ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2015
Inactivition of CDKL3 mildly inhibits proliferation of cells at VZ/SVZ in brain.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- CDKL3 is a promising biomarker for diagnosis and prognosis prediction in patients with hepatocellular carcinoma.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- The Impact of Mmu17 Non-Hsa21 Orthologous Genes in the Ts65Dn Mouse Model of Down Syndrome: The Gold Standard Refuted.Biological psychiatry · 2023Article
- Inhibition of CDKL3 downregulates STAT1 thus suppressing prostate cancer development.Cell death & disease · 2023Article
- Identification of CDKL3 as a critical regulator in development of glioma through regulating RRM2 and the JNK signaling pathway.Cancer science · 2021Article
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Authors and funding
2 authors at 2 institutions in 1 country.
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Abstract
CDKL3 has an important role in regulating cell growth and/or differentiation, and its inactivation is recently reported to be related to non-syndromic mild mental retardation (MR). MR is a common neurological disorder, predominantly characterized by impaired cognitive function. Though genetic factors play a very important role in the pathogenesis of MR, to date, only few genes linked to MR have been characterized and understood very well. Here, we investigated the role of the CDKL3 in the proliferation of cells surrounding the brain ventricle, and the results showed down-regulating CDKL3 by the method of RNAi in the cells surrounding the brain ventricle of the mouse embryo at E15 may inhibit their proliferation. As our previous study had shown that Cdkl3 mRNA expression is developmentally regulated in the central nervous system, peaking during late embryonic and early postnatal stages which are the key stages of neurite formation and maturation, furtherly, the present findings indicated that CDKL3 may be involved in proliferation of cells surrounding the brain ventricle where neuronal progenitor cells are enriched during the late embryo stage, supporting the notion that CDKL3 inactivation contributes to non-syndromic mild MR.
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