KLF8 antibody - N-terminal region (ARP31533_P050)
- Known as:
- KLF8 (anti-) - N-terminal region (ARP31533_P050)
- Catalog number:
- arp31533_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KLF8 antibody - N-terminal region (ARP31533_P050)
Related genes to: KLF8 antibody - N-terminal region (ARP31533_P050)
- Gene:
- KLF8 NIH gene
- Name:
- Kruppel like factor 8
- Previous symbol:
- -
- Synonyms:
- BKLF3, ZNF741, DXS741
- Chromosome:
- Xp11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-14
- Date modifiied:
- 2016-06-03
Related products to: KLF8 antibody - N-terminal region (ARP31533_P050)
Related articles to: KLF8 antibody - N-terminal region (ARP31533_P050)
- Objective This study aims to investigate the expression, phenotypic changes, and mechanisms of action of guanylate-binding protein 2 (GBP2) in the process of silica-induced pulmonary fibrosis. Methods The expression and localization of GBP2 in silicotic lung tissue were detected by immunohistochemical staining and immunofluorescence. An in vitro cell model was constructed, and methods such as Western blot and real-time quantitative reverse transcription polymerasechain reaction were utilized to investigate the function of GBP2 in different cell lines following silica stimulation. The mechanism of action of GBP2 in various cell lines was elucidated using Western blot analysis. Results GBP2 was highly expressed in the lung tissue of patients with silicosis. Immunohistochemical staining and immunofluorescence have revealed that GBP2 was localized in macrophages and epithelial cells. In vitro cell experiments demonstrated that silicon dioxide stimulated THP-1 cells to activate the c-Jun pathway through GBP2, promoting the secretion of inflammatory factors and facilitating the occurrence of M2 macrophage polarization. In epithelial cells, GBP2 promoted the occurrence of epithelial to mesenchymal transition (EMT) by upregulating Krueppel-like factor 8 (KLF8). Conclusion GBP2 not only activates c-Jun in macrophages to promote the production of inflammatory factors and the occurrence of M2 macrophage polarization, but also activates the transcription factor KLF8 in epithelial cells to induce EMT, collectively promoting the progression of silicosis. - Source: PubMed
Chen MaoqianWu JingLi XuanZhou JiaweiLiu YafengGuo JianqiangCheng AnqiHu Dong - To validate the clinical utility of a previously identified circulating tumor DNA methylation marker (meth-ctDNA) panel for disease detection and survival outcomes, meth-ctDNA markers were compared to PSA levels and PSMA PET/CT findings in men with different stages of prostate cancer (PCa). - Source: PubMed
Publication date: 2025/02/25
Kluge KilianLotz VincentEinspieler HolgerHaberl DavidSpielvogel ClemensAmereller DominikKramer GeroGrubmüller BernhardShariat ShahrokhHaug AlexanderHacker MarcusKenner LukasEgger Gerda - This study aimed to analyze the role of circSEC24A in non-small cell lung cancer (NSCLC) and its underlying mechanism. - Source: PubMed
Publication date: 2024/10/28
Xiong WeiYang Jinhua - Polycystic ovary syndrome (PCOS) is the most common metabolic and endocrine disorder affecting women of reproductive age. The pathogenesis of PCOS is influenced by factors such as race, genetics, environment, hyperandrogenemia, hyperinsulinemia, and obesity. However, the molecular mechanisms linking RNA modification and PCOS remain underexplored. This study aims to investigate the potential genetic and molecular pathways connecting RNA modification with PCOS through bioinformatics analyses. - Source: PubMed
Publication date: 2024/08/23
Quan KeweiNing ShutingYou ZilinDeng Gaopi - Accurate prostate cancer (PCa) patient diagnosis and risk assessment are key to ensure the best outcome. Currently, low- and favorable intermediate-risk PCa patients may be offered AS due to the indolent nature of the disease. Nonetheless, deciding between active surveillance and curative-intent treatment remains an intricate task, as a subset of these patients may eventually progress, enduring poorer prognosis. Herein, we sought to construct risk calculators based on cancer biomarkers, enabling more accurate discrimination among patients which may benefit from active interventions.Ki67 immunoscore, GSTP1 and KLF8 promoter methylation levels () were assessed in PCa tissues. Study endpoints included overall and biochemical recurrence-free (BCR) survival. Combination with relevant clinicopathological parameters allowed for construction of graphical calculating tools (nomograms).Higher Ki67 index correlated with worse BCR-free survival, whereas higher KLF8 levels were associated with improved overall survival, especially in patients with lower-grade tumors. GSTP1 levels had no prognostic value. Among prognostic models tested, a BCR-risk calculator - ProstARK (including Ki67 and clinicopathologic parameters) - disclosed 79.17% specificity, 66.67% sensitivity, 55% positive predictive value, 86% negative predictive value, and 75.76% accuracy. Similar results were found using an independent PCa biopsy cohort, validating its prognostication ability.Combining clinicopathologic features and Ki67 index into a risk calculator enables easy and accurate implementation of a novel PCa prognostication tool. This nomogram may be useful for a more accurate selection of patients for active surveillance protocols. Nonetheless, validation in a larger, multicentric, set of diagnostic PCa biopsies is mandatory for further confirmation of these results. - Source: PubMed
Publication date: 2024/08/01
Albuquerque-Castro ÂngelaMacedo-Silva CatarinaOliveira-Sousa RúbenConstâncio VeraLobo JoãoCarneiro IsaHenrique RuiJerónimo Carmen