ArticleCell death & disease2010
Extraribosomal functions associated with the C terminus of the 37/67 kDa laminin receptor are required for maintaining cell viability.
Article in Cell death & disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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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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
28 citing papers in PubMed, 40 citations in OpenAlex.
- The m5C reader Ybx1 regulates embryonic cortical neurogenesis by promoting progenitor cell cycle progression.PLoS biology · 2025Article
- 37 kDa LRP::FLAG enhances telomerase activity and reduces ageing markers in vivo.Cellular and molecular life sciences : CMLS · 2025Article
- The dual role of ribosomal protein SA in pathogen infection: the key role of structure and localization.Molecular biology reports · 2024Review
- Channeling the Natural Properties of Sindbis Alphavirus for Targeted Tumor Therapy.International journal of molecular sciences · 2023Review
- Article
- Targeting the Extra-Cellular Matrix-Tumor Cell Crosstalk for Anti-Cancer Therapy: Emerging Alternatives to Integrin Inhibitors.Frontiers in oncology · 2020Review
- The Ribosome as a Missing Link in Prebiotic Evolution III: Over-Representation of tRNA- and rRNA-Like Sequences and Plieofunctionality of Ribosome-Related Molecules Argues for the Evolution of Primitive Genomes from Ribosomal RNA Modules.International journal of molecular sciences · 2019Article
- A dock derived compound against laminin receptor (37 LR) exhibits anti-cancer properties in a prostate cancer cell line model.Oncotarget · 2018Article
- Article
- How Ribosomes Translate Cancer.Cancer discovery · 2017Review
- The ribosomal protein gene RPL5 is a haploinsufficient tumor suppressor in multiple cancer types.Oncotarget · 2017Article
- Looking into laminin receptor: critical discussion regarding the non-integrin 37/67-kDa laminin receptor/RPSA protein.Biological reviews of the Cambridge Philosophical Society · 2016Review
- The Transition of the 37-Kda Laminin Receptor (Rpsa) to Higher Molecular Weight Species: Sumoylation or Artifact?Cellular & molecular biology letters · 2015Article
- Discovery of new small molecules inhibiting 67 kDa laminin receptor interaction with laminin and cancer cell invasion.Oncotarget · 2015Article
- Article
- Deciphering the complex three-way interaction between the non-integrin laminin receptor, galectin-3 and Neisseria meningitidis.Open biology · 2014Article
- Article
- Tumor-specific targeting with modified Sindbis viral vectors: evaluation with optical imaging and positron emission tomography in vivo.Molecular imaging and biology · 2013Article
- Downregulation of the non-integrin laminin receptor reduces cellular viability by inducing apoptosis in lung and cervical cancer cells.PloS one · 2013Article
- Laminin receptor 37/67LR regulates adhesion and proliferation of normal human intestinal epithelial cells.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The 37/67 kDa laminin receptor (LAMR) is a multifunctional protein, acting as an extracellular receptor, localizing to the nucleus, and playing roles in rRNA processing and ribosome assembly. LAMR is important for cell viability; however, it is unclear which of its functions are essential. We developed a silent mutant LAMR construct, resistant to siRNA, to rescue the phenotypic effects of knocking down endogenous LAMR, which include inhibition of protein synthesis, cell cycle arrest, and apoptosis. In addition, we generated a C-terminal-truncated silent mutant LAMR construct structurally homologous to the Archaeoglobus fulgidus S2 ribosomal protein and missing the C-terminal 75 residues of LAMR, which displays more sequence divergence. We found that HT1080 cells stably expressing either silent mutant LAMR construct still undergo arrest in the G1 phase of the cell cycle when treated with siRNA. However, the expression of full-length silent mutant LAMR rescues cell viability, whereas the expression of the C-terminal-truncated LAMR does not. Interestingly, we also found that both silent mutant constructs restore protein translation and localize to the nucleus. Our findings indicate that the ability of LAMR to regulate viability is associated with its C-terminal 75 residues. Furthermore, this function is distinct from its role in cell proliferation, independent of its ribosomal functions, and may be regulated by a nonnuclear localization.
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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.