ArticleJournal of virology2002
Direct participation of Sam68, the 68-kilodalton Src-associated protein in mitosis, in the CRM1-mediated Rev nuclear export pathway.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 71 citations in OpenAlex.
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- Review
- HIV infection of non-classical cells in the brain.Retrovirology · 2023Review
- Protein arginine methylation in viral infection and antiviral immunity.International journal of biological sciences · 2023Review
- High expression of Sam68 contributes to metastasis by regulating vimentin expression and a motile phenotype in oral squamous cell carcinoma.Oncology reports · 2022Article
- Role of Sam68 in Sunitinib induced renal cell carcinoma apoptosis.Cancer medicine · 2022Article
- Apoptosis and Autophagy in Picornavirus Infection.Frontiers in microbiology · 2019Review
- Astrocytes as an HIV Reservoir: Mechanism of HIV Infection.Current HIV research · 2016Review
- Analysis of the interaction between host factor Sam68 and viral elements during foot-and-mouth disease virus infections.Virology journal · 2015Article
- STAT3 and its phosphorylation are involved in HIV-1 Tat-induced transactivation of glial fibrillary acidic protein.Current HIV research · 2015Article
- Inhibition of HIV-1 transcription and replication by a newly identified cyclin T1 splice variant.The Journal of biological chemistry · 2013Article
- RNA-binding protein Sam68 controls synapse number and local β-actin mRNA metabolism in dendrites.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Formation of trans-activation competent HIV-1 Rev:RRE complexes requires the recruitment of multiple protein activation domains.PloS one · 2012Article
- Translational regulation of HIV-1 replication by HIV-1 Rev cellular cofactors Sam68, eIF5A, hRIP, and DDX3.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Article
- Bortezomib induces the formation of nuclear poly(A) RNA granules enriched in Sam68 and PABPN1 in sensory ganglia neurons.Neurotoxicity research · 2010Article
- Sam68 relocalization into stress granules in response to oxidative stress through complexing with TIA-1.Experimental cell research · 2009Article
- Identification of a Sam68 ribonucleoprotein complex regulated by epidermal growth factor.The Journal of biological chemistry · 2009Article
- Inhibition of HIV-1 entry by extracts derived from traditional Chinese medicinal herbal plants.BMC complementary and alternative medicine · 2009Article
- Sam68 regulates translation of target mRNAs in male germ cells, necessary for mouse spermatogenesis.The Journal of cell biology · 2009Article
- An adaptor role for cytoplasmic Sam68 in modulating Src activity during cell polarization.Molecular and cellular biology · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Human immunodeficiency virus type 1 (HIV-1) replication requires efficient nuclear export of incompletely spliced and unspliced HIV-1 mRNA transcripts, which is achieved by Rev expression at an early stage of the viral life cycle. We have recently shown that expression of Sam68, the 68-kDa Src-associated protein in mitosis, is able to alleviate Rev function block in astrocytes by promoting Rev nuclear export. In the present study, we utilized an antisense RNA expression strategy to down-modulate constitutive Sam68 expression and examined its effect on Rev function, HIV-1 gene expression, and viral replication. These results showed that down-modulation of constitutive Sam68 expression markedly inhibited HIV-1 production in 293T cells and viral replication in T lymphocytes such as Jurkat and CEM cells, as well as human peripheral blood mononuclear cells (PBMCs). Rev-dependent in trans complementation and reporter gene assays further demonstrated that inhibition of HIV-1 gene expression by Sam68 down-modulation was due to impeded Rev activity. Moreover, digital fluorescence microscopic imaging revealed that down-modulation of Sam68 expression caused exclusive nuclear retention and colocalization of both Rev and CRM1. Taken together, these data suggest that adequate Sam68 expression is required for Rev function and, thereby, for HIV-1 gene expression and viral replication, and they support the notion that Sam68 is directly involved in the CRM1-mediated Rev nuclear export pathway.
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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.