ArticleMolecular and cellular biology2009
An adaptor role for cytoplasmic Sam68 in modulating Src activity during cell polarization.
Article in Molecular and cellular biology, 2009. 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, 68 citations in OpenAlex.
- SAM68 is a multifunctional post-transcriptional regulator of cardiomyocyte differentiation.Nucleic acids research · 2026Article
- Sam68 is a druggable vulnerability point in cancer stem cells.Cancer metastasis reviews · 2024Review
- Picornavirus 3C Proteins Intervene in Host Cell Processes through Proteolysis and Interactions with RNA.Viruses · 2023Review
- Sam68 promotes osteogenic differentiation of aortic valvular interstitial cells by TNF-α/STAT3/autophagy axis.Journal of cell communication and signaling · 2023Article
- Article
- Hepatic Sam68 Regulates Systemic Glucose Homeostasis and Insulin Sensitivity.International journal of molecular sciences · 2022Article
- Research progress on RNA-binding proteins in breast cancer.Oncology letters · 2022Review
- Article
- Ablation of Sam68 in adult mice increases thermogenesis and energy expenditure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Sam68 promotes hepatic gluconeogenesis via CRTC2.Nature communications · 2021Article
- Mechanisms and consequences of subcellular RNA localization across diverse cell types.Traffic (Copenhagen, Denmark) · 2020Review
- SAM68 interaction with U1A modulates U1 snRNP recruitment and regulates mTor pre-mRNA splicing.Nucleic acids research · 2019Article
- Phosphoproteomics Analysis Identifies Novel Candidate Substrates of the Nonreceptor Tyrosine Kinase,Molecular & cellular proteomics : MCP · 2018Article
- Clinical significance and effect of Sam68 expression in gastric cancer.Oncology letters · 2018Article
- Transcriptome profiling in preadipocytes identifies long noncoding RNAs as Sam68 targets.Oncotarget · 2017Article
- The p53 status can influence the role of Sam68 in tumorigenesis.Oncotarget · 2016Article
- Sam68 functions as a transcriptional coactivator of the p53 tumor suppressor.Nucleic acids research · 2016Article
- Analysis of the interaction between host factor Sam68 and viral elements during foot-and-mouth disease virus infections.Virology journal · 2015Article
- Inhibition of Sam68 triggers adipose tissue browning.The Journal of endocrinology · 2015Article
- SAM68: Signal Transduction and RNA Metabolism in Human Cancer.BioMed research international · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Src-associated substrate during mitosis with a molecular mass of 68 kDa (Sam68) is predominantly nuclear and is known to associate with proteins containing the Src homology 3 (SH3) and SH2 domains. Although Sam68 is a Src substrate, little is known about the signaling pathway that link them. Src is known to be activated transiently after cell spreading, where it modulates the activity of small Rho GTPases. Herein we report that Sam68-deficient cells exhibit loss of cell polarity and cell migration. Interestingly, Sam68-deficient cells exhibited sustained Src activity after cell attachment, resulting in the constitutive tyrosine phosphorylation and activation of p190RhoGAP and its association with p120rasGAP. Consistently, we observed that Sam68-deficient cells exhibited deregulated RhoA and Rac1 activity. By using total internal reflection fluorescence microscopy, we observed Sam68 near the plasma membrane after cell attachment coinciding with phosphorylation of its C-terminal tyrosines and association with Csk. These findings show that Sam68 localizes near the plasma membrane during cell attachment and serves as an adaptor protein to modulate Src activity for proper signaling to small Rho GTPases.
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What OpenQuestion holds
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.