LINC00507 Is Specifically Expressed in the Primate Cortex and Has Age-Dependent Expression Patterns

Ward, Melanie; Chen, Bei Jun; Iyer, Anand M.; Aronica, Eleonora; Janitz, Michael

doi:10.1007/s12031-016-0745-4

Cited by 17 publications

(10 citation statements)

References 32 publications

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“…There were five CNVs that overlapped in length with CNVs in DECIPHER and ClinGen that were identified in multiple individuals with intellectual disability and behavioral abnormalities: (a) a 600‐kb deletion (chr16:21839340‐22440319) encompassing 10 genes ( EEF2K ; CDR2 ; RRN3P3 ; POLR3E ; NPIPB4 ; C16orf52 ; MFSD13B ; UQCRC2 ; PDZD9 and VWA3A ) affecting EEF2K (which encodes postsynaptic eukaryotic elongation factor 2 kinase and balance inhibitory and excitatory synaptic transmission;) and CDR2 (which encodes cerebellar degeneration related protein 2, a major candidate gene of the 6p12.2 microdeletion syndrome [OMIM 136570]); (b) a 3.5 Mb duplication (chr22:41887922‐45396440) that impacts 70 genes some of which are implicated in autism ( TCF20 ), steroid‐dependent stress and anxiety (TSPO), drug metabolism ( CYP2D6 ), synaptic transmission ( PACSIN2 ), neuronal homeostasis ( MPPED1 ), with others specifically expressed in brain ( LINC00634 , SHISA8 ); (c) a 3‐Mb duplication (chr11:23211700‐26188592), affecting LUZ2P , a brain‐specific protein of unknown function; ( d ) a 1.7 Mb duplication (chr19:27791257‐29562474) affecting several noncoding RNAs and genes ( LINC01532 ; LOC102724908 ; LOC100420587 ; LINC00906 ; LOC101927151 ; LOC102724958 ; and LINC00662 ) whose function is unknown; and (e) a 1.3‐Mb duplication (chr12:127396986‐128 705 029) affecting several noncoding RNAs including LINC00507 , which is specifically and age‐dependently expressed in brain, suggesting it may be involved in the brain development of higher primates …”

Section: Resultsmentioning

confidence: 99%

Rare copy number variation in extremely impulsively violent males

Vevera

Zarrei

Hartmannová

et al. 2018

Genes Brain and Behavior

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The genetic correlates of extreme impulsive violence are poorly understood, and there have been no studies that have systematically characterized a large group of affected individuals both clinically and genetically. We performed a genome‐wide rare copy number variant (CNV) analysis in 281 males from four Czech prisons who met strict clinical criteria for extreme impulsive violence. Inclusion criteria included age ≥ 18 years, an ICD‐10 diagnosis of Dissocial Personality Disorder, and the absence of an organic brain disorder. Participants underwent a structured psychiatric assessment to diagnose extreme impulsive violence and then provided a blood sample for genetic analysis. DNA was genotyped and CNVs were identified using Illumina HumanOmni2.5 single‐nucleotide polymorphism array platform. Comparing with 10851 external population controls, we identified 828 rare CNVs (frequency ≤ 0.1% among control samples) in 264 participants. The CNVs impacted 754 genes, with 124 genes impacted more than once (2‐25 times). Many of these genes are associated with autosomal dominant or X‐linked disorders affecting adult behavior, cognition, learning, intelligence, specifically expressed in the brain and relevant to synapses, neurodevelopment, neurodegeneration, obesity and neuropsychiatric phenotypes. Specifically, we identified 31 CNVs of clinical relevance in 31 individuals, 59 likely clinically relevant CNVs in 49 individuals, and 17 recurrent CNVs in 65 individuals. Thus, 123 of 281 (44%) individuals had one to several rare CNVs that were indirectly or directly relevant to impulsive violence. Extreme impulsive violence is genetically heterogeneous and genomic analysis is likely required to identify, further research and specifically treat the causes in affected individuals.

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Section: Resultsmentioning

confidence: 99%

Rare copy number variation in extremely impulsively violent males

Vevera

Zarrei

Hartmannová

et al. 2018

Genes Brain and Behavior

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“…These age-dependent changes in the expression of lncRNAs in the prefrontal cortex reflect cognitive declines with age. LINC00507, which has ribosomebinding activity and micropeptide-coding potential, is specific to cortical regions in primates 82 , suggesting that its downregulation with age is associated with cognitive decline. Another lncRNA, BC200, inhibits local mRNA translation in dendrites and synapses 83,84 .…”

Section: Lncrnas Display High Regional Specificity In Aging Human Brainsmentioning

confidence: 99%

Advances in transcriptome analysis of human brain aging

Ham

Lee

2020

Exp Mol Med

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Aging is associated with gradual deterioration of physiological and biochemical functions, including cognitive decline. Transcriptome profiling of brain samples from individuals of varying ages has identified the whole-transcriptome changes that underlie age-associated cognitive declines. In this review, we discuss transcriptome-based research on human brain aging performed by using microarray and RNA sequencing analyses. Overall, decreased synaptic function and increased immune function are prevalent in most regions of the aged brain. Age-associated gene expression changes are also cell dependent and region dependent and are affected by genotype. In addition, the transcriptome changes that occur during brain aging include different splicing events, intersample heterogeneity, and altered levels of various types of noncoding RNAs. Establishing transcriptome-based hallmarks of human brain aging will improve the understanding of cognitive aging and neurodegenerative diseases and eventually lead to interventions that delay or prevent brain aging.

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“…An emerging area of research is in the ability of certain lncRNAs to encode small proteins, called micropeptides, challenging the theory that they are just non-coding molecules. Indeed, micropeptide-generating lncRNAs have been found in the brain (Mills et al, 2016 ). In addition, a large portion of tissue-specific lncRNAs are in the brain (Derrien et al, 2012 ) suggesting that they play an important role in neuronal function.…”

Section: Sleep-related Non-coding Rnasmentioning

confidence: 99%

Sleep Deprivation and the Epigenome

Gaine

Chatterjee

Abel

2018

Front. Neural Circuits

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Sleep deprivation disrupts the lives of millions of people every day and has a profound impact on the molecular biology of the brain. These effects begin as changes within a neuron, at the DNA and RNA level, and result in alterations in neuronal plasticity and dysregulation of many cognitive functions including learning and memory. The epigenome plays a critical role in regulating gene expression in the context of memory storage. In this review article, we begin by describing the effects of epigenetic alterations on the regulation of gene expression, focusing on the most common epigenetic mechanisms: (i) DNA methylation; (ii) histone modifications; and (iii) non-coding RNAs. We then discuss evidence suggesting that sleep loss impacts the epigenome and that these epigenetic alterations might mediate the changes in cognition seen following disruption of sleep. The link between sleep and the epigenome is only beginning to be elucidated, but clear evidence exists that epigenetic alterations occur following sleep deprivation. In the future, these changes to the epigenome could be utilized as biomarkers of sleep loss or as therapeutic targets for sleep-related disorders.

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LINC00507 Is Specifically Expressed in the Primate Cortex and Has Age-Dependent Expression Patterns

Cited by 17 publications

References 32 publications

Rare copy number variation in extremely impulsively violent males

Rare copy number variation in extremely impulsively violent males

Advances in transcriptome analysis of human brain aging

Sleep Deprivation and the Epigenome

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