ArticlePloS one2013
Targeted ANP32E mutant mice do not demonstrate obvious movement defects.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Anp32e promotes renal interstitial fibrosis by upregulating the expression of fibrosis-related proteins.International journal of biological sciences · 2022Article
- The gut microbiota influences skeletal muscle mass and function in mice.Science translational medicine · 2019Article
- ANP32B deficiency impairs proliferation and suppresses tumor progression by regulating AKT phosphorylation.Cell death & disease · 2016Article
- Cracking the ANP32 whips: important functions, unequal requirement, and hints at disease implications.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe ANP32 family of proteins have been implicated in neuronal function through biochemical and cellular biology studies in neurons, as well as by recent behavioural studies of a gene-trapped loss-of-function mutation of Anp32e in mice, particularly with respect to fine motor function. A second targeted allele of the Anp32e, however, did not appear to demonstrate neurological phenotypes. METHODOLOGY/PRINCIPAL
findingsUsing a stringently controlled cohort of ten-generation backcrossed, co-caged, sex-matched, littermate pairs, we assayed for potential motor defects in the targeted ANP32E-deficient mice. We found no phenotypic difference in any assays.
conclusionSince it is unlikely that the gene-trap is a more complete loss-of-function, our results suggest that ANP32E has no appreciable effect on motor functions and that genetic background differences most likely account for the gene-trap phenomena.
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Registered trials
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