| Title | The product of par-4, a gene induced during apoptosis, interacts selectively with the atypical isoforms of protein kinase C. |
| Publication Type | Journal Article |
| Year of Publication | 1996 |
| Authors | Diaz-Meco MT, Municio MM, Frutos S, Sanchez P, Lozano J, Sanz L, Moscat J |
| Journal | Cell |
| Volume | 86 |
| Issue | 5 |
| Pagination | 777-86 |
| Date Published | 1996 Sep 06 |
| ISSN | 0092-8674 |
| Keywords | 3T3 Cells, Amino Acid Sequence, Animals, Apoptosis, Apoptosis Regulatory Proteins, Bacterial Proteins, Base Sequence, Carrier Proteins, Cell Line, Chlorocebus aethiops, Cloning, Molecular, Enzyme Inhibitors, Humans, Intracellular Signaling Peptides and Proteins, Isoenzymes, Mice, Molecular Sequence Data, Promoter Regions, Genetic, Protein Binding, Protein Kinase C, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-mos, Proto-Oncogene Proteins c-raf, Recombinant Fusion Proteins, Sequence Alignment, Sequence Homology, Amino Acid, Serine Endopeptidases, Zinc Fingers |
| Abstract | The atypical PKCs are involved in a number of important cellular functions, including cell proliferation. We report here that the product of the par-4 gene specifically interacts with the regulatory domains of zeta PKC and lambda/LPKC, which dramatically inhibits their enzymatic activity. This is particularly challenging, because expression of par-4 has been shown to correlate with growth inhibition and apoptosis. Results are shown here demonstrating that the expression of par-4 in NIH-3T3 cells induces morphological changes typical of apoptosis, which are abrogated by cotransfection of either wild-type zeta PKC or lambda/LPKC, but not by their respective kinase-inactive mutants. These findings support a role for the atypical PKC subspecies in the control of cell growth and survival. |
| DOI | 10.1016/s0092-8674(00)80152-x |
| Alternate Journal | Cell |
| PubMed ID | 8797824 |
Related Faculty:
Maria Diaz-Meco Conde, Ph.D.