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Last update 08 May 2025

KLF9

Last update 08 May 2025

Basic Info

Synonyms

Basic transcription element-binding protein 1, BTE-binding protein 1, BTEB

+ [6]

Introduction

Transcription factor that binds to GC box promoter elements. Selectively activates mRNA synthesis from genes containing tandem repeats of GC boxes but represses genes with a single GC box. Acts as an epidermal circadian transcription factor regulating keratinocyte proliferation (PubMed:22711835).

Drugs associated with KLF9

Transcription Factor Inhibitors (Adynxx)

Target

KLF15 x KLF6 x KLF9

Mechanism

KLF15 inhibitors [+2]

Active Org.-

Originator Org.

Adynxx, Inc.

Active Indication-

Inactive Indication

Inflammatory pain [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with KLF9

100 Translational Medicine associated with KLF9

0 Patents (Medical) associated with KLF9

447

Literatures (Medical) associated with KLF9

01 Dec 2025·Human & Experimental Toxicology

KLF9 mediates NLRP3 inflammasome and reactive oxygen species to mediate pyroptosis in trophoblasts

Article

Author: Chen, Min ; Li, Qian

IntroductionThe objective of this study was to explore the effect of KLF9 on oxidative stress (OS) and NLRP3-mediated inflammation in preeclampsia (PE).Methods Lipopolysaccharide (LPS)+adenosine triphosphate (ATP)-induced HTR-8/SVneo cells were used as an in vitro PE inflammation cell model. shRNA was used to interfere with KLF9 expression (sh-KLF9) to assess the transfection efficiency and the effect of KLF9 on cell proliferation, migration, and invasion. ELISA was performed to detect OS-related factors and inflammatory cytokines. Reactive oxygen species (ROS) levels and pyroptosis were analyzed using DCFH-DA and TUNEL staining. LPS and ATP induced HTR-8/SVneo cells were co-transfected with sh-PRDX6/sh-KLF9 to explore the potential regulatory effect of KLF9 on PRDX6. Results LPS+ATP stimulation increased KLF9 expression in the PE cell model. Specifically, reducing KLF9 levels alleviated morphological damage and enhanced proliferation, migration, and invasion in the in vitro PE cell models. Moreover, inhibiting KLF9 expression decreased protein expression of NLRP3, GSDMD-N, cleaved caspase-1, and cleaved-IL-1β, suppressing cell death in LPS+ATP-induced HTR-8/SVneo cells. Analysis of OS indicators revealed that downregulating KLF9 expression restrained intracellular ROS production, decreased MDA expression, and increased SOD and CAT levels. KLF9 regulated the transcription of PRDX6 to attenuate OS and pyroptosis. Knockdown of PRDX6 partially abolished the effect of KLF9 downregulation on OS and pyroptosis of LPS+ATP-induced HTR-8/SVneo cells, as evidenced by the inhibition of cell proliferation, migration, and invasion, as well as the enhanced activity of the NLRP3 inflammasome. ConclusionDownregulation of KLF9 enhances trophoblast cell invasion and reduces OS and NLRP3 inflammasome activation-mediated pyroptosis.

01 May 2025·Journal of Hepatology

Multi-modal analysis of human hepatic stellate cells identifies novel therapeutic targets for metabolic dysfunction-associated steatotic liver disease

Article

Author: Brenner, David A ; Miciano, Charlene ; Preissl, Sebastian ; Han, Cuijuan ; Wang, Allen ; Glass, Christopher K. ; Glass, Christopher K ; Poirion, Olivier B. ; Liu, Xiao ; Hou, Xiaomeng ; Sakane, Sadatsugu ; Carvalho-Gontijo Weber, Raquel ; Rosenthal, Sara Brin ; Miller, Michael ; Kisseleva, Tatiana ; Lee, Wonseok ; Buchanan, Justin ; Diggle, Karin ; Poirion, Olivier B ; Brenner, David A. ; Chilin-Fuentes, Daisy ; Ren, Bing ; Kim, Hyun Young ; Housseini, Mojgan ; Zhao, Huayi

BACKGROUND & AIMSMetabolic dysfunction-associated steatotic liver disease ranges from metabolic dysfunction-associated steatotic liver (MASL) to metabolic dysfunction-associated steatohepatitis (MASH) with fibrosis. Transdifferentiation of hepatic stellate cells (HSCs) into fibrogenic myofibroblasts plays a critical role in the pathogenesis of MASH liver fibrosis. We compared transcriptome and chromatin accessibility of human HSCs from NORMAL, MASL, and MASH livers at single-cell resolution. We aimed to identify genes that are upregulated in activated HSCs and to determine which of these genes are key in the pathogenesis of MASH fibrosis.METHODSEighteen human livers were profiled using single-nucleus (sn)RNA-seq and snATAC-seq. High priority targets were identified, then tested in 2D human HSC cultures, 3D human liver spheroids, and HSC-specific gene knockout mice.RESULTSMASH-enriched activated HSC subclusters are the major source of extracellular matrix proteins. We identified a set of concurrently upregulated and more accessible core genes (GAS7, SPON1, SERPINE1, LTBP2, KLF9, EFEMP1) that drive activation of HSCs. Expression of these genes was regulated via crosstalk between lineage-specific (JUNB/AP1), cluster-specific (RUNX1/2) and signal-specific (FOXA1/2) transcription factors. The pathological relevance of the selected targets, such as SERPINE1 (PAI-1), was demonstrated using dsiRNA-based HSC-specific gene knockdown or pharmacological inhibition of PAI-1 in 3D human MASH liver spheroids, and HSC-specific Serpine1 knockout mice.CONCLUSIONThis study identified novel gene targets and regulatory mechanisms underlying activation of fibrogenic HSCs in MASH, and demonstrated that genetic or pharmacological inhibition of select genes suppressed liver fibrosis.IMPACT AND IMPLICATIONSHerein, we present the results of a multi-modal sequencing analysis of human hepatic stellate cells (HSCs) from NORMAL, MASL (metabolic dysfunction-associated steatotic liver), and metabolic dysfunction-associated steatohepatitis (MASH) livers. We identified additional subclusters that were not detected by previous studies and characterized the mechanism by which HSCs are activated in MASH livers, including the transcriptional machinery that induces the transdifferentiation of HSCs into myofibroblasts. For the first time, we described the pathogenic role of activated HSC-derived PAI-1 (a product of the SERPINE1 gene) in the development of MASH liver fibrosis. Targeting the RUNX1/2-SERPINE1 axis could be a novel strategy for the treatment of liver fibrosis in patients.

01 May 2025·Poultry Science

Identify key transcript factors of adipocyte differentiation in abdominal fat of broilers based on ATAC-seq and RNA-seq

Article

Author: Wang, Chaohui ; Sun, Xi ; Liu, Xiaoying ; Yang, Xiaojun ; Qiao, Zhihao ; Liu, Yanli

Intensive breeding has resulted in excessive deposition of abdominal fat tissue (AFT) in broilers, leading to significant economic loss in the poultry industry. Understanding the molecular mechanisms underlying AFT development is essential for informed breeding strategies. In the current study, we elucidated dynamic changes of chromatin accessibility and transcriptional reprogramming in AFT at D14 and D42 in broilers based on integrated analysis of RNA-seq and ATAC-seq. RNA-seq analysis manifested significant transcriptional differences in AFT development, identifying 1323 up- and 1285 down-regulated differential expression genes (DEGs) as well as 63 up- and 58 down-regulated transcription factors (TFs) at D42 compared to those at D14. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of total DEGs revealed significant enrichment in pathways related to DNA replication, cell adhesion molecules, cell cycle, p53 signaling pathway, fatty acid degradation, fatty acid biosynthesis and steroid biosynthesis. Gene set enrichment analysis (GSEA) further indicated that autophagy, MAPK signaling pathway and inositol phosphate metabolism were up-regulated at D42 compared to D14, whereas cell cycle, DNA replication and steroid biosynthesis were down-regulated. Additionally, ATAC-seq analysis identified 394 gain and 1195 loss differentially accessible peaks (DPs) in AFT between D14 and D42, associated with 319 and 905 genes, respectively. These gain or loss genes were enriched in p53 signaling pathway, PPAR signaling pathway, fat digestion and absorption, FoxO signaling pathway and glycerol lipid metabolism. Integration analysis of ATAC-seq and RNA-seq data revealed 25 up-regulated and 75 down-regulated DEGs overlapping with genes linked to gain and loss DPs, respectively. Notably, ACACA, SCD, SREBF1and KLF9 exhibited significantly lower expression at D42 compared to D14. DNA motifs analysis identified NFIX and MYB as loss motifs, overlapping with down-regulated TFs, suggesting their potential role in AFT regulation. Furthermore, MYB and NFIX exhibited potential binding sites in the promoter regions of lipid metabolism-related genes (ELOVL6, PPARγ, FABP4, ACACA and SCD). Overall, these results will provide a theoretical basis for investigating the epigenetic modification and transcriptional regulation of AFT development in broilers.

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KLF9

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