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Showing 1-6 of 6 results for "557360" within Papers
A-Ching Chao et al.
Biochimica et biophysica acta. Molecular cell research, 1867(4), 118628-118628 (2019-12-31)
One neurotoxic mechanism of amyloid-beta peptide (Aβ), the major component of senile plaques in the brains of Alzheimer's disease (AD) patients, is to trigger cell cycle reentry in fully differentiated neurons. However, the detailed underlying mechanisms remain unclear. Using Aβ25-35-treated
Arzu Ulu et al.
Cellular signalling, 80, 109926-109926 (2021-01-20)
The Neuroepithelial transforming gene 1 (Net1) is a RhoA subfamily guanine nucleotide exchange factor that is overexpressed in a number of cancers and contributes to cancer cell motility and proliferation. Net1 also plays a Rho GTPase independent role in mitotic
Jonathan Martinez-Fabregas et al.
Cell reports, 33(12), 108545-108545 (2020-12-29)
Cytokines are highly pleiotropic ligands that regulate the immune response. Here, using interleukin-6 (IL-6) as a model system, we perform detailed phosphoproteomic and transcriptomic studies in human CD4+ T helper 1 (Th-1) cells to address the molecular bases defining cytokine
Sandipan Ray et al.
Life science alliance, 2(6) (2019-12-04)
Determining the exact targets and mechanisms of action of drug molecules that modulate circadian rhythms is critical to develop novel compounds to treat clock-related disorders. Here, we have used phenotypic proteomic profiling (PPP) to systematically determine molecular targets of four
Taichi Igarashi et al.
Nature communications, 14(1), 4991-4991 (2023-08-18)
Activation of the KRAS oncogene is a source of replication stress, but how this stress is generated and how it is tolerated by cancer cells remain poorly understood. Here we show that induction of KRASG12V expression in untransformed cells triggers
Christiana Kontaxi et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 43(11), 2002-2020 (2023-02-10)
Cyclin-dependent kinase-like 5 (CDKL5) deficiency disorder (CDD) is a severe early-onset epileptic encephalopathy resulting mainly from de novo mutations in the X-linked CDKL5 gene. To determine whether loss of presynaptic CDKL5 function contributes to CDD, we examined synaptic vesicle (SV)
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