ArticleAging cell2010
The telomeric protein SNM1B/Apollo is required for normal cell proliferation and embryonic development.
Article in Aging cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 26 citations in OpenAlex.
- Mapping the genetic landscape of the DNA damage response with Cas12a-based combinatorial knockout screens.bioRxiv : the preprint server for biology · 2026Article
- DNA-PK controls Apollo's access to leading-end telomeres.Nucleic acids research · 2024Article
- DNA-PK and the TRF2 iDDR inhibit MRN-initiated resection at leading-end telomeres.Nature structural & molecular biology · 2023Article
- Dual targeting of Saccharomyces cerevisiae Pso2 to mitochondria and the nucleus, and its functional relevance in the repair of DNA interstrand crosslinks.G3 (Bethesda, Md.) · 2022Article
- Inherited human Apollo deficiency causes severe bone marrow failure and developmental defects.Blood · 2022Article
- A phosphate binding pocket is a key determinant of exo- versus endo-nucleolytic activity in the SNM1 nuclease family.Nucleic acids research · 2021Article
- Systematic evaluation of the effect of polyadenylation signal variants on the expression of disease-associated genes.Genome research · 2021Article
- Cyclic Peptidic Mimetics of Apollo Peptides Targeting Telomeric Repeat Binding Factor 2 (TRF2) and Apollo Interaction.ACS medicinal chemistry letters · 2018Article
- SNM1B/Apollo in the DNA damage response and telomere maintenance.Oncotarget · 2017Review
- OLA1, a Translational Regulator of p21, Maintains Optimal Cell Proliferation Necessary for Developmental Progression.Molecular and cellular biology · 2016Article
- The SNM1B/APOLLO DNA nuclease functions in resolution of replication stress and maintenance of common fragile site stability.Human molecular genetics · 2013Article
- How will telomeric complex be further contributed to our longevity? - the potential novel biomarkers of telomere complex counteracting both aging and cancer.Protein & cell · 2013Review
- Ku70 functions in addition to nonhomologous end joining in pancreatic β-cells: a connection to β-catenin regulation.Diabetes · 2013Article
- Characterization of the human SNM1A and SNM1B/Apollo DNA repair exonucleases.The Journal of biological chemistry · 2012Article
- Artemis interacts with the Cul4A-DDB1DDB2 ubiquitin E3 ligase and regulates degradation of the CDK inhibitor p27.Cell cycle (Georgetown, Tex.) · 2011Article
- Snm1B/Apollo functions in the Fanconi anemia pathway in response to DNA interstrand crosslinks.Human molecular genetics · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Conserved metallo β-Lactamase and β-CASP (CPSF-Artemis-Snm1-Pso2) domain nuclease family member SNM1B/Apollo is a shelterin-associated protein that localizes to telomeres through its interaction with TRF2. To study its in vivo role, we generated a knockout of SNM1B/Apollo in a mouse model. Snm1B/Apollo homozygous null mice die at birth with developmental delay and defects in multiple organ systems. Cell proliferation defects were observed in Snm1B/Apollo mutant mouse embryonic fibroblasts (MEFs) owing to high levels of telomeric end-to-end fusions. Deficiency of the nonhomologous end-joining (NHEJ) factor Ku70, but not p53, rescued the developmental defects and lethality observed in Snm1B/Apollo mutant mice as well as the impaired proliferation of Snm1B/Apollo-deficient MEFs. These findings demonstrate that SNM1B/Apollo is required to protect telomeres against NHEJ-mediated repair, which results in genomic instability and the consequent multi-organ developmental failure. Although Snm1B/Apollo-deficient MEFs exhibited high levels of apoptosis, abrogation of p53-dependent programmed cell death did not rescue the multi-organ developmental failure in the mice.
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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.