ArticleCell cycle (Georgetown, Tex.)2009
CAML loss causes anaphase failure and chromosome missegregation.
Article in Cell cycle (Georgetown, Tex.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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
14 citing papers in PubMed, 23 citations in OpenAlex.
- Tail Anchored protein insertion mediated by CAML and TRC40 links to neuromuscular function in mice.PLoS genetics · 2025Article
- Article
- An Early Neoplasia Index (ENI10), Based on Molecular Identity of CD10 Cells and Associated Stemness Biomarkers, is a Predictor of Patient Outcome in Many Cancers.Cancer research communications · 2023Article
- Identifying novel genes for amyotrophic lateral sclerosis by integrating human brain proteomes with genome-wide association data.Journal of neurology · 2023Article
- CTCF is essential for proper mitotic spindle structure and anaphase segregation.bioRxiv : the preprint server for biology · 2023Article
- The ATPase activity of Asna1/TRC40 is required for pancreatic progenitor cell survival.Development (Cambridge, England) · 2018Article
- Yet another hump for CAML: support of cell survival independent of tail-anchored protein insertion.Cell death & disease · 2017Article
- CAML mediates survival of Myc-induced lymphoma cells independent of tail-anchored protein insertion.Cell death discovery · 2017Article
- Tail-anchored Protein Insertion in Mammals: FUNCTION AND RECIPROCAL INTERACTIONS OF THE TWO SUBUNITS OF THE TRC40 RECEPTOR.The Journal of biological chemistry · 2016Article
- Essential role for CAML in follicular B cell survival and homeostasis.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- CAML regulates Bim-dependent thymocyte death.Cell death and differentiation · 2010Article
- Mechanisms of chromosomal instability.Current biology : CB · 2010Review
- Cancer as a metabolic disease.Nutrition & metabolism · 2010Article
- Effect of calcium-modulating cyclophilin ligand on human immunodeficiency virus type 1 particle release and cell surface expression of tetherin.Journal of virology · 2009Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Calcium modulating cyclophilin ligand (CAML) is a ubiquitously expressed cytoplasmic protein that is implicated in the EGFR and LCK signaling pathways and required for early embryonic and thymocyte development. To further define the critical biological functions of CAML at the cellular level, we generated CAML-deleted mouse embryonic fibroblasts (MEFs) using an in vitro Cre-loxP mediated conditional knockout system. We found that CAML(-/-) MEFs have severely impaired proliferation and a strong reduction of normal anaphases. The primary mitotic defect of CAML(-/-) MEFs is that duplicated chromosomes fail to segregate in anaphase, resulting in nuclear bisection by the cleavage furrow as cells decondense their DNA and exit mitosis, highly reminiscent of the "cut" phenotype in fission yeast. This phenotype is due to spindle dysfunction rather than inability to resolve physical connections between sister chromatids. Furthermore, CAML(-/-) MEFs display defects often seen in cells with mitotic checkpoint gene deficiencies, including lagging and misaligned chromosomes and chromatin bridges. Consistent with this, we found that CAML(-/-) MEFs have a modestly weakened spindle assembly checkpoint (SAC) and increased aneuploidy. Thus, our data identify CAML as a novel chromosomal instability gene and suggest that CAML protein acts as a key regulator of mitotic spindle function and a modulator of SAC maintenance.
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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.