ArticleMolecular endocrinology (Baltimore, Md.)2011
Adapter protein SH2B1beta binds filamin A to regulate prolactin-dependent cytoskeletal reorganization and cell motility.
Article in Molecular endocrinology (Baltimore, Md.), 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, 27 citations in OpenAlex.
- Centrosomal JAK2 Tyrosine Kinase Regulates Primary Cilia Length, Cell Proliferation, and Cilia Orientation During Cell Migration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Endogenous SH2B1 protein localizes to lamellipodia and filopodia: platinum replica electron-microscopy study.microPublication biology · 2025Article
- Prolactin-induced tyrosyl phosphorylation of PAK1 facilitates epithelial-mesenchymal transition.microPublication biology · 2024Article
- The nucleolar δ isoform of adapter protein SH2B1 enhances morphological complexity and function of cultured neurons.Journal of cell science · 2022Article
- ENC1 Facilitates Colorectal Carcinoma Tumorigenesis and Metastasis via JAK2/STAT5/AKT Axis-Mediated Epithelial Mesenchymal Transition and Stemness.Frontiers in cell and developmental biology · 2021Article
- Association of theNutrients · 2020Article
- SH2B1 promotes epithelial-mesenchymal transition through the IRS1/β-catenin signaling axis in lung adenocarcinoma.Molecular carcinogenesis · 2018Article
- The Dyslexia-susceptibility Protein KIAA0319 Inhibits Axon Growth Through Smad2 Signaling.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Growth hormone-releasing hormone receptor antagonists inhibit human gastric cancer through downregulation of PAK1-STAT3/NF-κB signaling.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Tyrosyl phosphorylated serine-threonine kinase PAK1 is a novel regulator of prolactin-dependent breast cancer cell motility and invasion.Advances in experimental medicine and biology · 2015Review
- SH2B1 regulation of energy balance, body weight, and glucose metabolism.World journal of diabetes · 2014Review
- Review
- RACK1 interacts with filamin-A to regulate plasma membrane levels of the cystic fibrosis transmembrane conductance regulator.American journal of physiology. Cell physiology · 2013Article
- PAK1 regulates breast cancer cell invasion through secretion of matrix metalloproteinases in response to prolactin and three-dimensional collagen IV.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Phosphorylation of the adaptor protein SH2B1β regulates its ability to enhance growth hormone-dependent macrophage motility.Journal of cell science · 2013Article
- Tyrosyl phosphorylated PAK1 regulates breast cancer cell motility in response to prolactin through filamin A.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Article
- Autocrine prolactin: an emerging market for homegrown (prolactin) despite the imports.Genes & development · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Prolactin (PRL) regulates cytoskeletal rearrangement and cell motility. PRL-activated Janus tyrosine kinase 2 (JAK2) phosphorylates the p21-activated serine-threonine kinase (PAK)1 and the Src homology 2 (SH2) domain-containing adapter protein SH2B1β. SH2B1β is an actin-binding protein that cross-links actin filaments, whereas PAK1 regulates the actin cytoskeleton by different mechanisms, including direct phosphorylation of the actin-binding protein filamin A (FLNa). Here, we have used a FLNa-deficient human melanoma cell line (M2) and its derivative line (A7) that stably expresses FLNa to demonstrate that SH2B1β and FLNa are required for maximal PRL-dependent cell ruffling. We have found that in addition to two actin-binding domains, SH2B1β has a FLNa-binding domain (amino acids 200-260) that binds directly to repeats 17-23 of FLNa. The SH2B1β-FLNa interaction participates in PRL-dependent actin rearrangement. We also show that phosphorylation of the three tyrosines of PAK1 by JAK2, as well as the presence of FLNa, play a role in PRL-dependent cell ruffling. Finally, we show that the actin- and FLNa-binding-deficient mutant of SH2B1β (SH2B1β 3Δ) abolished PRL-dependent ruffling and PRL-dependent cell migration when expressed along with PAK1 Y3F (JAK2 tyrosyl-phosphorylation-deficient mutant). Together, these data provide insight into a novel mechanism of PRL-stimulated regulation of the actin cytoskeleton and cell motility via JAK2 signaling through FLNa, PAK1, and SH2B1β. We propose a model for PRL-dependent regulation of the actin cytoskeleton that integrates our findings with previous studies.
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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 Socratic graph.