<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>144(3)</volume><submitter>Uberall F</submitter><pubmed_abstract>Expression of transforming Ha-Ras L61 in NIH3T3 cells causes profound morphological alterations which include a disassembly of actin stress fibers. The Ras-induced dissolution of actin stress fibers is blocked by the specific PKC inhibitor GF109203X at concentrations which inhibit the activity of the atypical aPKC isotypes lambda and zeta, whereas lower concentrations of the inhibitor which block conventional and novel PKC isotypes are ineffective. Coexpression of transforming Ha-Ras L61 with kinase-defective, dominant-negative (DN) mutants of aPKC-lambda and aPKC-zeta, as well as antisense constructs encoding RNA-directed against isotype-specific 5' sequences of the corresponding mRNA, abrogates the Ha-Ras-induced reorganization of the actin cytoskeleton. Expression of a kinase-defective,</pubmed_abstract><journal>The Journal of cell biology</journal><pagination>413-25</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2132909</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Evidence that atypical protein kinase C-lambda and atypical protein kinase C-zeta participate in Ras-mediated reorganization of the F-actin cytoskeleton.</pubmed_title><pmcid>PMC2132909</pmcid><pubmed_authors>Maly K</pubmed_authors><pubmed_authors>Grunicke HH</pubmed_authors><pubmed_authors>Villunger A</pubmed_authors><pubmed_authors>Mwanjewe J</pubmed_authors><pubmed_authors>Baier G</pubmed_authors><pubmed_authors>Hellbert K</pubmed_authors><pubmed_authors>Spitaler M</pubmed_authors><pubmed_authors>Kampfer S</pubmed_authors><pubmed_authors>Uberall F</pubmed_authors><pubmed_authors>Baier-Bitterlich G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Evidence that atypical protein kinase C-lambda and atypical protein kinase C-zeta participate in Ras-mediated reorganization of the F-actin cytoskeleton.</name><description>Expression of transforming Ha-Ras L61 in NIH3T3 cells causes profound morphological alterations which include a disassembly of actin stress fibers. The Ras-induced dissolution of actin stress fibers is blocked by the specific PKC inhibitor GF109203X at concentrations which inhibit the activity of the atypical aPKC isotypes lambda and zeta, whereas lower concentrations of the inhibitor which block conventional and novel PKC isotypes are ineffective. Coexpression of transforming Ha-Ras L61 with kinase-defective, dominant-negative (DN) mutants of aPKC-lambda and aPKC-zeta, as well as antisense constructs encoding RNA-directed against isotype-specific 5' sequences of the corresponding mRNA, abrogates the Ha-Ras-induced reorganization of the actin cytoskeleton. Expression of a kinase-defective,</description><dates><release>1999-01-01T00:00:00Z</release><publication>1999 Feb</publication><modification>2025-04-05T08:52:02.299Z</modification><creation>2019-06-06T15:54:03Z</creation></dates><accession>S-EPMC2132909</accession><cross_references><pubmed>9971737</pubmed><doi>10.1083/jcb.144.3.413</doi></cross_references></HashMap>