ArticleMolecular biology of the cell2001
Src family kinases are required for prolactin induction of cell proliferation.
Article in Molecular biology of the cell, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 106 citations in OpenAlex.
- Identification of conserved gene expression changes across common glomerular diseases by spatial transcriptomics.Journal of nephrology · 2025Article
- Aripiprazole alleviates the high prolactin levels induced by amisulpride via distinct molecular mechanisms: a network pharmacology and molecular docking study.BMC psychiatry · 2025Article
- Prolactin promotes crop epithelial proliferation of domestic pigeons (Columba livia) through the Hippo signaling pathway.Journal of animal science · 2023Article
- Fyn expression is associated with the response of patients with locally advanced uterine cervical squamous cell carcinoma to neoadjuvant chemotherapy.Molecular and clinical oncology · 2022Article
- Plectin promotes tumor formation by B16 mouse melanoma cells via regulation of Rous sarcoma oncogene activity.BMC cancer · 2022Article
- Orchestration of signaling by structural disorder in class 1 cytokine receptors.Cell communication and signaling : CCS · 2020Article
- Targeting Fyn Kinase in Alzheimer's Disease.Biological psychiatry · 2018Review
- Prolactin Biology and Laboratory Measurement: An Update on Physiology and Current Analytical Issues.The Clinical biochemist. Reviews · 2018Review
- Src tyrosyl phosphorylates cortactin in response to prolactin.Biochemical and biophysical research communications · 2015Article
- Article
- New insights in prolactin: pathological implications.Nature reviews. Endocrinology · 2015Review
- Prolactin Promotes Breast Cancer Cell Migration through Actin Cytoskeleton Remodeling.Frontiers in endocrinology · 2015Article
- Prolactin and growth hormone affect metaphase-II chromosomes in aging oocytes via cumulus cells using similar signaling pathways.Frontiers in genetics · 2015Article
- Article
- Fyn regulates adipogenesis by promoting PIKE-A/STAT5a interaction.Molecular and cellular biology · 2013Article
- Prolactin gene expression in primary central nervous system tumors.Journal of negative results in biomedicine · 2013Article
- Life stage differences in mammary gland gene expression profile in non-human primates.Breast cancer research and treatment · 2012Article
- Prolactin-stimulated activation of ERK1/2 mitogen-activated protein kinases is controlled by PI3-kinase/Rac/PAK signaling pathway in breast cancer cells.Cellular signalling · 2011Article
- Fyn: a novel molecular target in cancer.Cancer · 2010Review
- SRC family kinases are required for limb trajectory selection by spinal motor axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prolactin (PRL) is a pleiotropic cytokine promoting cellular proliferation and differentiation. Because PRL activates the Src family of tyrosine kinases (SFK), we have studied the role of these kinases in PRL cell proliferation signaling. PRL induced [(3)H]thymidine incorporation upon transient transfection of BaF-3 cells with the PRL receptor. This effect was inhibited by cotransfection with the dominant negative mutant of c-Src (K>A295/Y>F527, SrcDM). The role of SFK in PRL-induced proliferation was confirmed in the BaF-3 PRL receptor-stable transfectant, W53 cells, where PRL induced Fyn and Lyn activation. The SFK-selective inhibitors PP1/PP2 and herbimycin A blocked PRL-dependent cell proliferation by arresting the W53 cells in G1, with no evident apoptosis. In parallel, PP1/PP2 inhibited PRL induction of cell growth-related genes c-fos, c-jun, c-myc, and odc. These inhibitors have no effect on PRL-mediated activation of Ras/Mapk and Jak/Start pathways. In contrast, they inhibited the PRL-dependent stimulation of the SFKs substrate Sam68, the phosphorylation of the tyrosine phosphatase Shp2, and the PI3K-dependent Akt and p70S6k serine kinases. Consistently, transient expression of SrcDM in W53 cells also blocked PRL activation of Akt. These results demonstrate that activation of SFKs is required for cell proliferation induced by PRL.
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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.