ArticleOncogene2007
The p85 regulatory subunit of PI3K mediates TSH-cAMP-PKA growth and survival signals.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 65 citations in OpenAlex.
- Development of Marine-Lenhart Syndrome during the Course of Acromegaly.Internal medicine (Tokyo, Japan) · 2026Article
- TSH upregulates CYP4B1 through the PI3K/AKT/CREB pathway to promote cardiac hypertrophy.Journal of endocrinological investigation · 2025Article
- Article
- Sex Hormones and Inflammation Role in Oral Cancer Progression: A Molecular and Biological Point of View.Journal of oncology · 2020Review
- p85α Inactivates MMP-2 and Suppresses Bladder Cancer Invasion by Inhibiting MMP-14 Transcription and TIMP-2 Degradation.Neoplasia (New York, N.Y.) · 2019Article
- Growth hormone and insulin-like growth factor 1 affect the severity of Graves' disease.Endocrinology, diabetes & metabolism case reports · 2017Article
- G protein-coupled receptors (GPCRs) That Signal via Protein Kinase A (PKA) Cross-talk at Insulin Receptor Substrate 1 (IRS1) to Activate the phosphatidylinositol 3-kinase (PI3K)/AKT Pathway.The Journal of biological chemistry · 2016Article
- PDE1C deficiency antagonizes pathological cardiac remodeling and dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- NF-κB Essential Modulator (NEMO) Is Critical for Thyroid Function.The Journal of biological chemistry · 2016Article
- Insulin Receptor Substrate 1, the Hub Linking Follicle-stimulating Hormone to Phosphatidylinositol 3-Kinase Activation.The Journal of biological chemistry · 2016Article
- Switch in signaling control of mTORC1 activity after oncoprotein expression in thyroid cancer cell lines.The Journal of clinical endocrinology and metabolism · 2014Article
- β-Arrestin-1 mediates thyrotropin-enhanced osteoblast differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- The p85 regulatory subunit of PI3K mediates cAMP-PKA and insulin biological effects on MCF-7 cell growth and motility.TheScientificWorldJournal · 2014Article
- Mechanism of sperm capacitation and the acrosome reaction: role of protein kinases.Asian journal of andrology · 2012Review
- PKA and GAB2 play central roles in the FSH signaling pathway to PI3K and AKT in ovarian granulosa cells.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Identification of microRNAs that mediate thyroid cell growth induced by TSH.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Overexpression of 14-3-3ζ in cancer cells activates PI3K via binding the p85 regulatory subunit.Oncogene · 2012Article
- Article
- A stress response pathway regulates DNA damage through β2-adrenoreceptors and β-arrestin-1.Nature · 2011Article
- Prion protein interaction with stress-inducible protein 1 enhances neuronal protein synthesis via mTOR.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phosphatidylinositol 3-kinase (PI3K) is necessary for thyroid stimulating hormone (TSH)-induced cell cycle progression. To determine the molecular mechanism linking PI3K to TSH, we have identified a serine residue in p85alpha(PI3K) phosphorylated by protein kinase A (PKA) in vitro and in vivo. Expression of an alanine mutant (p85A) abolished cyclic AMP/TSH-induced cell cycle progression and was lethal in thyroid cells (FRTL-5). The aspartic version of the p85alpha(PI3K) (p85D) inhibited apoptosis following TSH withdrawal. The p85alpha(PI3K) wild type not the p85A bound PKA regulatory subunit RIIbeta in cells stimulated with cAMP or TSH. The binding of the aspartic version of p85alpha(PI3K) to RIIbeta was independent of cAMP or TSH stimulation. Similarly, binding of PI3K to p21Ras and activation of AKT, a downstream PI3K target, were severely impaired in cells expressing the p85A mutant. Finally, we found that the catalytic activity of PI3K was stimulated by TSH in cells expressing the wild-type p85alpha(PI3K) but not in cells expressing p85A. This latter mutant did not affect the epidermal growth factor-stimulated PI3K activity. We suggest that (1) TSH-cAMP-induced PKA phosphorylates p85alpha(PI3K) at serine 83, (2) phosphorylated p85alpha(PI3K) binds RIIbeta-PKA and targets PKAII to the membrane, and (3) PI3K activity and p21Ras binding to PI3K increase and activate PI3K downstream targets. This pathway is essential for the transmission of TSH-cAMP growth signals.
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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.