Varaico: Literature-Extracted Genetic Variants

Gene:CDK5
Variant:p.D144N
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CDK5

NM_004935.4:p.D144N

Associated Papers

CDK5-PRMT1-WDR24 signaling cascade promotes mTORC1 signaling and tumor growth.

Yin S et al.

Cell Reports, 2023

Identification and characterization of a novel phosphoregulatory site on cyclin-dependent kinase 5.

Roach BL et al.

Biochemical and Biophysical Research Communications, 2018

Inhibition of CDK5 Alleviates the Cardiac Phenotypes in Timothy Syndrome.

Song L et al.

Stem Cell Reports, 2017

28648896 (PubMed )
Supplement: mmc1.pdf

The roles of Cdk5-mediated subcellular localization of FOXO1 in neuronal death.

Zhou J et al.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2015

Effects of p35 Mutations Associated with Mental Retardation on the Cellular Function of p35-CDK5.

Takada S et al.

Plos One, 2015

Acetylation of cyclin-dependent kinase 5 is mediated by GCN5.

Lee J et al.

Biochemical and Biophysical Research Communications, 2014

Ubiquitin C-terminal hydrolase L1 (UCH-L1) acts as a novel potentiator of cyclin-dependent kinases to enhance cell proliferation independently of its hydrolase activity.

Kabuta T et al.

The Journal of Biological Chemistry, 2013

RNAi screening in primary human hepatocytes of genes implicated in genome-wide association studies for roles in type 2 diabetes identifies roles for CAMK1D and CDKAL1, among others, in hepatic glucose regulation.

Haney S et al.

Plos One, 2013

Stabilization and activation of p53 induced by Cdk5 contributes to neuronal cell death.

Lee JH et al.

Journal of Cell Science, 2007

Cyclin-dependent kinase 5 differentially regulates the transcriptional activity of the glucocorticoid receptor through phosphorylation: clinical implications for the nervous system response to glucocorticoids and stress.

Kino T et al.

Molecular Endocrinology (baltimore, Md.), 2007

Regulation of cyclin-dependent kinase 5 and p53 by ERK1/2 pathway in the DNA damage-induced neuronal death.

Lee JH et al.

Journal of Cellular Physiology, 2007

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Regarding the variants extracted from papers and shown text snippets from research papers, the following holds: "Some rights reserved. This work permits non-commercial use, distribution and reproduction in any medium, provided the original author and source are credited."