ArticleMolecular and cellular biology2000
Atypical protein kinases Clambda and -zeta associate with the GTP-binding protein Cdc42 and mediate stress fiber loss.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 83 citations in OpenAlex.
- The Dual Roles of the Atypical Protein Kinase Cs in Cancer.Cancer cell · 2019Review
- Article
- Def-6, a novel regulator of small GTPases in podocytes, acts downstream of atypical protein kinase C (aPKC) λ/ι.The American journal of pathology · 2013Article
- Signal mechanisms underlying low-dose endothelial monocyte-activating polypeptide-II-induced opening of the blood-tumor barrier.Journal of molecular neuroscience : MN · 2012Article
- Protein kinase Cι expression and oncogenic signaling mechanisms in cancer.Journal of cellular physiology · 2011Review
- PRKC-ζ Expression Promotes the Aggressive Phenotype of Human Prostate Cancer Cells and Is a Novel Target for Therapeutic Intervention.Genes & cancer · 2010Article
- RHOA and PRKCZ control different aspects of cell motility in pancreatic cancer metastatic clones.Molecular cancer · 2010Article
- Protein kinase Ciota is required for pancreatic cancer cell transformed growth and tumorigenesis.Cancer research · 2010Article
- Atypical protein kinase C activity is required for extracellular matrix degradation and invasion by Src-transformed cells.Journal of cellular physiology · 2009Article
- Protein kinase C iota: human oncogene, prognostic marker and therapeutic target.Pharmacological research · 2007Review
- Essential role of protein kinase C zeta in transducing a motility signal induced by superoxide and a chemotactic peptide, fMLP.The Journal of cell biology · 2007Article
- The formin mDia regulates GSK3beta through novel PKCs to promote microtubule stabilization but not MTOC reorientation in migrating fibroblasts.Molecular biology of the cell · 2006Article
- Mosaic Eyes is a novel component of the Crumbs complex and negatively regulates photoreceptor apical size.Development (Cambridge, England) · 2006Article
- mTOR-independent translational control of the extrinsic cell death pathway by RalA.Molecular and cellular biology · 2006Article
- Protein kinase Ciota is required for Ras transformation and colon carcinogenesis in vivo.The Journal of cell biology · 2004Article
- Atypical protein kinase C (PKCzeta/lambda) is a convergent downstream target of the insulin-stimulated phosphatidylinositol 3-kinase and TC10 signaling pathways.The Journal of cell biology · 2004Article
- Phosphorylation of critical serine residues in Gem separates cytoskeletal reorganization from down-regulation of calcium channel activity.Molecular and cellular biology · 2004Article
- Regulation of type II transforming-growth-factor-beta receptors by protein kinase C iota.The Biochemical journal · 2003Article
- Small GTP-binding protein TC10 differentially regulates two distinct populations of filamentous actin in 3T3L1 adipocytes.Molecular biology of the cell · 2002Article
- PC phosphorylation increases the ability of AFAP-110 to cross-link actin filaments.Molecular biology of the cell · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Both the Rho family of low-molecular-weight GTP-binding proteins and protein kinases C (PKCs) mediate responses to a variety of extracellular and intracellular signals. They share many downstream targets, including remodeling of the actin cytoskeleton, activation of p70(S6) kinase and c-jun N-terminal kinase (JNK), and regulation of transcription and cell proliferation. We therefore investigated whether Rho family GTP-binding proteins bind to PKCs. We found that Cdc42 associates with atypical PKCs (aPKCs) PKCzeta and -lambda in a GTP-dependent manner. The regulatory domain of the aPKCs mediates the interaction. Expression of activated Cdc42 results in the translocation of PKClambda from the nucleus into the cytosol, and Cdc42 and PKClambda colocalize at the plasma membrane and in the cytoplasm. Expression of activated Cdc42 leads to a loss of stress fibers, as does overexpression of either the wild type or an activated form of PKClambda. Kinase-dead PKClambda and -zeta constructs acted as dominant negatives and restored stress fibers in cells expressing the activated V12 Cdc42 mutant, indicating that Cdc42-dependent loss of stress fibers requires aPKCs. Kinase-dead PKClambda and -zeta and dominant-negative N17 Cdc42 also blocked Ras-induced loss of stress fibers, suggesting that this pathway may also be important for Ras-dependent cytoskeletal changes. N17 Rac did not block Ras-induced loss of stress fibers, nor did kinase-dead PKClambda block V12 Rac-stimulated loss of stress fibers. These results indicate that Cdc42 and Rac use different pathways to regulate stress fibers.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.