Suppr超能文献

其表达受到转录因子 的调控,其沉默促进视网膜神经元的神经分化。

Is Regulated by the Transcription Factor , and Its Silencing Promotes Neural Differentiation in Retinal Neurons.

机构信息

Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou 510060, China.

出版信息

Int J Mol Sci. 2022 Nov 10;23(22):13860. doi: 10.3390/ijms232213860.

Abstract

Previous studies have indicated that () plays an important role in neural development and degenerative diseases. However, the bioactivity and regulatory mechanism of expression in retinal neurocytes remain unclear. In the present study, our data indicated that maintains the state of neuronal precursor cells. silencing induces differentiation in 661W cells. , a marker of precursor cells, was significantly decreased in parallel with silencing in 661W cells, whereas (), a marker of differentiated neurons, was significantly increased. Neurite outgrowth was increased by ~4.0-fold in -silenced cells. Moreover, DNA affinity purification assays and ChIP assays demonstrated that () regulates transcription in 661W cells. Silencing or overexpressing could significantly regulate the expression of and affect its promoter inducibility. Furthermore, the expression of generally occurred in parallel with that of in developing mouse retinas. Both and are expressed in the neonatal mouse retina but are developmentally silenced with age. Exogenous significantly inhibited neural activity by decreasing synaptophysin and neurite outgrowth. Thus, this study demonstrated that is transcriptionally regulated by . / silencing is involved in neuronal differentiation and maturation.

摘要

先前的研究表明,()在神经发育和退行性疾病中发挥着重要作用。然而,()在视网膜神经细胞中的生物活性和调控机制仍不清楚。本研究中,我们的数据表明,()维持神经前体细胞的状态。沉默()会诱导 661W 细胞分化。与 661W 细胞中的()沉默平行的是,神经前体细胞的标志物 ()显著降低,而分化神经元的标志物 ()显著增加。沉默()的细胞中,神经突生长增加了约 4.0 倍。此外,DNA 亲和纯化分析和 ChIP 分析表明,()在 661W 细胞中调控()的转录。沉默或过表达()可以显著调节()的表达,并影响其启动子的诱导能力。此外,在发育中的小鼠视网膜中,()的表达通常与()的表达平行。()和 ()均在新生小鼠视网膜中表达,但随年龄增长而发育沉默。外源性()通过减少突触小泡蛋白和神经突生长显著抑制神经活性。因此,本研究表明,()受 调控。/沉默参与神经元的分化和成熟。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b47d/9694312/03728fcd3846/ijms-23-13860-g001.jpg

相似文献

4
BRCA1 silencing is associated with failure of DNA repairing in retinal neurocytes.
PLoS One. 2014 Jun 11;9(6):e99371. doi: 10.1371/journal.pone.0099371. eCollection 2014.
5
Heterarchy of transcription factors driving basal and luminal cell phenotypes in human urothelium.
Cell Death Differ. 2017 May;24(5):809-818. doi: 10.1038/cdd.2017.10. Epub 2017 Mar 10.
8
GATA-3 regulates differentiation-specific loricrin gene expression in keratinocytes.
Exp Dermatol. 2012 Nov;21(11):859-64. doi: 10.1111/exd.12023.
9
Transcriptional repression of Gata3 is essential for early B cell commitment.
Immunity. 2013 May 23;38(5):930-42. doi: 10.1016/j.immuni.2013.01.014. Epub 2013 May 16.
10
GATA3 acts upstream of FOXA1 in mediating ESR1 binding by shaping enhancer accessibility.
Genome Res. 2013 Jan;23(1):12-22. doi: 10.1101/gr.139469.112. Epub 2012 Nov 21.

本文引用的文献

3
BRCA1-associated R-loop affects transcription and differentiation in breast luminal epithelial cells.
Nucleic Acids Res. 2019 Jun 4;47(10):5086-5099. doi: 10.1093/nar/gkz262.
4
GATA3 Promotes the Neural Progenitor State but Not Neurogenesis in 3D Traumatic Injury Model of Primary Human Cortical Astrocytes.
Front Cell Neurosci. 2019 Feb 11;13:23. doi: 10.3389/fncel.2019.00023. eCollection 2019.
7
Role of BRCA1 in Neuronal Death in Alzheimer's Disease.
ACS Chem Neurosci. 2018 May 16;9(5):870-872. doi: 10.1021/acschemneuro.8b00149. Epub 2018 Apr 10.
8
White Blood Cell BRCA1 Promoter Methylation Status and Ovarian Cancer Risk.
Ann Intern Med. 2018 Mar 6;168(5):326-334. doi: 10.7326/M17-0101. Epub 2018 Jan 16.
9
Twist1 regulates embryonic hematopoietic differentiation through binding to and promoter regions.
Blood Adv. 2017 Aug 31;1(20):1672-1681. doi: 10.1182/bloodadvances.2017006056. eCollection 2017 Sep 12.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验