Results 31 to 40 of about 9,925 (218)

Wnt/β-catenin signaling stimulates the expression and synaptic clustering of the autism-associated Neuroligin 3 gene [PDF]

open access: yes, 2018
Indexación: Scopus.Synaptic abnormalities have been described in individuals with autism spectrum disorders (ASD). The cell-adhesion molecule Neuroligin-3 (Nlgn3) has an essential role in the function and maturation of synapses and NLGN3 ASD-associated ...
Andrade, V.M.   +9 more
core   +1 more source

The Omnipresence of DYRK1A in Human Diseases

open access: yesInternational Journal of Molecular Sciences, 2022
The increasing population will challenge healthcare, particularly because the worldwide population has never been older. Therapeutic solutions to age-related disease will be increasingly critical. Kinases are key regulators of human health and represent promising therapeutic targets for novel drug candidates.
Estelle Deboever   +3 more
openaire   +2 more sources

Rescue of the abnormal skeletal phenotype in Ts65Dn Down syndrome mice using genetic and therapeutic modulation of trisomic Dyrk1a [PDF]

open access: yes, 2015
Trisomy 21 causes skeletal alterations in individuals with Down syndrome (DS), but the causative trisomic gene and a therapeutic approach to rescue these abnormalities are unknown.
Abeysekera, Irushi   +3 more
core   +1 more source

Inhibition of DYRK1A disrupts neural lineage specificationin human pluripotent stem cells

open access: yeseLife, 2017
Genetic analysis has revealed that the dual specificity protein kinase DYRK1A has multiple roles in the development of the central nervous system. Increased DYRK1A gene dosage, such as occurs in Down syndrome, is known to affect neural progenitor cell ...
Stephanie F Bellmaine   +8 more
doaj   +1 more source

Altered age‐linked regulation of plasma DYRK1A in elderly cognitive complainers (INSIGHT‐preAD study) with high brain amyloid load

open access: yesAlzheimer’s & Dementia: Translational Research & Clinical Interventions, 2020
Introduction An effective therapy has not yet been developed for Alzheimer's disease (AD), in part because pathological changes occur years before clinical symptoms manifest.
Jean M. Delabar   +9 more
doaj   +1 more source

Structural analysis of pathogenic mutations in the DYRK1A gene in patients with developmental disorders. [PDF]

open access: yes, 2017
Haploinsufficiency in DYRK1A is associated with a recognizable developmental syndrome, though the mechanism of action of pathogenic missense mutations is currently unclear.
Ajoy Sarkar   +32 more
core   +2 more sources

Identification and analysis of a selective DYRK1A inhibitor

open access: yesBiomedicine & Pharmacotherapy, 2022
The dysregulation of DYRK1A is implicated in many diseases such as cancer, diabetes, and neurodegenerative diseases. Alzheimer's disease is one of the most common neurodegenerative disease and has elevated interest in DYRK1A research. Overexpression of DYRK1A has been linked to the formation of tau aggregates.
Lin, Tony Eight   +11 more
openaire   +3 more sources

DCAF7/WDR68 is required for normal levels of DYRK1A and DYRK1B.

open access: yesPLoS ONE, 2018
Overexpression of the Dual-specificity Tyrosine Phosphorylation-Regulated Kinase 1A (DYRK1A) gene contributes to the retardation, craniofacial anomalies, cognitive impairment, and learning and memory deficits associated with Down Syndrome (DS).
Mina Yousefelahiyeh   +5 more
doaj   +1 more source

Insights from the protein interaction Universe of the multifunctional “Goldilocks” kinase DYRK1A

open access: yesFrontiers in Cell and Developmental Biology, 2023
Human Dual specificity tyrosine (Y)-Regulated Kinase 1A (DYRK1A) is encoded by a dosage-dependent gene located in the Down syndrome critical region of human chromosome 21.
Varsha Ananthapadmanabhan   +4 more
doaj   +1 more source

DYRK1A and the Cell Cycle [PDF]

open access: yes, 2020
The ability to halt the cell cycle is critical for cells to maintain tissue and organ size, to suppress tumors and abnormal growth, and exists as a helpful mechanism to pause the cell cycle for DNA repair.
Byers, Holly   +1 more
core   +1 more source

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