ArticleCancer research2008
Loss of the SSeCKS/Gravin/AKAP12 gene results in prostatic hyperplasia.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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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
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Contribution of the -160C/A polymorphism in the E-cadherin promoter to cancer risk: a meta-analysis of 47 case-control studies.PloS one · 2012Pooled it
- A-Kinase-Anchoring Protein Subtypes Differentially Regulate GPCR Signaling and Function in Human Airway Smooth Muscle.American journal of respiratory cell and molecular biology · 2025Article
- AKAP12 Variant 1 Knockout Enhances Vascular Endothelial Cell Motility.Journal of vascular research · 2025Article
- Sex differences in the role of AKAP12 in behavioral function of middle-aged mice.Biology of sex differences · 2024Article
- Protein kinase A and local signaling in cancer.The Biochemical journal · 2024Review
- Transcriptomic Profiles of AKAP12 Deficiency in Mouse Corpus Callosum.Bioinformatics and biology insights · 2024Article
- 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
- AKAP12 ameliorates liver injury via targeting PI3K/AKT/PCSK6 pathway.Redox biology · 2022Article
- Exploring the ovine sperm transcriptome by RNAseq techniques. I Effect of seasonal conditions on transcripts abundance.PloS one · 2022Article
- Roles of A-kinase Anchor Protein 12 in Astrocyte and Oligodendrocyte Precursor Cell in Postnatal Corpus Callosum.Stem cell reviews and reports · 2021Article
- Whole-genome SNP markers reveal conservation status, signatures of selection, and introgression in Chinese Laiwu pigs.Evolutionary applications · 2021Article
- ARHGEF18/p114RhoGEF Coordinates PKA/CREB Signaling and Actomyosin Remodeling to Promote Trophoblast Cell-Cell Fusion During Placenta Morphogenesis.Frontiers in cell and developmental biology · 2021Article
- AKAP12 Supports Blood-Brain Barrier Integrity against Ischemic Stroke.International journal of molecular sciences · 2020Article
- Identification of single-nucleotide variants associated with susceptibility to Salmonella in pigs using a genome-wide association approach.BMC veterinary research · 2020Article
- AKAP12 deficiency impairs VEGF-induced endothelial cell migration and sprouting.Acta physiologica (Oxford, England) · 2020Article
- Disruption of AKAP-PKA Interaction Induces Hypercontractility With Concomitant Increase in Proliferation Markers in Human Airway Smooth Muscle.Frontiers in cell and developmental biology · 2020Article
- Akap12beta supports asymmetric heart development via modulating the Kupffer's vesicle formation in zebrafish.BMB reports · 2019Article
- A-kinase anchoring protein 12 is downregulated in human hepatocellular carcinoma and its deficiency in mice aggravates thioacetamide-induced liver injury.Oncology letters · 2018Article
- SSeCKS/Akap12 suppresses metastatic melanoma lung colonization by attenuating Src-mediated pre-metastatic niche crosstalk.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
SSeCKS/Gravin/AKAP12 (SSeCKS) is a kinase scaffolding protein that encodes metastasis-suppressor activity through the suppression of Src-mediated oncogenic signaling and vascular endothelial growth factor expression. SSeCKS expression is down-regulated in Src- and Ras-transformed fibroblasts, in human cancer cell lines and in several types of human cancer, including prostate. Normal human and mouse prostates express abundant SSeCKS in secretory epithelial cells and, to a lesser extent, in the surrounding mesenchyme. Here, we show that the loss of SSeCKS results in prostatic hyperplasia in the anterior and ventral lobes as well as increased levels of apoptosis throughout the prostate. Dysplastic foci were observed less frequently but were associated with the loss of E-cadherin staining and the loss of high molecular weight cytokeratin-positive basal epithelial cells. SSeCKS-null prostate tissues expressed significantly higher relative levels of AKT(poS473) compared with wild-type controls, suggesting that SSeCKS attenuates phosphatidylinositol-3-OH kinase signaling. The data suggest that SSeCKS-null mice have increased susceptibility for oncogenic transformation in the prostate.
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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.