ArticleOncogene2002
Functional interaction of Sam68 and heterogeneous nuclear ribonucleoprotein K.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Heterogeneous nuclear ribonucleoprotein K promotes cap-independent translation initiation of retroviral mRNAs.Nucleic acids research · 2024Article
- The SINEB1 element in the long non-coding RNA Malat1 is necessary for TDP-43 proteostasis.Nucleic acids research · 2020Article
- Sam68 Promotes Hepatitis C Virus Replication by Interaction with Stem-Loop 2 of Viral 5' Untranslated Region.Journal of virology · 2019Article
- A hnRNP K⁻AR-Related Signature Reflects Progression toward Castration-Resistant Prostate Cancer.International journal of molecular sciences · 2018Article
- Sam68 Is Required for DNA Damage Responses via Regulating Poly(ADP-ribosyl)ation.PLoS biology · 2016Article
- Sam68/KHDRBS1 is critical for colon tumorigenesis by regulating genotoxic stress-induced NF-κB activation.eLife · 2016Article
- Analysis of the interaction between host factor Sam68 and viral elements during foot-and-mouth disease virus infections.Virology journal · 2015Article
- Nuclear Protein Sam68 Interacts with the Enterovirus 71 Internal Ribosome Entry Site and Positively Regulates Viral Protein Translation.Journal of virology · 2015Article
- SAM68: Signal Transduction and RNA Metabolism in Human Cancer.BioMed research international · 2015Review
- The transcriptional co-activator SND1 is a novel regulator of alternative splicing in prostate cancer cells.Oncogene · 2014Article
- Role of Sam68 in post-transcriptional gene regulation.International journal of molecular sciences · 2013Review
- Sam68 modulates the promoter specificity of NF-κB and mediates expression of CD25 in activated T cells.Nature communications · 2013Article
- Identification of a Sam68 ribonucleoprotein complex regulated by epidermal growth factor.The Journal of biological chemistry · 2009Article
- Heterogeneous nuclear ribonucleoprotein K represses the production of pro-apoptotic Bcl-xS splice isoform.The Journal of biological chemistry · 2009Article
- Identification of c-Src tyrosine kinase substrates using mass spectrometry and peptide microarrays.Journal of proteome research · 2008Article
- SUMO modification of Sam68 enhances its ability to repress cyclin D1 expression and inhibits its ability to induce apoptosis.Oncogene · 2006Article
- The tumour-suppressor protein ASPP1 is nuclear in human germ cells and can modulate ratios of CD44 exon V5 spliced isoforms in vivo.Oncogene · 2006Article
- A novel function for Sam68: enhancement of HIV-1 RNA 3' end processing.RNA (New York, N.Y.) · 2004Article
- Sam68 exerts separable effects on cell cycle progression and apoptosis.BMC cell biology · 2004Article
- Protein kinase CK2 phosphorylation regulates the interaction of Kaposi's sarcoma-associated herpesvirus regulatory protein ORF57 with its multifunctional partner hnRNP K.Nucleic acids research · 2004Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Sam68 is a target of the c-Src tyrosine kinase. We previously showed that overexpression of Sam68 functionally substitutes for, as well as synergies with, HIV-1 Rev in Rev-response element (RRE)-mediated gene expression and virus replication. Here we describe the identification of heterogeneous nuclear ribonucleoprotein K (hnRNP K) as a protein that specifically interacts with Sam68 in vitro and in vivo. HnRNP K did not bind to RRE-RNA directly, but formed a super complex with Sam68 and RRE in vitro. RNase treatment did not change the strength of binding of hnRNP K to Sam68. We demonstrated that hnRNP K significantly inhibited Sam68-mediated, but not Rev-mediated, RRE-dependent gene expression. We further showed that Sam68, but not a non-functional mutant Sam68p21, inhibited transcriptional activation of CT element by hnRNP K. Interestingly, the Sam68p21 with a single amino acid substitution in the nuclear localization domain exhibited less affinity for hnRNP K in vitro. We propose that the direct interaction of Sam68 and hnRNP K adversely affect the activities of both proteins in signal transduction pathways of both transcriptional and post-transcriptional events.
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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.