Results 41 to 50 of about 3,929,505 (299)
Aptamers as Valuable Molecular Tools in Neurosciences [PDF]
Aptamers are short nucleic acids that interact with a variety of targets with high affinity and specificity. They have been shown to inhibit biological functions of cognate target proteins, and they are identifiable by anin vitroselection process, also termed SELEX (Systematic Evolution of Ligands by EXponential enrichment).
Olga, Wolter, Günter, Mayer
openaire +2 more sources
Leucine‐rich glioma inactivated 1 (LGI1) is a ganglioside‐binding protein
Neuronal hyperexcitability associated with a decrease/absence of the extracellular protein LGI1 has been suggested to be primarily due to the downregulation of Kv1 channel expression. The molecular mechanisms underlying this decrease have not yet been elucidated.
Kévin Debreux +7 more
wiley +1 more source
Miami Neuroscience Institute - Spring 2020
https://scholarlycommons.baptisthealth.net/bg-bh-neuroscience-news/1001/thumbnail ...
Miami Neuroscience Institute
core +1 more source
Summary: Synaptic structural plasticity, the expansion of dendritic spines in response to synaptic stimulation, is essential for experience-dependent plasticity and is driven by branched actin polymerization. The WAVE regulatory complex (WRC) is confined
Belal Shohayeb +7 more
doaj +1 more source
Summary: The microtubule-associated tau protein forms pathological inclusions that accumulate in an age-dependent manner in tauopathies including Alzheimer's disease (AD). Since age is the major risk factor for AD, we examined endogenous tau species that
Connor M. Wander +11 more
doaj +1 more source
Summary: Mutations in the human fasciculation and elongation protein zeta 1 (FEZ1) gene are found in schizophrenia and Jacobsen syndrome patients. Here, using human cerebral organoids (hCOs), we show that FEZ1 expression is turned on early during brain ...
Yinghua Qu +5 more
doaj +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source
Cancer‐associated mutations in endometriosis reframe a benign disease through molecular oncology
This review aims to comprehensively analyse cancer‐associated somatic mutations (CAMs) present in endometriotic lesions, emphasizing their biological roles, spatial distribution and implications for translational applications in medicine. By contextualizing a benign state within a genomic framework, this analysis seeks to establish its value as a ...
Clarissa Mujacic +15 more
wiley +1 more source
Summary: Light sensitivity of the vertebrate retina relies on the integrity of photoreceptors, including rods and cones. Research in patients with Alzheimer's disease (AD) and in AD transgenic mice reports that accumulated amyloid-β (Aβ) plaques in the ...
Jie Zhang +4 more
doaj +1 more source
Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim +11 more
wiley +1 more source

