KLF10

Last update 08 May 2025

Basic Info

Synonyms

EGR-alpha, EGRA, KLF10

+ [7]

Introduction

Transcriptional repressor which binds to the consensus sequence 5'-GGTGTG-3'. Plays a role in the regulation of the circadian clock; binds to the GC box sequence in the promoter of the core clock component ARTNL/BMAL1 and represses its transcriptional activity. Regulates the circadian expression of genes involved in lipogenesis, gluconeogenesis, and glycolysis in the liver. Represses the expression of PCK2, a rate-limiting step enzyme of gluconeogenesis (By similarity). May play a role in the cell cycle regulation.

100 Clinical Results associated with KLF10

100 Translational Medicine associated with KLF10

0 Patents (Medical) associated with KLF10

367

Literatures (Medical) associated with KLF10

01 Jun 2025·The Pharmacogenomics Journal

Exploring pharmacogenetic factors influencing hydroxyurea response in tanzanian sickle cell disease patients: a genomic medicine approach

Article

Author: Nzunda, Collin ; Alimohamed, Mohamed Zahir ; Chamba, Clara ; Sangeda, Raphael Z ; Karim, Salman ; Mgaya, Josephine ; Ngowi, Doreen ; Yonazi, Mbonea ; Buchard, Eliud ; Saukiwa, Emmanuel ; Chimusa, Emile R ; Johansen, Julieth ; Kaywanga, Frida ; Urio, Florence ; Novelli, Enrico ; Dandara, Collet ; Solomon, David ; Makani, Julie ; Kindole, Christina ; Nkya, Siana ; Christopher, Heavenlight

In sub-Saharan Africa, sickle cell disease (SCD) remains a significant public health challenge. Despite the discovery of SCD over a century ago, progress in developing and accessing effective treatments has been limited. Hydroxyurea is the primary drug used for managing SCD and associated with improving clinical outcomes. However, up to 30% of patients do not respond to hydroxyurea, likely due to genetic factors. This study involved 148 individuals with SCD investigated the association of hydroxyurea response with genetic variants across 13 loci associated with HbF synthesis and drug metabolism, focusing on MYB, HBB, HBG1, HBG2, BCL11A, KLF10, HAO2, NOS1, ARG2, SAR1A, CYP2C9, and CYP2E1. Significant associations with hydroxyurea response were identified in CYP2C9, CYP2E1, KLF10, BCL11A, ARG2, HBG1, SAR1A, MYB, and NOS1 loci. Furthermore, pathway enrichment and gene-gene interaction analyses provide deeper insights into the genetic mechanisms underlying hydroxyurea treatment response, highlighting potential avenues for personalized therapy in SCD management.

01 Apr 2025·Cytotechnology

FXYD6 is transcriptionally activated by KLF10 to suppress the aggressiveness of gastric cancer cells

Article

Author: Zhou, Xin ; Liu, Chao ; Xu, Rui ; Wang, Guangsheng ; Zhu, Chenyu

Despite improvements in therapeutic approaches, the mortality rate of gastric cancer (GC) remains unacceptably high. Evidence suggests that FXYD domain containing ion transport regulator 6 (FXYD6) is downregulated in GC. However, its exact function and the molecular mechanism in GC are still unclear. FXYD6 expression in different cell lines was estimated using RT-qPCR. Western blotting was employed for protein expression detection. Cell counting kit-8 assay, colony formation assay, and flow cytometry were implemented to assess GC cell viability, proliferation, and apoptosis, respectively. Bioinformatics analysis as well as chromatin immunoprecipitation and luciferase reporter assays were utilized for verifying FXYD6 interaction with the transcription factor Krüppel-like factor 10 (KLF10). The results showed that FXYD6 displayed a decreased level in GC cell lines. Impaired proliferative ability and enhanced apoptotic capacity were observed in GC cells overexpressing FXYD6. KLF10 expression is positively correlated with FXYD6 expression in GC samples. KLF10 binds to the FXYD6 promoter to enhance its transcription. FXYD6 depletion counteracted KLF10 upregulation-triggered reduction in GC cell proliferation and elevation in apoptosis. In conclusion, KLF10 activates FXYD6 transcription, thereby impeding GC cell proliferation and promoting cell apoptosis.

01 Mar 2025·Cell Proliferation

Single‐nucleus transcriptomics reveals subsets of degenerative myonuclei after rotator cuff tear‐induced muscle atrophy

Article

Author: Sun, Ziying ; Zhang, Hanwen ; Wang, Zheng ; Liu, Yuan ; Yang, Xiaojiang ; Lai, Chengteng ; Wang, Yang ; Lu, Zhihao ; Lv, Zhongyang ; Wang, Xingyun ; Qiao, Chenfeng ; Lin, Jintao ; Cheng, Xi ; Sun, Wenshuang ; Meng, Jia ; Qian, Hong ; Yuan, Tao ; Bao, Nirong

AbstractRotator cuff tear (RCT) is the primary cause of shoulder pain and disability and frequently trigger muscle degeneration characterised by muscle atrophy, fatty infiltration and fibrosis. Single‐nucleus RNA sequencing (snRNA‐seq) was used to reveal the transcriptional changes in the supraspinatus muscle after RCT. Supraspinatus muscles were obtained from patients with habitual shoulder dislocation (n = 3) and RCT (n = 3). In response to the RCT, trajectory analysis showed progression from normal myonuclei to ANKRD1+ myonuclei, which captured atrophy‐and fatty infiltration‐related regulons (KLF5, KLF10, FOSL1 and BHLHE40). Transcriptomic alterations in fibro/adipogenic progenitors (FAPs) and muscle satellite cells (MuSCs) have also been studied. By predicting cell–cell interactions, we observed communication alterations between myofibers and muscle‐resident cells following RCT. Our findings reveal the plasticity of muscle cells in response to RCT and offer valuable insights into the molecular mechanisms and potential therapeutic targets of RCT.

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KLF10

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