ArticleProtein & cell2012
Generation of Calhm1 knockout mouse and characterization of calhm1 gene expression.
Article in Protein & cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Microglial Calhm2 regulates neuroinflammation and contributes to Alzheimer's disease pathology.Science advances · 2021Article
- A novel mCell research · 2019Article
- Calhm2 governs astrocytic ATP releasing in the development of depression-like behaviors.Molecular psychiatry · 2018Article
- CALHM1 deficiency impairs cerebral neuron activity and memory flexibility in mice.Scientific reports · 2016Article
- Salty taste deficits in CALHM1 knockout mice.Chemical senses · 2014Article
- How do taste cells lacking synapses mediate neurotransmission? CALHM1, a voltage-gated ATP channel.BioEssays : news and reviews in molecular, cellular and developmental biology · 2013Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disease among elderly people worldwide. Several genes have been validated to be associated with AD, and calcium homeostasis modulator 1 (Calhm1) is the latest suspected one. To investigate the biological and pathological function of Calhm1 systematically, we generated a Calhm1 conventional knockout mouse. However, both the male and female of elderly Calhm1 knockout (KO) mice showed similar ability to their wild type littermates in spatial learning and memory retrieving. Surprisingly, we found that Calhm1 mRNA could not be detected in mouse brains at different ages, although it is expressed in the human brain tissues. We further found that CpG islands (CGIs) of both mouse and human Calhm1 were hypermethylated, whereas CGI of mouse Calhm2 was hypomethylated. In addition, transcriptional active marker H3K4Di occupied on promoters of human Calhm1 and mouse Calhm2 at a considerable level in brain tissues, while the occupancy of H3K4Di on promoter of mouse Calhm1 was rare. In sum, we found that mouse Calhm1 was of rare abundance in brain tissues. So it might not be suitable to utilize the knockout murine model to explore biological function of Calhm1 in the pathogenesis of AD.
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Registered trials
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