ArticleJournal of cellular physiology2014
Nemo-like kinase regulates postnatal skeletal homeostasis.
Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Microglia regulate brain progranulin levels through the endocytosis/lysosomal pathway.JCI insight · 2021Article
- Nemo-Like Kinase in Development and Diseases: Insights from Mouse Studies.International journal of molecular sciences · 2020Review
- An antibody to Notch3 reverses the skeletal phenotype of lateral meningocele syndrome in male mice.Journal of cellular physiology · 2020Article
- Loss ofAmerican journal of physiology. Endocrinology and metabolism · 2019Article
- Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Nemo-like kinase (Nlk) is related to the mitogen-activated protein (MAP) kinases and known to regulate signaling pathways involved in osteoblastogenesis. In vitro Nlk suppresses osteoblastogenesis, but the consequences of the Nlk inactivation in the skeleton in vivo are unknown. To study the function of Nlk, Nlk(loxP/loxP) mice, where the Nlk exon2 is flanked by lox(P) sequences, were mated with mice expressing the Cre recombinase under the control of the paired-related homeobox gene 1 (Prx1) enhancer (Prx1-Cre), the Osterix (Osx-Cre) or the osteocalcin/bone gamma carboxyglutamate protein (Bglap-Cre) promoter. Prx1-Cre;Nlk(Δ/Δ) mice did not exhibit a skeletal phenotype except for a modest increase in trabecular number and connectivity observed only in 3-month-old male mice. Osx-Cre;Nlk(Δ/Δ) male and female mice exhibited an increase in trabecular bone volume secondary to an increased trabecular number at 3 months of age. Bone histomorphometry revealed a decrease in osteoclast number and eroded surface in male mice, and decreased osteoblast number and function in female mice. Expression of osteoprotegerin mRNA was increased in calvarial extracts, explaining the decreased osteoclast and osteoblast number. The conditional deletion of Nlk in mature osteoblasts (Bglap-Cre;Nlk(Δ/Δ) ) resulted in no skeletal phenotype in 1- to 6-month-old male or female mice. In conclusion, when expressed in undifferentiated osteoblasts, Nlk is a negative regulator of skeletal homeostasis possibly by targeting signals that regulate osteoclastogenesis and bone resorption.
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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.