ArticleGenes2016
Regulation of BLM Nucleolar Localization.
Article in Genes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- G-quadruplexes regulate chromatin accessibility and gene expression in Bloom Syndrome.bioRxiv : the preprint server for biology · 2026Article
- Article
- Hyper-recombination in ribosomal DNA is driven by long-range resection-independent RAD51 accumulation.Nature communications · 2024Article
- Functions of the Bloom Syndrome Helicase N-terminal Intrinsically Disordered Region.bioRxiv : the preprint server for biology · 2024Article
- CRISPR/Cas9-mediated knockout of the ubiquitin variant UbKEKS reveals a role in regulating nucleolar structures and composition.Biology open · 2023Article
- The BLM helicase is a new therapeutic target in multiple myeloma involved in replication stress survival and drug resistance.Frontiers in immunology · 2022Article
- BLM interaction with EZH2 regulates MDM2 expression and is a poor prognostic biomarker for prostate cancer.American journal of cancer research · 2021Article
- Keeping ribosomal DNA intact: a repeating challenge.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019Review
- RECQ helicase disease and related progeroid syndromes: RECQ2018 meeting.Mechanisms of ageing and development · 2018Review
- A tri-serine cluster within the topoisomerase IIα-interaction domain of the BLM helicase is required for regulating chromosome breakage in human cells.Human molecular genetics · 2018Article
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
Defects in coordinated ribosomal RNA (rRNA) transcription in the nucleolus cause cellular and organismal growth deficiencies. Bloom's syndrome, an autosomal recessive human disorder caused by mutated recQ-like helicase BLM, presents with growth defects suggestive of underlying defects in rRNA transcription. Our previous studies showed that BLM facilitates rRNA transcription and interacts with RNA polymerase I and topoisomerase I (TOP1) in the nucleolus. The mechanisms regulating localization of BLM to the nucleolus are unknown. In this study, we identify the TOP1-interaction region of BLM by co-immunoprecipitation of in vitro transcribed and translated BLM segments and show that this region includes the highly conserved nuclear localization sequence (NLS) of BLM. Biochemical and nucleolar co-localization studies using site-specific mutants show that two serines within the NLS (S1342 and S1345) are critical for nucleolar localization of BLM but do not affect the functional interaction of BLM with TOP1. Mutagenesis of both serines to aspartic acid (phospho-mimetic), but not alanine (phospho-dead), results in approximately 80% reduction in nucleolar localization of BLM while retaining the biochemical functions and nuclear localization of BLM. Our studies suggest a role for this region in regulating nucleolar localization of BLM via modification of the two serines within the NLS.
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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.