KLF11 antibody - N-terminal region (ARP30042_T100)
- Known as:
- KLF11 (anti-) - N-terminal region (ARP30042_T100)
- Catalog number:
- arp30042_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KLF11 antibody - N-terminal region (ARP30042_T100)
Related genes to: KLF11 antibody - N-terminal region (ARP30042_T100)
- Gene:
- KLF11 NIH gene
- Name:
- Kruppel like factor 11
- Previous symbol:
- TIEG2
- Synonyms:
- Tieg3, MODY7
- Chromosome:
- 2p25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-02
- Date modifiied:
- 2016-10-05
Related products to: KLF11 antibody - N-terminal region (ARP30042_T100)
Related articles to: KLF11 antibody - N-terminal region (ARP30042_T100)
- Transforming growth factor-β1 (TGF-β1) and tumor necrosis factor-α (TNF-α) are central regulators of vascular inflammation and remodeling in coronary artery disease. However, their cell-type-specific and context-dependent effects in primary human coronary artery endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) remain incompletely defined. Primary human coronary artery endothelial cells (pHCAECs) and smooth muscle cells (pHCASMCs) were stimulated with TGF-β1 (10 ng/mL), TNF-α (100 ng/mL), or their combination. Canonical SMAD2/3 activation, Krüppel-like factor 11 (KLF11) expression, cytoskeletal and junctional remodeling, vascular cell adhesion molecule-1 (VCAM-1) expression, migration dynamics (wound healing and confluent assays), and endothelial tube formation were assessed using immunofluorescence microscopy, live-cell imaging, and quantitative trajectory analysis. Both cytokines were associated with increased nuclear pSMAD2/3 signal in ECs and VSMCs, consistent with functional interplay between inflammatory and TGF-β-related signaling pathways. In pHCAECs, TNF-α robustly induced VCAM-1 functional expression and disrupted VE-cadherin continuity, whereas TGF-β1 primarily promoted cytoskeletal remodeling without strong inflammatory activation. TGF-β1 increased endothelial migration velocity and accumulated distance. In contrast, TNF-α preferentially enhanced Euclidean displacement and directional persistence, shifting the migratory pattern toward more directed movement most evident under combined TGF-β1 + TNF-α stimulation. Notably, TGF-β1 significantly reduced endothelial tube formation, indicating impaired network organization rather than proangiogenic activity. In pHCASMCs, TGF-β1 enhanced migratory activity, particularly in confluent monolayers, whereas TNF-α enhanced directional displacement. KLF11 was induced by TGF-β1 in both pHCAECs and pHCASMCs. In pHCAECs, TNF-α also increased KLF11 and co-stimulation promoted nuclear enrichment, whereas in pHCASMCs TNF-α alone was not effective and combined treatment amplified the TGF-β1 response, supporting cell-type-specific integration of inflammatory and TGF-β-dependent signals. TGF-β1 and TNF-α differentially regulate the inflammatory activation and migration of primary human coronary vascular cells in a cell-type- and structural-context-dependent manner. TGF-β1 enhances migratory force generation, whereas TNF-α reinforces directional polarization, and their integration determines effective vascular repair dynamics. Canonical SMAD2/3 activation does not uniformly predict functional outcome, and KLF11 was identified as a context-sensitive transcription-associated factor showing differential nuclear localization in response to cytokine stimulation, representing a hypothesis-generating observation for future mechanistic studies. - Source: PubMed
Publication date: 2026/04/29
Bonowicz-Kozłowska KlaudiaJerka DominikaTwardak DamianKleszczyński KonradGagat Maciej - The gene can cause maturity-onset diabetes of the young type 7 (MODY7). Currently, there are few reports on MODY7 cases and their clinical and functional characteristics. This study aimed to analyze the clinical and functional features of the R29Q variant to provide a basis for the diagnosis and treatment of this disease. - Source: PubMed
Publication date: 2026/03/11
Qiao YidanJiang YanyanZhang MengyangSong YiSong DanXin YingQin GuijunLiu Yanxia - Contrast-induced acute kidney injury (CI-AKI) represents a major clinical complication in cardiovascular interventions with limited preventive options. This study investigated whether the FXR agonist CDCA protects against CI-AKI via transcriptional upregulation of Krüppel-like factor 11 (KLF11) and subsequent inhibition of the JAK2/STAT3 pathway. - Source: PubMed
Publication date: 2026/03/18
Su Bo-WeiYang Hai-XiaWang Wen-HaoWen LinCui Xiao-HuiBao Ya-NanRen Hui-WenWang Guan-YuHu Wen-JuanYuan Ru-QiangWen Rui-KangLuan Zhi-Lin - The global distribution and frequency of maturity onset diabetes of the young (MODY) vary, necessitating investigation across diverse ethnic groups. This study aimed to investigate MODY gene variants and phenotypic characteristics among young Bangladeshi individuals with nonobese, nonautoimmune youth-onset diabetes. Fifty participants with diabetes (onset < 35 years, BMI < 25 kg/m², negative for islet autoantibodies, detectable C-peptide, and a family history of DM) and 50 young individuals with normoglycemia were enrolled. Targeted next-generation sequencing (NGS) was performed on a panel of 14 known MODY genes. Candidate MODY-gene variants were identified in 20% (10/50) of the diabetes cohort. There were 11 heterozygous missense variants across eight genes: HNF1A, PDX1, NEUROD1, KLF11, PAX4 (three variants), BLK, ABCC8 (two variants), and KCNJ11. No variants met the ACMG/AMP criteria for ‘Pathogenic’ or ‘Likely Pathogenic’ classification; all identified variants were categorized as variants of uncertain significance (VUS). No significant phenotypic differences were observed between individuals with diabetes who carried identified variants and those who did not. In conclusion, this study identified candidate MODY variants (all classified as VUS) in one-fifth of the Bangladeshi nonobese, nonautoimmune youth-onset diabetes cohort. These findings provide a preliminary indication of a distinct genetic pattern characterized by a low frequency of common variants and a relative abundance of variants in rare MODY-associated genes. These findings are hypothesis-generating and highlight potential genetic targets for future functional validation to confirm pathogenicity and to support definitive MODY diagnoses. - Source: PubMed
Publication date: 2026/03/17
Hasan MashfiqulSultana NusratShil Kishore KumarAbdus-Salam Sayad BinNayem Maksudur RahmanOliver MerinaPadinjyarekara AswathiGolani TamannaRabbi Mohammad Fazle AlamSalimullah MdAkhteruzzaman SharifHasanat Muhammad Abul - This study aimed to investigate the function of KLF11 in regulating radiosensitivity (RT) in esophageal squamous cell carcinoma (ESCC) and to elucidate the underlying mechanisms. - Source: PubMed
Publication date: 2026/01/20
Xia YaoxiongWang JiazhuZhao DongmeiLi YanliLi SongqinLi ManDong RenyiWang Li