ArticleMolecular and cellular biology2001
Cse1l is essential for early embryonic growth and development.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Chromosome Segregation-1-like Gene Participates in Ferroptosis in Human Ovarian Granulosa Cells via Nucleocytoplasmic Transport.Antioxidants (Basel, Switzerland) · 2024Article
- CSE1L/CAS regulates cell proliferation through CDK signalling in mouse spermatogenesis.Cell proliferation · 2022Article
- A Novel Mutation in Cse1l Disrupts Brain and Eye Development with Specific Effects on Pax6 Expression.Journal of developmental biology · 2021Article
- CSE1L silencing impairs tumor progression via MET/STAT3/PD-L1 signaling in lung cancer.American journal of cancer research · 2021Article
- Cellular apoptosis susceptibility protein (CAS) suppresses the proliferation of breast cancer cells by upregulated cyp24a1.Medical oncology (Northwood, London, England) · 2020Article
- CSE1L participates in regulating cell mitosis in human seminoma.Cell proliferation · 2019Article
- Elucidating the Host Interactome of EV-A71 2C Reveals Viral Dependency Factors.Frontiers in microbiology · 2019Article
- Expression of CAS/CSE1L, the Cellular Apoptosis Susceptibility Protein, Correlates With Neoplastic Progression in Barrett's Esophagus.Applied immunohistochemistry & molecular morphology : AIMM · 2018Article
- Article
- Roles of the CSE1L-mediated nuclear import pathway in epigenetic silencing.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Quantitative trait loci mapping for feed conversion efficiency in crucian carp (Carassius auratus).Scientific reports · 2017Article
- CAS (CSE1L) signaling pathway in tumor progression and its potential as a biomarker and target for targeted therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- The Cellular Apoptosis Susceptibility Protein (CAS) Promotes Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)-induced Apoptosis and Cell Proliferation.The Journal of biological chemistry · 2016Article
- Divergent LIN28-mRNA associations result in translational suppression upon the initiation of differentiation.Nucleic acids research · 2014Article
- Article
- Correlations between cytoplasmic CSE1L in neoplastic colorectal glands and depth of tumor penetration and cancer stage.Journal of translational medicine · 2013Article
- CSE1L, a novel microvesicle membrane protein, mediates Ras-triggered microvesicle generation and metastasis of tumor cells.Molecular medicine (Cambridge, Mass.) · 2012Article
- Cse1l is a negative regulator of CFTR-dependent fluid secretion.Current biology : CB · 2010Article
- Cellular apoptosis susceptibility (CSE1L/CAS) protein in cancer metastasis and chemotherapeutic drug-induced apoptosis.Journal of experimental & clinical cancer research : CR · 2010Review
- CSE1L/CAS, the cellular apoptosis susceptibility protein, enhances invasion and metastasis but not proliferation of cancer cells.Journal of experimental & clinical cancer research : CR · 2008Article
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
No grant is acknowledged in the PubMed record.
Abstract
The CSE1L gene, the human homologue of the yeast chromosome segregation gene CSE1, is a nuclear transport factor that plays a role in proliferation as well as in apoptosis. CSE1 and CSE1L are essential genes in Saccharomyces cerevisiae and mammalian cells, as shown by conditional yeast mutants and mammalian cell culture experiments with antisense-mediated depletion of CSE1L. To analyze whether CSE1L is also essential in vivo and whether its absence can be compensated for by other genes or mechanisms, we have cloned the murine CSE1L gene (Cse1l) and analyzed its tissue- and development-specific expression: Cse1l was detected at embryonic day 7.0 (E7.0), E11.0, E15.0, and E17.0, and in adults, high expression was observed in proliferating tissues. Subsequently, we inactivated the Cse1l gene in embryonic stem cells to generate heterozygous and homozygous knockout mice. Mice heterozygous for Cse1l appear normal and are fertile. However, no homozygous pups were born after interbreeding of heterozygous mice. In 30 heterozygote interbreeding experiments, 50 Cse1l wild-type mice and 100 heterozygotes were born but no animal with both Cse1l alleles deleted was born. Embryo analyses showed that homozygous mutant embryos were already disorganized and degenerated by E5.5. This implicates with high significance (P < 0.0001, Pearson chi-square test) an embryonically lethal phenotype of homozygous murine CSE1 deficiency and suggests that Cse1l plays a critical role in early embryonic development.
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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.