ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010
Role of the PI3-kinase signaling pathway in trafficking of the surfactant protein A receptor P63 (CKAP4) on type II pneumocytes.
Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Surfactant proteins A and D nucleotide variants: association with retinal vascular disease.Pediatric research · 2026Article
- A network map of cytoskeleton-associated protein 4 (CKAP4) mediated signaling pathway in cancer.Journal of cell communication and signaling · 2023Article
- Repurpose but also (nano)-reformulate! The potential role of nanomedicine in the battle against SARS-CoV2.Journal of controlled release : official journal of the Controlled Release Society · 2021Review
- Neurobiochemical Cross-talk Between COVID-19 and Alzheimer's Disease.Molecular neurobiology · 2021Review
- From Anti-SARS-CoV-2 Immune Responses to COVID-19 via Molecular Mimicry.Antibodies (Basel, Switzerland) · 2020Article
- Cytoskeleton-Associated Protein 4, a Promising Biomarker for Tumor Diagnosis and Therapy.Frontiers in molecular biosciences · 2020Review
- Serum cytoskeleton-associated protein 4 as a biomarker for the diagnosis of hepatocellular carcinoma.OncoTargets and therapy · 2019Article
- The Dickkopf1-cytoskeleton-associated protein 4 axis creates a novel signalling pathway and may represent a molecular target for cancer therapy.British journal of pharmacology · 2017Review
- CKAP4 is a Dickkopf1 receptor and is involved in tumor progression.The Journal of clinical investigation · 2016Article
- How many lives does CLIMP-63 have?Biochemical Society transactions · 2015Review
- Alteration in the Wnt microenvironment directly regulates molecular events leading to pulmonary senescence.Aging cell · 2014Article
- Article
- Characterization of the Niemann-Pick C pathway in alveolar type II cells and lamellar bodies of the lung.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Antiproliferative factor regulates connective tissue growth factor (CTGF/CCN2) expression in T24 bladder carcinoma cells.Molecular biology of the cell · 2012Article
- Surfactant and its role in the pathobiology of pulmonary infection.Microbes and infection · 2012Review
- Membrane Trafficking of Collecting Duct Water Channel Protein AQP2 Regulated by Akt/AS160.Electrolyte & blood pressure : E & BP · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Surfactant protein A (SP-A) plays an important role in the maintenance of lung lipid homeostasis. Previously, an SP-A receptor, P63 (CKAP4), on type II pneumocyte plasma membranes (PM) was identified by chemical cross-linking techniques. An antibody to P63 blocked the specific binding of SP-A to pneumocytes and the ability of SP-A to regulate surfactant secretion. The current report shows that another biological activity of SP-A, the stimulation of surfactant uptake by pneumocytes, is inhibited by P63 antibody. cAMP exposure resulted in enrichment of P63 on the cell surface as shown by stimulation of SP-A binding, enhanced association of labeled P63 antibody with type II cells, and promotion of SP-A-mediated liposome uptake, all of which were inhibited by competing P63 antibody. Incubation of A549 and type II cells with SP-A also increased P63 localization on the PM. The phosphatidylinositol 3-kinase (PI3-kinase) signaling pathway was explored as a mechanism for the transport of this endoplasmic reticulum (ER)-resident protein to the PM. Treatment with LY-294002, an inhibitor of the PI3-kinase pathway, prevented the SP-A-induced PM enrichment of P63. Exposure of pneumocytes to SP-A or cAMP activated Akt (PKB). Blocking either PI3-kinase or Akt altered SP-A-mediated lipid turnover. The data demonstrate an important role for the PI3-kinase-Akt pathway in intracellular transport of P63. The results add to the growing body of evidence that P63 is critical for SP-A receptor-mediated interactions with type II pneumocytes and the resultant regulation of surfactant turnover.
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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.