Human Klf4 mRNA 20 ug
- Known as:
- Human Klf4 mRNA 20 ug
- Catalog number:
- MR300A-2
- Product Quantity:
- 20 ug
- Category:
- -
- Supplier:
- SBI
- Gene target:
- Human Klf4 mRNA 20
Related genes to: Human Klf4 mRNA 20 ug
- 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
Related products to: Human Klf4 mRNA 20 ug
Related articles to: Human Klf4 mRNA 20 ug
- Endothelial cells (ECs) are key regulators in vascular homeostasis, and their physiological state depends on hemodynamic forces produced by the blood flow. Laminar shear stress (LSS) maintains endothelial integrity, whereas oscillatory shear stress (OSS) leads to endothelial dysfunction and subsequently to cardiovascular disease. Here, we delineated the proteomic signatures of human umbilical vein endothelial cells (HUVECs) exposed to a protective flow (LSS) or a disturbed flow (OSS) in comparison to static conditions, using trapped ion mobility spectrometry coupled with parallel accumulation-serial fragmentation. OSS induced limited changes in cell morphology and the proteomic profile, whereas LSS triggered major modifications in cell shape and a proteomic signature related to the cell surface and extracellular matrix. Membrane subproteomic profiling confirmed the identification of membrane effectors involved in flow-mediated responses and in silico integrating promoter analysis suggested Krüppel-like Factor 4 (KLF4) as an important transcriptional regulator of this effector cluster. Using a novel EC model, TeloHAECs, we demonstrated that KLF4 likely contributes to LSS-induced alignment and elongation by increasing the expression of , , , and and that KLF4 is involved in and expression. Collectively, these findings provide a robust discovery data set on EC proteomic profiles related to flow and a refined view of KLF4-associated regulatory signatures at the level of membrane protein-coding genes in response to LSS. - Source: PubMed
Publication date: 2026/07/06
Réthoré LéaBarré BenjaminGuihot Anne-LaureGrimaud LindaProux CoralyneBoissard AliceHenry CécileGuette CatherineGuillonneau FrançoisHenrion DanielLegros ChristianLegendre Claire - This study aimed to investigate the role of the m6A demethylase ALKBH5 in RIPostC against CI/R injury and its underlying regulatory mechanism. A rat model of CI/R was established using the MCAO method. Subsequently, RIPostC was performed to evaluate its therapeutic potential against CI/R injury. The effects of overexpressing ALKBH5 and KLF4 on CI/R injury were also examined in the rat model. A cellular model of CI/R was established by inducing OGD/R in PC12 cells. The effects of ALKBH5 and KLF4 on cellular function in the CI/R model were investigated, and the specific regulatory role of ALKBH5 in the mA modification of KLF4 was elucidated. The mRNA expression of ALKBH5 and KLF4 in acute ischemic stroke patients and healthy individuals was measured by RT-qPCR. The results demonstrated that ALKBH5 and KLF4 expression was decreased in acute ischemic stroke patients, as well as in CI/R rats and OGD/R-induced cells. RIPostC treatment alleviated MCAO-induced neurological deficits, reduced cerebral infarct volume, apoptosis, and inflammatory cytokine levels. Furthermore, RIPostC upregulated the expression of ALKBH5 and KLF4 in CI/R rats. Overexpression of ALKBH5 and KLF4 further enhanced the therapeutic efficacy of RIPostC in CI/R rats. Overexpression of ALKBH5 and KLF4 alleviated OGD/R-induced cellular injury. Mechanistically, overexpression of ALKBH5 upregulated KLF4 expression by promoting m6A demethylation of KLF4 mRNA. In conclusion, overexpression of ALKBH5 upregulates KLF4 by promoting mA demethylation, thereby attenuating CI/R injury. - Source: PubMed
Publication date: 2026/07/05
Wang AimeiWu WeiqiYin MeiWang YingZhou MingruiLiu LuluLi ChunyanMiao Wei - Lung adenocarcinoma (LUAD) is the most common lung cancer histological subtype. Although the unfolded protein response (UPR) has been linked to various human diseases, its role in LUAD remains unclear. To identify UPR-related genes, we applied various methods, including weighted gene co-expression network analysis, differential expression analysis, and multivariate Cox regression. Ten machine learning algorithms were used to construct a UPR-related signature (UPRRS), which was validated using multiple public LUAD datasets. The UPRRS was integrated into a nomogram used in clinical practice for prognosis prediction. We also evaluated predicted drug sensitivity patterns across different risk subgroups. We identified 33 UPR-associated hub genes. A UPRRS was developed through systematic evaluation of 101 machine-learning combinations, exhibiting stable prognostic performance across multiple cohorts. Integration of the UPRRS into a nomogram facilitated the construction of a quantitative prognostic model. Significant differences in biological processes and tumor microenvironment immune cell infiltration were observed between the high- and low-risk UPRRS groups. All five UPRRS genes (ALDH2, FKBP4, KLF4, LAIR1, SIDT2) were validated at the protein level in LUAD cell lines, and FKBP4 was further confirmed by IHC in clinical tissues. Functional experiments showed that FKBP4 knockdown inhibited proliferation, migration, and invasion of A549 and H1975 cells, supporting a potential role for FKBP4 in LUAD progression. Our UPRRS provides a promising tool for prognostic stratification and may offer additional insights into tumor immune microenvironment characterization and therapeutic response prediction in LUAD. - Source: PubMed
Publication date: 2026/07/04
Jiao RuiWu ChengyangZhang TaoYan HanyuHe WeidongWang ZhaoyangYan Xiaolong - Cerebral ischemia/reperfusion injury (CI/RI) is a critical pathological process in ischemic stroke. Pyroptosis plays a central role in the development of CI/RI. NOD-like receptor protein 3 (NLRP3) inflammasome is a key initiator of pyroptosis and is associated with neuroinflammation. Although Tanshinone IIA (Tan-IIA) downregulates NLRP3 expression, its role in NLRP3-mediated neuronal pyroptosis during CI/RI remains unclear. In the current study, we aimed to evaluate the neuroprotective effects of Tan-IIA on CI/RI and elucidate the underlying molecular mechanisms. We used rat middle cerebral artery occlusion/reperfusion (MCAO/R) and PC12 cell oxygen-glucose deprivation/reoxygenation (OGD/R) models to investigate the underlying mechanisms. A range of methodologies were used, including neurological function scoring, western blotting, co-immunoprecipitation (Co-IP), dual-luciferase reporter assays, chromatin immunoprecipitation (ChIP), and cycloheximide (CHX) chase. Tan-IIA substantially improved neurological function, reduced cerebral infarction volume, and mitigated neuronal necrosis in MCAO/R rats. In PC12 cells, Tan-IIA showed a pronounced protective effect against OGD/R-induced damage in OGD/R. Mechanistically, in vitro evidence suggests that Tan-IIA upregulates Krüppel-like factor 4 (KLF4) expression. This, in turn, transcriptionally activates the Carboxy-terminus of Hsc70-interacting protein (CHIP). The increased CHIP expression appeared to promote ubiquitination and degradation of the NLRP3 protein, inhibiting the NLRP3 inflammasome activation, caspase-1 cleavage, and the maturation of interleukin (IL)-1β and IL-18, suppressing neuronal pyroptosis. Our findings suggest that Tan-IIA alleviates CI/RI at least in part through a KLF4/CHIP/NLRP3-related mechanism, with strong in vitro support for this pathway. Direct causal validation in vivo remains to be established. This study provides evidence of the protective role of Tan-IIA in experimental models of CI/RI. - Source: PubMed
Publication date: 2026/07/01
Zhong ZhenzhenHuang ZhilinWu ZhaopingNie XiaoyanLiang JiWen JunZhang Xiaobo - Pantothenic acid (PA), or vitamin B5, can be synthesized by gut commensals, but the contribution of microbial PA to metabolic health remains unclear. Here, we find that microbial PA supply is reduced in individuals with metabolic syndrome (MetS) and is associated with impaired gut barrier function and disease severity. Tracing microbial PA identifies Bacteroides fragilis as a key contributor, with panC required for PA biosynthesis, as confirmed by isotope tracing, bacterial culture, and germ-free colonization. In MetS models, colonization with wild-type, but not ΔpanC B. fragilis, restores PA, preserves gut barrier integrity, reduces endotoxemia, and improves metabolic dysfunction. Mechanistically, microbial PA requires host pantothenate kinase activity, as silencing pantothenate kinase 2/3 (PANK2/3) in colonic organoids and in vivo reduces coenzyme A (CoA)/acetyl-CoA metabolism, suppresses Krüppel-like factor 4 (KLF4)-associated differentiation programs, and blunts the protective effects of microbial PA. Finally, a plant-derived polysaccharide enriches PA-producing Bacteroides and restores colonic PA, highlighting a strategy for colonic homeostasis and metabolic health. - Source: PubMed
Publication date: 2026/07/01
Luo ZichenXiao ZihanYuan TianjieWang XuanShi ChenXu WeichenChong YingHou XionglinWu PeifengLi MingxiaoHe XiaofangZhou YiZhang TaoJi XinyuSu KeChen TaoWang XuzhuoXie TongDi LiuqingLi HoukaiXu BinCheng HaiboShan Jinjun