ArticleDevelopmental biology2011
LKB1 regulates development and the stress response in Dictyostelium.
Article in Developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Polyphenols and Exercise in Mitochondrial Biogenesis: Focus on Age-Related CNS Disorders.Molecular neurobiology · 2025Review
- The transcription factor Spores Absent A is a PKA dependent inducer of Dictyostelium sporulation.Scientific reports · 2018Article
- 'Biogeneric' developmental processes: drivers of major transitions in animal evolution.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- Isoflurane suppresses the self-renewal of normal mouse neural stem cells in a p53-dependent manner by activating the Lkb1-p53-p21 signalling pathway.Molecular medicine reports · 2015Article
- MicroRNA-17 promotes normal ovarian cancer cells to cancer stem cells development via suppression of the LKB1-p53-p21/WAF1 pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Protein kinase LKB1 promotes RAB7-mediated neuropilin-1 degradation to inhibit angiogenesis.The Journal of clinical investigation · 2014Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The serine/threonine kinase LKB1 is a master kinase that regulates a number of critical events such as cell transformation, polarization, development, stress response, and energy metabolism in metazoa. After multiple unsuccessful attempts of generating Dictyostelium lkb1-null cells, an RNAi-based knockdown approach proved effective. Depletion of lkb1 with a knockdown construct displayed severe reduction in prespore cell differentiation and precocious induction of prestalk cells, which were reminiscent of cells lacking GSK3. Similar to gsk3(-) cells, lkb1 depleted cells displayed lower GSK3 activity than wild type cells during development and compromised cAMP-mediated inhibition of the DIF-1 mediated ecmB induction. In response to stress insult, the kinase activity of LKB1, but not that of GSK3, increased. Therefore, LKB1 positively functions at the upstream of GSK3 during development and responds to stress insults independently from GSK3.
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Registered trials
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