Dev Biol       Date:  2010-02-01       Impact factor: 3.582

6.  A Novel Conserved Domain Mediates Dimerization of Protein Kinase D (PKD) Isoforms: DIMERIZATION IS ESSENTIAL FOR PKD-DEPENDENT REGULATION OF SECRETION AND INNATE IMMUNITY.

Authors:  Clara Aicart-Ramos; Sophia Dan Qing He; Marianne Land; Charles S Rubin
Journal:  J Biol Chem       Date:  2016-09-23       Impact factor: 5.157

7.  Drosophila atypical protein kinase C associates with Bazooka and controls polarity of epithelia and neuroblasts.

Authors:  A Wodarz; A Ramrath; A Grimm; E Knust
Journal:  J Cell Biol       Date:  2000-09-18       Impact factor: 10.539

8.  Developmental basis for intestinal barrier against the toxicity of graphene oxide.

Authors:  Mingxia Ren; Li Zhao; Xuecheng Ding; Natalia Krasteva; Qi Rui; Dayong Wang
Journal:  Part Fibre Toxicol       Date:  2018-06-22       Impact factor: 9.400

Review 9.  aPKC in neuronal differentiation, maturation and function.

Authors:  Sophie M Hapak; Carla V Rothlin; Sourav Ghosh
Journal:  Health Psychol Behav Med       Date:  2019-09-23
  9 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.