Cortical excitatory neurons become protected from cell division during neurogenesis in an Rb family-dependent manner

Oshikawa, Masaki; Okada, Keisuke; Nakajima, Kazunori; Ajioka, Itsuki

doi:10.1242/dev.095653

Cited by 22 publications

(27 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, p130, which mediates gene expression by direct binding to the transcription factor E2F, is also a key regulator of maintaining neuron survival among the Rb family members . Equally important, p130, particularly expressed in basal progenitors, is involved in producing and differentiating neurons . Interestingly, RBL2 is not completely coexpressed with E2F4 (as well as RB1 and RBL1) indicating that the gene might have an independent, to date unknown, function in neurodevelopment .…”

Section: Discussionsupporting

confidence: 82%

Biallelic loss‐of‐function variants in RBL2 in siblings with a neurodevelopmental disorder

Brunet

Radivojkov-Blagojevic

Lichtner

et al. 2020

Ann Clin Transl Neurol

View full text Add to dashboard Cite

The RBL2 locus has been associated with intelligence and educational attainment but not with a monogenic disorder to date. RBL2 encodes p130, a member of the retinoblastoma protein family, which is involved in mediating neuron survival and death. Previous studies on p130 knockout mice revealing embryonic death and impaired neurogenesis underscore the importance of RBL2 in brain development. Exome sequencing in two siblings with severe intellectual disability, stereotypies and dysmorphic features identified biallelic loss‐of‐function variants c.556C>T, p.(Arg186Ter) and a deletion of exon 13–17 in RBL2 (NM_005611.3), establishing RBL2 as a candidate gene for an autosomal recessive neurodevelopmental disorder.

show abstract

Section: Discussionsupporting

confidence: 82%

Biallelic loss‐of‐function variants in RBL2 in siblings with a neurodevelopmental disorder

Brunet

Radivojkov-Blagojevic

Lichtner

et al. 2020

Ann Clin Transl Neurol

View full text Add to dashboard Cite

show abstract

“…Similarly, up-regulation of p16 Ink4a is a consistent feature of cellular senescence and age-related morbidity in a range of in vitro and in vivo models. However, direct evidence supporting a role for p16 Ink4a in brain physiology is still deficient and is mostly supported by circumstantial evidence, including the involvement of p53 and Rb moieties in response to brain trauma, aetiology of neurodegenerative diseases or cancer [43,44,45,46,47,48,49,50]. …”

Section: Discussionmentioning

confidence: 99%

Segmental Aging Underlies the Development of a Parkinson Phenotype in the AS/AGU Rat

Khojah

Payne

McGuinness

et al. 2016

Cells

View full text Add to dashboard Cite

There is a paucity of information on the molecular biology of aging processes in the brain. We have used biomarkers of aging (SA β-Gal, p16Ink4a, Sirt5, Sirt6, and Sirt7) to demonstrate the presence of an accelerated aging phenotype across different brain regions in the AS/AGU rat, a spontaneous Parkinsonian mutant of PKCγ derived from a parental AS strain. P16INK4a expression was significantly higher in AS/AGU animals compared to age-matched AS controls (p < 0.001) and displayed segmental expression across various brain regions. The age-related expression of sirtuins similarly showed differences between strains and between brain regions. Our data clearly show segmental aging processes within the rat brain, and that these are accelerated in the AS/AGU mutant. The accelerated aging, Parkinsonian phenotype, and disruption to dopamine signalling in the basal ganglia in AS/AGU rats, suggests that this rat strain represents a useful model for studies of development and progression of Parkinson’s disease in the context of biological aging and may offer unique mechanistic insights into the biology of aging.

show abstract

“…Acute Rb family inactivation could force neurons underwent S-phase progression, indicating the potential involvement of Rb in the cell cycle reentry [16]. Berberine (BBR) possesses many pharmacological activities [17].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Retinoblastoma mRNA Degradation through Poly (A) Involved in the Neuroprotective Effect of Berberine against Cerebral Ischemia

et al. 2014

View full text Add to dashboard Cite

Berberine is one kind of isoquinoline alkaloid with anti-apoptotic effects on the neurons suffering ischemia. To address the explanation for these activities, the berberine-induced cell cycle arrest during neurons suffering ischemia/reperfusion had been studied in the present study. According to the in vitro neurons with oxygen-glucose deprivation and in vivo ICR mice with cerebral ischemia/reperfusion, it was found that berberine could protect the mRNA of retinoblastoma (Rb) from degradation through its function on the poly(A) tail. The prolonged half-life of retinoblastoma 1 (gene of Rb, RB1) mRNA level secures the protein level of retinoblastoma, which facilitates cell cycle arrest of neurons in the process of ischemia/reperfusion and subsequently avoids cells entering in the apoptotic process. The poly(A) tail of RB1 mRNA, as a newly identified target of berberine, could help people focus on the interaction between berberine and mRNA to further understand the biological activities and functions of berberine.

show abstract

Cortical excitatory neurons become protected from cell division during neurogenesis in an Rb family-dependent manner

Cited by 22 publications

References 47 publications

Biallelic loss‐of‐function variants in RBL2 in siblings with a neurodevelopmental disorder

Biallelic loss‐of‐function variants in RBL2 in siblings with a neurodevelopmental disorder

Segmental Aging Underlies the Development of a Parkinson Phenotype in the AS/AGU Rat

Inhibition of Retinoblastoma mRNA Degradation through Poly (A) Involved in the Neuroprotective Effect of Berberine against Cerebral Ischemia

Contact Info

Product

Resources

About