CK2α is essential for embryonic morphogenesis
Molecular and Cellular Biochemistry, ISSN: 0300-8177, Vol: 356, Issue: 1-2, Page: 209-216
2011
- 30Citations
- 32Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations30
- Citation Indexes30
- 30
- CrossRef24
- Captures32
- Readers32
- 32
Article Description
CK2 is a highly conserved serine-threonine kinase involved in biological processes such as embryonic development, circadian rhythms, inflammation, and cancer. Biochemical experiments have implicated CK2 in the control of several cellular processes and in the regulation of signal transduction pathways. Our laboratory is interested in characterizing the cellular, signaling, and molecular mechanisms regulated by CK2 during early embryonic development. For this purpose, animal models, including mice deficient in CK2 genes, are indispensable tools. Using CK2α gene-deficient mice, we have recently shown that CK2α is a critical regulator of mid-gestational morphoge-netic processes, as CK2α deficiency results in defects in heart, brain, pharyngeal arch, tail bud, limb bud, and somite formation. Morphogenetic processes depend upon the precise coordination of essential cellular processes in which CK2 has been implicated, such as proliferation and survival. Here, we summarize the overall phenotype found in CK2α mice and describe our initial analysis aimed to identify the cellular processes affected in CK2α mutants. © Springer Science+Business Media, LLC. 2011.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84855228464&origin=inward; http://dx.doi.org/10.1007/s11010-011-0961-8; http://www.ncbi.nlm.nih.gov/pubmed/21761203; http://link.springer.com/10.1007/s11010-011-0961-8; https://dx.doi.org/10.1007/s11010-011-0961-8; https://link.springer.com/article/10.1007/s11010-011-0961-8; http://www.springerlink.com/index/10.1007/s11010-011-0961-8; http://www.springerlink.com/index/pdf/10.1007/s11010-011-0961-8
Springer Science and Business Media LLC
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