GKLF EMSA Kit
- Known as:
- GKLF EMSA Kit
- Catalog number:
- AY1314
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- GKLF EMSA Kit
Related genes to: GKLF EMSA Kit
- Gene:
- KLF4 NIH gene
- Name:
- Kruppel like factor 4
- Previous symbol:
- -
- Synonyms:
- EZF, GKLF
- Chromosome:
- 9q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-14
- Date modifiied:
- 2016-10-05
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- While exercise-based rehabilitation is known to positively impact functionally related parameters, the role of genomic and epigenomic responses coordinated with cellular, extracellular matrix (ECM), mitochondrial, and microvascular adaptations remains insufficiently investigated. This narrative review summarizes mechanistic evidence linking exercise-associated mechanical, metabolic, hypoxia-redox, inflammatory, and hemodynamic stimuli with tissue remodeling and clinically relevant biomarkers. Current findings indicate that integrin-focal adhesion kinase (FAK) signaling and Hippo YAP/TAZ pathways contribute to mechanical signal transduction, cytoskeletal regulation, and gene expression, whereas metabolic adaptation, ATP homeostasis, and protein synthesis are regulated through AMPK-PGC-1α, SIRT1, and mTOR-dependent pathways. Epigenetic mechanisms, including DNA methylation, histone modifications, chromatin remodeling, and noncoding RNA regulation, further influence cell-specific responses in myofibers, satellite cells, fibro-adipogenic progenitors, endothelial cells, pericytes, and immune cells. In addition, VEGF-VEGFR2, eNOS-NO, and KLF2/KLF4 signaling, together with extracellular matrix turnover and inflammation resolution, contribute to tissue repair and microvascular adaptation during rehabilitation. Importantly, acute exercise-induced molecular responses should not be interpreted as direct evidence of sustained tissue adaptation. Circulating microRNAs, extracellular vesicles, cell-free DNA, collagen-related markers, and vascular proteins represent promising approaches for monitoring rehabilitation-related changes; however, their clinical translation remains limited by challenges related to tissue specificity, biomarker kinetics, analytical variability, and the need for standardized validation alongside structural and functional outcomes. - Source: PubMed
Publication date: 2026/09/10
Song HonghongLi JiaoXu HengPattanimuthu AnanthiMuthusamy ParamasivamLiu JunDu JunyingDu YiSun Chen - - Source: PubMed
- Fragrance products are widely used in daily life. Nevertheless, the biological effects associated with specific fragrance formulations remain insufficiently characterized due to the complexity of their chemical composition. This study aimed to provide an integrated multi-organ evaluation of the effects of inhaling a tested commercial fragrance formulation on oxidative stress, physiological parameters, neurotoxicity-related biomarkers, and gene expression in rats, and to assess the potential protective role of vitamin E. - Source: PubMed
Publication date: 2026/08/26
Al-Sowayan Noora SalehAl-Shebel Daniyah Khaled - Colorectal cancer (CRC) is a common cause of cancer-related deaths worldwide. Electron transfer flavoprotein dehydrogenase (ETFDH) is a novel prognostic biomarker for human CRC. However, the role and molecular mechanism of ETFDH in CRC are still unclear. DEGs in CRC development were identified using mRNA microarray datasets GSE23011, GSE44076, and GSE113513. Gene expression was determined using RT-qPCR and Western blot. Cell proliferation, migration, and invasion were detected by EdU, Colony formation, Transwell, and wound healing. Effects of CRC cells on CD8+ T cell apoptosis were analyzed using flow cytometry. Effects of ETFDH on CRC cell growth in vivo was analyzed using xenograft model. After JASPAR prediction, the binding between Transcription factor Kruppel-like factor 4 (KLF4) and ETFDH promoter was verified using ChIP and dual-luciferase reporter. ETFDH and KLF4 were decreased in CRC tissues and cells. ETFDH upregulation blocked CRC cell proliferation, migration, invasion, and repress the apoptosis of CD8+ T cells in vitro. ETFDH overexpression hindered CRC tumor growth in vivo. Mechanistically, KLF4 enhanced the transcriptional activity of ETFDH via binding to its promoter region. KLF4-activated ETFDH transcription suppresses CRC cell malignant behavior and decreases the apoptosis of CD8+T cells, which provides a promising therapeutic target for CRC. - Source: PubMed
Zeng YanLiu QiaozhenXu YaliZhao TongHu Zhiping - Stem cell aging significantly impairs therapeutic efficacy, requiring innovative strategies to restore potency. We present a microfluidic cell-compressing platform for reactivation (µ-CPR) designed to apply controlled hydrodynamic deformation to late-passage stem cells. This mechanical stimulation facilitates functional reactivation without external chemical cues. Within a defined window, µ-CPR reduces oxidative stress, SA-β-gal activity, and γ-H2A.X foci, while enhancing proliferation and increasing the expression of canonical stemness-associated markers, including OCT4, SOX2, and KLF4. Mechanical stimulation via µ-CPR induces coordinated structural remodeling: nuclei become more compact, actin cortex organization is restored, α-actinin redistributes to focal adhesions, and microtubule networks are restructured, suggesting reorganization of intracellular mechanical architecture. Transcriptomic and proteomic analyses reveal that this process reprograms extracellular matrix remodeling and DNA repair pathways while attenuating pro-fibrotic and senescence-associated secretory phenotype (SASP)-associated pathways. Crucially, this reactivation occurs without compromising fundamental stem cell hallmarks, preserving intrinsic immunophenotypes and multilineage differentiation potential. Functionally, µ-CPR-processed stem cells demonstrate enhanced in vitro wound closure and improved tissue repair in vivo, with efficacy dependent on the applied mechanical dose. This platform establishes a non-genetic, mechanobiological approach to functional stem cell reactivation, offering a scalable strategy for restoring stem cell function and providing a foundation for future cellular rejuvenation strategies. - Source: PubMed
Publication date: 2026/09/09
Jang Soo BinJeon Tak-IlKang Geun-HoSeo DonghwanKim HyeleeYeo HancheolSeok JaekwonLim Kyung MinDayem Ahmed AbdalKim Se JongSong KwonwooKwak YeonjooHur JeongsooChung Aram JCho Ssang-Goo