KRT4 Mouse Monoclonal Antibody
- Known as:
- KRT4 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003851-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- KRT4 Mouse Monoclonal Antibody
Related genes to: KRT4 Mouse Monoclonal Antibody
- Gene:
- KRT4 NIH gene
- Name:
- keratin 4
- Previous symbol:
- CYK4
- Synonyms:
- CK4, K4
- Chromosome:
- 12q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2017-12-06
Related products to: KRT4 Mouse Monoclonal Antibody
Related articles to: KRT4 Mouse Monoclonal Antibody
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Publication date: 2026/04/20
Wu GongpingYu WeitaoYao DongnuanMa XuemingFan ChengweiHou JuanjuanRen XuezhaoTian Junqiang - Although mucins are generally linked to aggressive tumor behavior and poor clinical outcomes, the role of MUC21 in oral squamous cell carcinoma (OSCC) remains unexplored. Previous studies suggest that MUC21 may inhibit cancer cell adhesion, indicating its potential significance in OSCC pathogenesis. - Source: PubMed
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Mao LishaKang JiaZou AnnaWang XiangpuGuo SiyuanChen SijiaSu YingGe LihuaYang JingWang Xuejiu - Precise control of keratinocyte proliferation and differentiation is critical for oral epithelial regeneration, yet the mechanobiological cues guiding these processes remain incompletely defined. Here, we systematically evaluated how electrospun polycaprolactone (PCL) scaffolds with defined fiber orientations (aligned vs. random) and diameters (600-800 nm, 1.2-1.7 µm, 2.0-2.5 µm) direct gingival keratinocyte fate. Using immortalized human gingival keratinocytes, we assessed cell and nuclear morphology, proliferation dynamics, differentiation marker expression, and the effects of basal keratin (KRT5/KRT14) knockdown. Quantitative morphological analysis revealed scaffold-dependent changes in cell shape: aligned medium-diameter fibers (with fiber diameters of 1.2-1.7 µm) induced pronounced cell and nuclear elongation, whereas random fibers (600-800 nm) promoted larger, more rounded cell and nuclear shapes. Time-resolved EdU assays indicated that aligned scaffolds supported sustained proliferation, whereas random scaffolds elicited a transient proliferative burst followed by a decline. Gene expression analysis (ddPCR) demonstrated that random scaffolds (especially 600-800 nm fibers) upregulated basal keratins (KRT5, KRT14) and early differentiation markers (KRT1, KRT10, KRT4, KRT13) relative to aligned scaffolds. At the protein level, differentiation markers involucrin (IVL) and filaggrin (FLG) were likewise elevated on random scaffolds, corroborating the mRNA findings. Functional KRT5/KRT14 knockdown experiments revealed scaffold-specific dependencies: cells on random scaffolds required these keratins for viability, whereas aligned cultures remained viable upon KRT5/14 loss. Furthermore, KRT5/14 depletion differentially altered downstream differentiation markers (IVL, KRT1) and mechanotransduction markers (LMNB1, YAP1) in a scaffold-dependent manner. Collectively, these findings establish fiber orientation and diameter as key design parameters for controlling keratinocyte fate. As a translational concept, layered scaffolds combining aligned and random fibers may enable spatially controlled proliferation and differentiation in engineered oral epithelia. - Source: PubMed
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