ArticleThe Journal of biological chemistry2011
Control of protein kinase C activity, phorbol ester-induced cytoskeletal remodeling, and cell survival signals by the scaffolding protein SSeCKS/GRAVIN/AKAP12.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- PTEN-regulated PI3K-p110 and AKT isoform plasticity controls metastatic prostate cancer progression.Oncogene · 2024Article
- Metastasis suppressor genes in clinical practice: are they druggable?Cancer metastasis reviews · 2023Review
- Article
- Targeted disruption of PKC from AKAP signaling complexes.RSC chemical biology · 2021Article
- Neuregulin‑1: An underlying protective force of cardiac dysfunction in sepsis (Review).Molecular medicine reports · 2020Review
- Absence of gravin-mediated signaling inhibits development of high-fat diet-induced hyperlipidemia and atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2019Article
- Neuregulin‑1 protects cardiac function in septic rats through multiple targets based on endothelial cells.International journal of molecular medicine · 2019Article
- SSeCKS/Akap12 suppresses metastatic melanoma lung colonization by attenuating Src-mediated pre-metastatic niche crosstalk.Oncotarget · 2018Article
- Metastasis suppressors: functional pathways.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- SSeCKS/AKAP12 scaffolding functions suppress B16F10-induced peritoneal metastasis by attenuating CXCL9/10 secretion by resident fibroblasts.Oncotarget · 2017Article
- Scaffolding during the cell cycle by A-kinase anchoring proteins.Pflugers Archiv : European journal of physiology · 2015Review
- Article
- AKAP signaling complexes: pointing towards the next generation of therapeutic targets?Trends in pharmacological sciences · 2013Review
- Article
- Enhanced cardiac function in Gravin mutant mice involves alterations in the β-adrenergic receptor signaling cascade.PloS one · 2013Article
- Suppression of tumor and metastasis progression through the scaffolding functions of SSeCKS/Gravin/AKAP12.Cancer metastasis reviews · 2012Review
- Pivotal Role of AKAP12 in the Regulation of Cellular Adhesion Dynamics: Control of Cytoskeletal Architecture, Cell Migration, and Mitogenic Signaling.Journal of signal transduction · 2012Article
- Physiologic and pathophysiologic roles of AKAP12.Science progressArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The product of the SSeCKS/GRAVIN/AKAP12 gene ("SSeCKS") is a major protein kinase (PK) C substrate that exhibits tumor- and metastasis-suppressing activity likely through its ability to scaffold multiple signaling mediators such as PKC, PKA, cyclins, calmodulin, and Src. Although SSeCKS and PKCα bind phosphatidylserine, we demonstrate that phosphatidylserine-independent binding of PKC by SSeCKS is facilitated by two homologous SSeCKS motifs, EG(I/V)(T/S)XWXSFK(K/R)(M/L)VTP(K/R)K(K/R)X(K/R)XXXEXXXE(E/D) (amino acids 592-620 and 741-769). SSeCKS binding to PKCα decreased kinase activity and was dependent on the two PKC-binding motifs. SSeCKS scaffolding of PKC was increased in confluent cell cultures, correlating with significantly increased SSeCKS protein levels and decreased PKCα activity, suggesting a role for SSeCKS in suppressing PKC activation during contact inhibition. SSeCKS-null mouse embryo fibroblasts displayed increased relative basal and phorbol ester (phorbol 12-myristate 13-acetate)-induced PKC activity but were defective in phorbol 12-myristate 13-acetate-induced actin cytoskeletal reorganization and cell shape change; these responses could be rescued by the forced expression of full-length SSeCKS but not by an SSeCKS variant deleted of its PKC-binding domains. Finally, the PKC binding sites in SSeCKS were required to restore cell rounding and/or decreased apoptosis in phorbol ester-treated LNCaP, LNCaP-C4-2, and MAT-LyLu prostate cancer cells. Thus, PKC-mediated remodeling of the actin cytoskeleton is likely regulated by the ability of SSeCKS to control PKC signaling and activity through a direct scaffolding function.
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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 OpenQuestion graph.