Редактирование: KLF5 (раздел)

==Publications==

{{medline-entry
|title=Senescence-associated genes and non-coding RNAs function in pancreatic cancer progression.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31997706
|abstract=Pancreatic cancer is a major cause of mortality with a poor diagnosis and prognosis that most often occurs in elderly patients. Few studies, however, focus on the interplay of age and pancreatic cancer at the transcriptional level. Here we evaluated the possible roles of age-dependent, differentially expressed genes (DEGs) in pancreatic cancer. These DEGs were used to construct a correlation network and clustered in six gene modules, among which two modules were highly correlated with patients' survival time. Integrating different datasets, including ATAC-Seq and ChIP-Seq, we performed multi-parallel analyses and identified eight age-dependent protein coding genes and two non-coding RNAs as potential candidates. These candidates, together with [[KLF5]], a potent functional transcription factor in pancreatic cancer, are likely to be key elements linking cellular senescence and pancreatic cancer, providing insights on the balance between them, as well as on diagnosis and subsequent prognosis of pancreatic cancer.

|keywords=* RNA-Seq
* Senescence
* gene Module
* non-coding RNA
* pancreatic Cancer
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7567515
}}
{{medline-entry
|title=[[EGR1]] promotes the cartilage degeneration and hypertrophy by activating the Krüppel-like factor 5 and β-catenin signaling.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31201921
|abstract=Osteoarthritis is one of the most common orthopedic diseases in elderly people who have lost their mobility. In this study，we observed abnormally high [[EGR1]] expression in the articular cartilage of patients with osteoarthritis. We also found significantly high [[EGR1]] expression in the articular cartilage of mice with destabilized medial meniscus (DMM)-induced osteoarthritis and 20-month-old mice. In vitro experiments indicated that IL-1β could significantly enhance [[EGR1]] expression in primary mouse chondrocytes. [[EGR1]] over-expression in chondrocytes using adenovirus could inhibit COl2A1 expression and enhance [[MMP9]] and [[MMP13]] expression. And silencing [[EGR1]], using RNAi, had the opposite effects. Moreover, [[EGR1]] over-expression accelerated chondrocyte hypertrophy in vitro, and [[EGR1]] knockdown reversed this effect. We then explored the underlying mechanism. [[EGR1]] over-expression increased Kruppel-Like Factor 5 ([[KLF5]]) protein level without influencing its synthesis. Enhanced [[EGR1]] expression induced its integration with [[KLF5]], leading to suppressed ubiquitination of [[KLF5]]. Moreover, [[EGR1]] prompted β-catenin nuclear transportation to control chondrocyte hypertrophy. Ectopic expression of [[EGR1]] in articular cartilage aggravated the degradation of the cartilage matrix in vivo. The [[EGR1]] inhibitor, ML264, protected chondrocytes from IL-1β-mediated cartilage matrix degradation in vitro and DMM-induced osteoarthritis in vivo. Above all, we demonstrate the effect and mechanisms of [[EGR1]] on osteoarthritis and provide evidence that the ML264 might be a potential drug for treating osteoarthritis in the future.
|mesh-terms=* Aging
* Animals
* Cartilage, Articular
* Chondrocytes
* Early Growth Response Protein 1
* Heterocyclic Compounds, 3-Ring
* Humans
* Interleukin-1beta
* Kruppel-Like Transcription Factors
* Matrix Metalloproteinase 9
* Mice
* Mice, Inbred C57BL
* Osteoarthritis
* RNA Interference
* RNA, Small Interfering
* Signal Transduction
* Ubiquitin
* Ubiquitination
* Up-Regulation
* beta Catenin
|keywords=* Chondrocyte
* EGR1
* KLF5
* Osteoarthritis
|full-text-url=https://sci-hub.do/10.1016/j.bbadis.2019.06.010
}}
{{medline-entry
|title=The Ets transcription factor [[EHF]] as a regulator of cornea epithelial cell identity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24142692
|abstract=The cornea is the clear, outermost portion of the eye composed of three layers: an epithelium that provides a protective barrier while allowing transmission of light into the eye, a collagen-rich stroma, and an endothelium monolayer. How cornea development and aging is controlled is poorly understood. Here we characterize the mouse cornea transcriptome from early embryogenesis through aging and compare it with transcriptomes of other epithelial tissues, identifying cornea-enriched genes, pathways, and transcriptional regulators. Additionally, we profiled cornea epithelium and stroma, defining genes enriched in these layers. Over 10,000 genes are differentially regulated in the mouse cornea across the time course, showing dynamic expression during development and modest expression changes in fewer genes during aging. A striking transition time point for gene expression between postnatal days 14 and 28 corresponds with completion of cornea development at the transcriptional level. Clustering classifies co-expressed, and potentially co-regulated, genes into biologically informative categories, including groups that exhibit epithelial or stromal enriched expression. Based on these findings, and through loss of function studies and ChIP-seq, we show that the Ets transcription factor [[EHF]] promotes cornea epithelial fate through complementary gene activating and repressing activities. Furthermore, we identify potential interactions between [[EHF]], [[KLF4]], and [[KLF5]] in promoting cornea epithelial differentiation. These data provide insights into the mechanisms underlying epithelial development and aging, identifying [[EHF]] as a regulator of cornea epithelial identity and pointing to interactions between Ets and KLF factors in promoting epithelial fate. Furthermore, this comprehensive gene expression data set for the cornea is a powerful tool for discovery of novel cornea regulators and pathways. 
|mesh-terms=* Aging
* Animals
* Cell Differentiation
* Cell Lineage
* Cornea
* Embryonic Development
* Epithelial Cells
* Gene Expression Profiling
* Gene Expression Regulation, Developmental
* Kruppel-Like Transcription Factors
* Mice
* Transcription Factors
|keywords=* Aging
* Chromatin Immunoprecipitation (ChiP)
* Cornea
* DNA Transcription
* Development
* Epithelium
* Eye
* Gene Expression
* Transcription/Developmental Factors
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3843046
}}