The road to ERK activation: Do neurons take alternate routes?

Zobon, Nadiatou T Miningou; Blackwell, Kim T.

doi:10.1016/j.cellsig.2020.109541

Cited by 31 publications

(29 citation statements)

References 160 publications

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“…It is traditionally believed that the ERK signal is mainly involved in proliferation, differentiation, learning and memory, development, synaptic plasticity and neural apoptosis Miningou & Blackwell, 2020). The role of ERK in neuronal migration and autism spectrum disorders (ASD) has long been ignored and has only been reported in recent years (Vithayathil et al, 2018;Xing et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Lack of dcf1 leads to neuronal migration delay, axonal swollen and autism-related deficits

Feng

Chen

Sun

et al. 2020

Preprint

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Perturbed neuronal migration and abnormal axonogenesis have been shown to be implicated in the pathogenesis of autism spectrum disorder (ASD). However, the molecular mechanism remains unknown. Here we demonstrate that dendritic cell factor 1(DCF1) is involved in neuronal migration and axonogenesis. The deletion of dcf1 in mice delays the localization of callosal projection neurons, while dcf1 overexpression restores normal migration. Delayed neurons appear as axon swelling and axonal boutons loss, resulting in a permanent deficit in the callosal projections.Western blot analysis indicates that absence of dcf1 leads to the abnormal activation of ERK signal. Differential protein expression assay shows that PEBP1, a negative regulator of the ERK signal, is significant downregulation in dcf1 KO mice. Direct interaction between DCF1 and PEBP1 is confirmed by Co-immunoprecipitation test, thus indicating that DCF1 regulates the ERK signal in a PEBP1-dependent pattern. As a result of the neurodevelopmental migration disorder, dcf1 deletion results in ASD-like behaviors in mice. This finding identifies a link between abnormal activated ERK signaling, delayed neuronal migration and autistic-like behaviors in humans.

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Section: Discussionmentioning

confidence: 99%

Lack of dcf1 leads to neuronal migration delay, axonal swollen and autism-related deficits

Feng

Chen

Sun

et al. 2020

Preprint

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“…ERK regulates cell migration through its phosphorylation of myosin light chain kinase (MLCK), focal adhesion kinase (FAK), calpain, and p21-activated kinase (PAK1). ERK (ERK1 and ERK2) is activated by its phosphorylation on Thr 202/185 and Tyr 204/187 (human sequences) by MAPK/ERK Kinases (MEKs) (Miningou and Blackwell 2020;Seger et al 1992). Upon phosphorylation, ERK is either seen to homodimerize or heterodimerize (Khokhlatchev et al 1998), which enhances ERK activity but reduces its translocation of ERK monomers to the nucleus.…”

Section: )mentioning

confidence: 99%

Adhesion-growth factor crosstalk regulates AURKB activation and ERK signaling in re-adherent fibroblasts

Inchanalkar

Balasubramanian

2021

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Aurora kinases despite their similarity have distinct roles in the cell cycle, which is regulated by cell-matrix adhesion and growth factors. This study reveals loss of adhesion and re-adhesion to differentially regulate Aurora kinases. AURKB activation that drops on the loss of adhesion recovers on re-adhesion in serum-deprived conditions but not in the presence of serum growth factors. A rapid 30min serum treatment of serum-deprived cells blocks the adhesion-dependent recovery of AURKB, which negatively corelates with Erk activation. AZD mediated inhibition of AURKB in serum-deprived re-adherent cells promotes Erk activation and membrane ruffling, comparable to presence of serum. These studies thus define a novel adhesion-growth factor-dependent regulation of AURKB that controls adhesion-dependent Erk activation in re-adherent fibroblasts.

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“…Numerous studies have demonstrated that ERK contributes to synaptic plasticity by controlling transcription and protein translation (for review Miningou and Blackwell, 2020;Peng et al, 2010), as well as increasing cell excitability by phosphorylating potassium channels (Schrader et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…Another critical molecule in synaptic plasticity and memory is extracelluar signal-regulated kinase (ERK) (English and Sweatt, 1997), as inhibition of ERK inhibits both hippocampal LTP and memory. Numerous studies have demonstrated that ERK contributes to synaptic plasticity by controlling transcription and protein translation (for review Miningou and Blackwell, 2020; Peng et al, 2010), as well as increasing cell excitability by phosphorylating potassium channels (Schrader et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…A critical molecule in induction of L-LTP and memory is extracellular signal-regulated kinase (ERK) (English and Sweatt, 1997). Numerous studies have demonstrated that ERK contributes to L-LTP induction by controlling the transcription and protein translation necessary for L-LTP (for review Miningou and Blackwell, 2020; Peng et al, 2010), as well as increasing cell excitability by phosphorylating potassium channels (Schrader et al, 2006). ERK is activated by a cascade of kinases (Buscà et al, 2016; Terrell and Morrison, 2019), which are activated by Ras family GTP binding proteins, which are controlled by diverse Guanine nucleotide Exchange Factors (GEFs) and GTPase Activating Proteins (GAPs).…”

Section: Introductionmentioning

confidence: 99%

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Temporal pattern and synergy influence activity of ERK signaling pathways during L-LTP induction

Blackwell

Zobon

2020

Preprint

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Long lasting long-term potentiation (L-LTP) is a cellular mechanism of learning and memory storage. Studies have demonstrated a requirement for the extracellular signal-regulated kinase (ERK) activation in L-LTP produced by a diversity of temporal stimulation patterns. Multiple signaling pathways converge to activate ERK, with different pathways being required for different stimulation patterns. We addressed the critical questions of whether maximal activation of ERK requires multiple pathways, and whether different temporal patterns select different signaling pathways for ERK activation. We developed a computational model of five signaling pathways (including two novel pathways) leading to ERK activation during L-LTP. Simulations show that calcium and cAMP work synergistically to activate ERK, and that stimuli given with large inter-trial intervals activate more ERK than shorter intervals, a temporal sensitivity similar to PKA but contrary to CaMKII. These results suggest that signaling pathways with different temporal sensitivity facilitate ERK activation to diversity of temporal patterns.

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The road to ERK activation: Do neurons take alternate routes?

Cited by 31 publications

References 160 publications

Lack of dcf1 leads to neuronal migration delay, axonal swollen and autism-related deficits

Lack of dcf1 leads to neuronal migration delay, axonal swollen and autism-related deficits

Adhesion-growth factor crosstalk regulates AURKB activation and ERK signaling in re-adherent fibroblasts

Temporal pattern and synergy influence activity of ERK signaling pathways during L-LTP induction

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