Редактирование: CEBPB

CCAAT/enhancer-binding protein beta (C/EBP beta) (Liver activator protein) (LAP) (Liver-enriched inhibitory protein) (LIP) (Nuclear factor NF-IL6) (Transcription factor 5) (TCF-5) [TCF5] [PP9092]

==Publications==

{{medline-entry
|title=Integrative Analysis of Hippocampus Gene Expression Profiles Identifies Network Alterations in Aging and Alzheimer's Disease.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29875655
|abstract=Alzheimer's disease (AD) is a neurodegenerative disorder contributing to rapid decline in cognitive function and ultimately dementia. Most cases of AD occur in elderly and later years. There is a growing need for understanding the relationship between aging and AD to identify shared and unique hallmarks associated with the disease in a region and cell-type specific manner. Although genomic studies on AD have been performed extensively, the molecular mechanism of disease progression is still not clear. The major objective of our study is to obtain a higher-order network-level understanding of aging and AD, and their relationship using the hippocampal gene expression profiles of young (20-50 years), aging (70-99 years), and AD (70-99 years). The hippocampus is vulnerable to damage at early stages of AD and altered neurogenesis in the hippocampus is linked to the onset of AD. We combined the weighted gene co-expression network and weighted protein-protein interaction network-level approaches to study the transition from young to aging to AD. The network analysis revealed the organization of co-expression network into functional modules that are cell-type specific in aging and AD. We found that modules associated with astrocytes, endothelial cells and microglial cells are upregulated and significantly correlate with both aging and AD. The modules associated with neurons, mitochondria and endoplasmic reticulum are downregulated and significantly correlate with AD than aging. The oligodendrocytes module does not show significant correlation with neither aging nor disease. Further, we identified aging- and AD-specific interactions/subnetworks by integrating the gene expression with a human protein-protein interaction network. We found dysregulation of genes encoding protein kinases (FYN, [[SYK]], [[SRC]], PKC, [[MAPK1]], ephrin receptors) and transcription factors (FOS, [[STAT3]], [[CEBPB]], [[MYC]], NFKβ, and EGR1) in AD. Further, we found genes that encode proteins with neuroprotective function (14-3-3 proteins, [[PIN1]], [[ATXN1]], [[BDNF]], VEGFA) to be part of the downregulated AD subnetwork. Our study highlights that simultaneously analyzing aging and AD will help to understand the pre-clinical and clinical phase of AD and aid in developing the treatment strategies.

|keywords=* PPI network
* aging
* co-expression network
* glial cells
* graph theory
* hippocampus
* neurodegenerative disease
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5974201
}}
{{medline-entry
|title=The microRNA miR-17-3p inhibits mouse cardiac fibroblast senescence by targeting Par4.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25472717
|abstract=The microRNA miR-17-92 cluster plays a fundamental role in heart development. The aim of this study was to investigate the effect of a member of this cluster, miR-17, on cardiac senescence. We examined the roles of miR-17 in senescence and demonstrated that miR-17-3p attenuates cardiac aging in the myocardium by targeting Par4 (also known as PAWR). This upregulates the downstream proteins [[CEBPB]], FAK, N-cadherin, vimentin, Oct4 and Sca-1 (also known as stem cell antigen-1), and downregulates E-cadherin. Par4 has been reported as a tumor suppressor gene that induces apoptosis in cancer cells, but not in normal cells. Repression of Par4 by miR-17-3p enhances the transcription of [[CEBPB]] and FAK, which promotes mouse cardiac fibroblast (MCF) epithelial-to-mesenchymal transition (EMT) and self-renewal, resulting in cellular senescence and apoptosis resistance. We conclude that Par4 can bind to the [[CEBPB]] promoter and inhibit its transcription. Decreased Par4 expression increases the amount of [[CEBPB]], which binds to the FAK promoter and enhances FAK transcription. Par4, [[CEBPB]] and FAK form a senescence signaling pathway, playing roles in modulating cell survival, growth, apoptosis, EMT and self-renewal. Through this novel senescence signaling axis, miR-17-3p represses Par4 expression, acting pleiotropically as a negative modulator of cardiac aging and cardiac fibroblast cellular senescence.
|mesh-terms=* Animals
* Apoptosis
* Apoptosis Regulatory Proteins
* CCAAT-Enhancer-Binding Protein-beta
* Cell Survival
* Cellular Senescence
* Epithelial-Mesenchymal Transition
* Fibroblasts
* Focal Adhesion Kinase 1
* Gene Expression Regulation, Neoplastic
* Humans
* Mice
* MicroRNAs
* Protein Binding
* Signal Transduction
|keywords=* Senescence
* miR-17
* microRNA
|full-text-url=https://sci-hub.do/10.1242/jcs.158360
}}