#9345. ERK/MAPK signalling in the developing brain: Perturbations and consequences

November 2026publication date
Proposal available till 18-05-2025
4 total number of authors per manuscript5500 $

The title of the journal is available only for the authors who have already paid for
Journal’s subject area:
Behavioral Neuroscience;
Cognitive Neuroscience;
Neuropsychology and Physiological Psychology;
Places in the authors’ list:
place 1place 2place 3place 4
FreeFreeFreeFree
2350 $1200 $1050 $900 $
Contract №9345.1 Contract №9345.2 Contract №9345.3 Contract №9345.4
1 place - free (for sale)
2 place - free (for sale)
3 place - free (for sale)
4 place - free (for sale)

Abstract:
The extracellular regulated kinase/microtubule-associated protein kinase (ERK/MAPK) signalling pathway transduces signals that cause an alteration in the ongoing metabolic pathways and modifies gene expression patterns; thus, influencing cellular behaviour. ERK/MAPK signalling is essential for the proper development of the nervous system from neural progenitor cells derived from the embryonic mesoderm. Several signalling molecules that regulate the well-coordinated process of neurodevelopment transduce developmental information through the ERK/MAPK signalling pathway. The ERK/MAPK is a potential novel therapeutic target in several neurodevelopmental disorders, however, despite years of study, there is still significant uncertainty about the exact mechanism by which the ERK/MAPK signalling pathway elicits specific responses in neurodevelopment. Here, we will review the evidence highlighting the role of ERK/MAPK signalling in neurodevelopment. We will also discuss the structural implication and behavioural deficits associated with perturbed ERK/MAPK signalling pathway in cortical development, whilst examining its contribution to the neuropathology of several neurodevelopmental disorders, such as Autism Spectrum Disorder, Schizophrenia, Fragile X, and Attention Deficit Hyperactive Disorder.
Keywords:
Brain development; ERK/MAPK; Neural progenitors; Neurodevelopmental disorders; RAF family

Contacts :
0