ArticleMolecular and cellular biology2006
Mechanistic studies of the mitotic activation of Mos.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Mechanistic study of TRPM2-Ca(2+)-CAMK2-BECN1 signaling in oxidative stress-induced autophagy inhibition.Autophagy · 2016Article
- Two pore channel 2 (TPC2) inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH.The Journal of biological chemistry · 2013Article
- Two pore channel 2 differentially modulates neural differentiation of mouse embryonic stem cells.PloS one · 2013Article
- Inhibition of cardiomyocytes differentiation of mouse embryonic stem cells by CD38/cADPR/Ca2+ signaling pathway.The Journal of biological chemistry · 2012Article
- A novel fluorescent cell membrane-permeable caged cyclic ADP-ribose analogue.The Journal of biological chemistry · 2012Article
- Kicked by Mos and tuned by MPF-the initiation of the MAPK cascade in Xenopus oocytes.HFSP journal · 2009Article
- CK2alpha/CK1alpha chimeras are sensitive to regulation by the CK2beta subunit.Molecular and cellular biochemistry · 2008Article
- A novel role for Cdk1/cyclin B in regulating B-raf activation at mitosis.Molecular biology of the cell · 2008Article
- Search for the genes involved in oocyte maturation and early embryo development in the hen.BMC genomics · 2008Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The protein kinase Mos is responsible for the activation of MEK1 and p42 mitogen-activated protein kinase during Xenopus oocyte maturation and during mitosis in Xenopus egg extracts. Here we show that the activation of Mos depends upon the phosphorylation of Ser 3, a residue previously implicated in the regulation of Mos stability; the dephosphorylation of Ser 105, a previously unidentified phosphorylation site conserved in Mos proteins; and the regulated dissociation of Mos from CK2beta. Mutation of Ser 3 to alanine and/or mutation of Ser 105 to glutamate produces a Mos protein that is defective for M-phase activation, as assessed by in vitro kinase assays, and defective for induction of oocyte maturation and maintenance of the spindle assembly checkpoint in extracts. Interestingly, Ser 105 is situated at the beginning of helix alphaC in the N-terminal lobe of the Mos kinase domain. Changes in the orientation of this helix have been previously implicated in the activation of Cdk2 and Src family tyrosine kinases. Our work suggests that Ser 105 dephosphorylation represents a novel mechanism for reorienting helix alphaC.
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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.