ArticleMolecular and cellular biology2016
SPRED1 Interferes with K-ras but Not H-ras Membrane Anchorage and Signaling.
Article in Molecular and cellular biology, 2016. 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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Who cites it
18 citing papers in PubMed.
- Downregulation of SPRED1 drives keratinocyte hyperproliferation in psoriasis via activation of the ERK-RSK1 signaling axis.iScience · 2026Article
- The impact of RAS on cell differentiation in health and disease.The Biochemical journal · 2025Review
- The role of SPRED1 mutation in melanoma.European journal of medical research · 2025Review
- Identification of an H-Ras nanocluster disrupting peptide.Communications biology · 2024Article
- Accessory proteins of the RAS-MAPK pathway: moving from the side line to the front line.Communications biology · 2021Review
- Promotion of cancer cell stemness by Ras.Biochemical Society transactions · 2021Review
- Mechanisms of Ras Membrane Organization and Signaling: Ras Rocks Again.Biomolecules · 2020Review
- SPRED proteins and their roles in signal transduction, development, and malignancy.Genes & development · 2020Review
- Structural Insights into the SPRED1-Neurofibromin-KRAS Complex and Disruption of SPRED1-Neurofibromin Interaction by Oncogenic EGFR.Cell reports · 2020Article
- Article
- Ras Pathways on Prox1 and Lymphangiogenesis: Insights for Therapeutics.Frontiers in cardiovascular medicine · 2020Review
- Understanding a complicated Gal-1.Neuro-oncology · 2019Article
- Feedback regulation of RTK signaling in development.Developmental biology · 2019Review
- Article
- Oncogenic Ras Isoforms Signaling Specificity at the Membrane.Cancer research · 2018Review
- Opposite feedback from mTORC1 to H-ras and K-ras4B downstream of SREBP1.Scientific reports · 2017Article
- Rapalogs can promote cancer cell stemness in vitro in a Galectin-1 and H-ras-dependent manner.Oncotarget · 2017Article
- Strong Association of Polymorphism inAvicenna journal of medical biotechnologyArticle
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ras/mitogen-activated protein kinase (MAPK) signaling pathway is tightly controlled by negative feedback regulators, such as the tumor suppressor SPRED1. The SPRED1 gene also carries loss-of-function mutations in the RASopathy Legius syndrome. Growth factor stimulation translocates SPRED1 to the plasma membrane, triggering its inhibitory activity. However, it remains unclear whether SPRED1 there acts at the level of Ras or Raf. We show that pharmacological or galectin-1 (Gal-1)-mediated induction of B- and C-Raf-containing dimers translocates SPRED1 to the plasma membrane. This is facilitated in particular by SPRED1 interaction with B-Raf and, via its N terminus, with Gal-1. The physiological significance of these novel interactions is supported by two Legius syndrome-associated mutations that show diminished binding to both Gal-1 and B-Raf. On the plasma membrane, SPRED1 becomes enriched in acidic membrane domains to specifically perturb membrane organization and extracellular signal-regulated kinase (ERK) signaling of active K-ras4B (here, K-ras) but not H-ras. However, SPRED1 also blocks on the nanoscale the positive effects of Gal-1 on H-ras. Therefore, a combinatorial expression of SPRED1 and Gal-1 potentially regulates specific patterns of K-ras- and H-ras-dependent signaling output. More broadly, our results open up the possibility that related SPRED and Sprouty proteins act in a similar Ras and Raf isoform-specific manner.
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