MicroRNA-339-5p Down-regulates Protein Expression of β-Site Amyloid Precursor Protein-Cleaving Enzyme 1 (BACE1) in Human Primary Brain Cultures and Is Reduced in Brain Tissue Specimens of Alzheimer Disease Subjects

Long, Justin M.; Ray, Balmiki; Lahiri, Debomoy K.

doi:10.1074/jbc.m113.518241

Cited by 160 publications

(97 citation statements)

References 97 publications

(116 reference statements)

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“…There are 128 genes in the duplicated region on 11q23.3-q25; mutations found in 40 of these genes are considered to be the molecular basis of other diseases as summarized below: BACE1, located at 11q23.3, has been reportedly involved in cerebral deposition of amyloid beta peptide, which is an early indicator of Alzheimer disease (Vassar et al, 1999). Gene knockout and overexpression experiments showed that BACE1 was related with nervous system development (Long et al, 2014). BSX, located at 11q24.1, is a DNA-binding protein and a transcriptional activator found to be essential for fetal growth and development (Chu and Ohtoshi, 2007).…”

Section: Discussionmentioning

confidence: 99%

A rare case of trisomy 11q23.3-11q25 and trisomy 22q11.1-22q11.21

Ps¹,

Hf²,

Chen³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Partial duplication of the long arm of chromosome 11 and the partial trisomy of 22q are uncommon karyotypic abnormalities. Here, we report the case of a 6-year-old girl who showed partial trisomy of 11q and 22q, as a result of a maternal balanced reciprocal translocation (11;22), and exhibited dysmorphic features, severe intellectual disability, brain malformations, and speech delay related to this unique chromosomal abnormality. Array comparative genomic hybridization (array CGH) revealed a gain in copy number on the long arm of chromosome 11, spanning at least 18.22 Mb. Additionally, there was a gain in copy number on the long arm of chromosome 22, spanning at least 3.46 Mb. FISH analysis using a chromosome 11 short arm telomere probe (11p14.2), a chromosome 11 long arm telomere probe (11q24.3), and a chromosome 22 long arm telomere probe (22q13.33) confirmed the origin of the marker chromosome. It has been confirmed by the State Key Laboratory of Medical Genetics of China that this is the first reported instance of the karyotype 47,XX, +der (22

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Section: Discussionmentioning

confidence: 99%

A rare case of trisomy 11q23.3-11q25 and trisomy 22q11.1-22q11.21

Ps¹,

Hf²,

Chen³

et al. 2016

Genet. Mol. Res.

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“…Therefore, miR-135b may be a potential candidate for the treatment of AD through inhibiting BACE1. In addition, several other miRs have been observed to directly target BACE1, including the miR-29 family, miR-124, miR-195 and miR-339-5p, and thus may contribute to the treatment of AD (4,(27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-135b has a neuroprotective role via targeting of β-site APP-cleaving enzyme 1

Zhang

Xing

Guo

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. MicroRNAs (miRs) are a class of endogenous small non-coding RNAs that have been revealed to negatively mediate the expression of their target genes at the post-transcriptional level. Recently, particular miRs have demonstrated an involvement in the pathogenesis of Alzheimer's disease (AD). However, the specific role of miR-135b in AD has yet to be elucidated. The present study aimed to investigate the neuroprotective role of miR-135b, in addition to its underlying mechanism. Herein, reverse transcription-quantitative polymerase chain reaction was conducted to determine miR-135b expression levels in the peripheral blood samples of patients with AD and age-matched normal controls. The data of the present study revealed that the expression levels of miR-135b were significantly reduced in the peripheral blood of AD patients compared with normal controls (P<0.01). In vitro MTT analyses identified that the overexpression of miR-135b significantly enhanced the proliferation of hippocampal cells (P<0.01). Furthermore, in vivo analysis using a Y-maze test indicated that injection with miR-135b mimics into the third ventricle of anesthetized SAMP8 mice significantly enhanced their learning and memory capacities (P<0.01). Molecular mechanism investigations identified β-site APP-cleaving enzyme 1 (BACE1) as a direct target gene of miR-135b, and the latter was identified to negatively mediate the protein expression levels of BACE1 in hippocampal cells, in addition to hippocampal tissues, of SAMP8 mice. Based on the aforementioned findings, we propose that miR-135b has a neuroprotective role via direct targeting of BACE1 and, thus, may be used for the treatment of AD.

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“…For example, several miRNA species, such as miR-101, miR-153 and miR-339-5p are dysregulated in AD (Long and Lahiri, 2011a;Long and Lahiri, 2011b;Long et al, 2014). In this context, p35 expression can be post-transcriptionally suppressed by miRNAs 103 and 107 (miR-103 and miR-107, respectively) (Moncini et al, 2011).…”

Section: Post-transcriptional Regulation Of P35 and Cdk5mentioning

confidence: 99%

Cdk5 activity in the brain – multiple paths of regulation

Shah

Lahiri

2014

Journal of Cell Science

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165

124

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Cyclin dependent kinase-5 (Cdk5), a family member of the cyclindependent kinases, plays a pivotal role in the central nervous system. During embryogenesis, Cdk5 is indispensable for brain development and, in the adult brain, it is essential for numerous neuronal processes, including higher cognitive functions such as learning and memory formation. However, Cdk5 activity becomes deregulated in several neurological disorders, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, which leads to neurotoxicity. Therefore, precise control over Cdk5 activity is essential for its physiological functions. This Commentary covers the various mechanisms of Cdk5 regulation, including several recently identified protein activators and inhibitors of Cdk5 that control its activity in normal and diseased brains. We also discuss the autoregulatory activity of Cdk5 and its regulation at the transcriptional, post-transcriptional and post-translational levels. We finally highlight physiological and pathological roles of Cdk5 in the brain. Specific modulation of these protein regulators is expected to provide alternative strategies for the development of effective therapeutic interventions that are triggered by deregulation of Cdk5.

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MicroRNA-339-5p Down-regulates Protein Expression of β-Site Amyloid Precursor Protein-Cleaving Enzyme 1 (BACE1) in Human Primary Brain Cultures and Is Reduced in Brain Tissue Specimens of Alzheimer Disease Subjects

Cited by 160 publications

References 97 publications

A rare case of trisomy 11q23.3-11q25 and trisomy 22q11.1-22q11.21

A rare case of trisomy 11q23.3-11q25 and trisomy 22q11.1-22q11.21

MicroRNA-135b has a neuroprotective role via targeting of β-site APP-cleaving enzyme 1

Cdk5 activity in the brain – multiple paths of regulation

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