Cytokeratin 19, CK19 recombinant protein
- Known as:
- Cytokeratin 19, CK19 Rec. protein
- Catalog number:
- BRP1007
- Product Quantity:
- 100 μg
- Category:
- -
- Supplier:
- Biospect
- Gene target:
- Cytokeratin 19 CK19 recombinant protein
Related genes to: Cytokeratin 19, CK19 recombinant protein
- Gene:
- KRT19 NIH gene
- Name:
- keratin 19
- Previous symbol:
- -
- Synonyms:
- K19, CK19, K1CS, MGC15366
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-11
- Date modifiied:
- 2016-03-09
Related products to: Cytokeratin 19, CK19 recombinant protein
Related articles to: Cytokeratin 19, CK19 recombinant protein
- In adult females of most hystricomorph rodents (animals in the suborder Hystricomorpha, such as guinea pigs), the vagina is open only during heat period; for the remainder of the estrous cycle, it is occluded by a structure resembling the human hymen-known as the "vaginal closure membrane" (VCM). This process of periodic formation and regression of the VCM persists throughout the animal's entire life, from puberty until death. To date, the underlying mechanisms explaining why only this small subset of rodents periodically forms a VCM remain largely unelucidated. In this study, we compared the epithelium structure around the external vaginal orifice between guinea pigs and mice, revealed that a hairless epidermal transition zone exists in guinea pig but not mice. The proliferation of keratin (Krt) 10-positive epithelial cells in this zone plays key roles in VCM formation. Hormone treatment in ovariectomized guinea pigs revealed progesterone may promote the formation and thickening of VCM. Ki67 cytoplasmic localization and strong expression of progenitor cell marker Krt19 in epithelial cells at external vaginal orifice of guinea pigs but not mice indicated that the VCM formation in guinea pigs is most likely a tissue remodeling process. And in addition, we identified a novel population of stem cells expressing pluripotency markers at the external vaginal orifice of guinea pigs. Our findings suggest that, in guinea pigs, pluripotent stem cells may reside within the epithelial tissue of the vaginal opening region of adult females and is responsible for VCM formation. - Source: PubMed
Publication date: 2026/07/20
Wang ShanshanZheng Zhengui - Human induced pluripotent stem cell (iPSC)-derived neural cells (NCs) and cardiomyocytes (CMs) show significant promise for clinical applications in regenerative medicine. Because the manufacturing of iPSC-derived products faces challenges in quality reproducibility, cost, and manufacturing time, closed automated culture systems have been developed. Recently, an efficient and noninvasive cell monitoring system based on extracellular markers secreted by cells represents a new strategy for closed systems. Extracellular vesicles (EVs), secreted by cells, contain proteins involved in stem cell differentiation; however, EV proteins in the cell culture medium are difficult to analyze because of their low abundance. Thus, their changes during cell differentiation, and the relationship between EV and cell proteins, remain unclear. In this study, we investigated the changes in EV proteins during iPSC differentiation into NCs and CMs using data-independent acquisition LC/MS/MS (DIA-MS), a highly comprehensive and quantitative approach. We observed significant positive correlations between the EV protein abundance and cellular protein expression levels during differentiation on days 0-7, and identified signature proteins characteristic of NCs and CMs. Among these, trophoblast glycoprotein (TPBG) for NC differentiation and keratin, type I cytoskeletal 19 (KRT19) for CM differentiation were particularly increased in both cells and EVs. Moreover, TPBG and KRT19 levels at day 7 showed similar trends to the differences in differentiation observed among the cell lines, as determined by flow cytometry. These findings suggest that these EV proteins may serve as predictive markers for monitoring differentiation into NC and CM. - Source: PubMed
Publication date: 2026/07/17
Mikami MeiKatsuno EriHoshina ShunsukeTakashita KanseiTakakura DaisukeKawasaki Nana - Ovarian steroid cell tumors-not otherwise specified (SCT-NOS) is a rare category of sex cord-stromal tumor, however, its pathophysiology is unclear. A comprehensive cellular atlas of ovarian SCT-NOS remains lacking. - Source: PubMed
Publication date: 2026/07/17
Huang FeilingChen HongyanMei SongXue HuadanWang QinLu ZhaohuiZhang PengChen Rong - Oral diseases and placental disorders are closely associated with adverse pregnancy outcomes, and accumulating evidence supports their crosstalk that constitutes the "oral-placental axis". This study integrated scientometric and bioinformatic approaches to systematically analyze global research trends, collaboration networks, research hotspots, and core molecular-microbial mechanisms of the oral-placental axis covering the period from 2016 to 2025. A total of 196 eligible publications were retrieved from the Web of Science Core Collection, Scopus, and PubMed. Bibliometric visualization was performed using VOSviewer, CiteSpace, and R-bibliometrix, and bioinformatic analysis was conducted to identify shared genes, signaling pathways, and microbial links between oral and placental diseases. The results revealed an annual publication growth rate of 5.03%, with the United States, China, and Australia as major contributing countries, the University of Queensland as the leading institution, and Gomez-Arango Luisa F. and Nitert Marloes Dekker as the most influential authors. Core keywords included preterm birth, periodontal diseases, gestational diabetes mellitus, and oral microbiome, reflecting a research shift from phenotypic association to mechanistic exploration such as microbial vertical transmission and inflammatory signaling. Mechanistic analyses identified shared hub genes (e.g., KRT19, ADAMDEC1, AQP9, SPAG4, PLAT) and key pathways, predominantly primary immunodeficiency and complement and coagulation cascades. Pathogenic bacteria including and mediated adverse pregnancy outcomes via hematogenous spread and placental barrier disruption. This study established a bidirectional regulatory model of the oral-placental axis involving shared risks, microbial transmission, and systemic inflammation, providing a theoretical basis for preconception oral intervention and precise prevention during pregnancy, and supporting the integration of oral care into routine perinatal management. - Source: PubMed
Publication date: 2026/06/30
Zhang BeiyingYun ZhouhuiYuan YiLi LijieXiong Zhihui - Aurora kinase A (AURKA) is frequently overexpressed in gastrointestinal cancers. Helicobacter pylori (H. pylori) infection is a significant risk factor for gastric carcinogenesis. LGR5, a stem cell marker in the stomach, plays an important role in gastric tumorigenesis. This study investigates the link between AURKA and LGR5 in response to H. pylori infection in gastric cancer. We analyzed publicly available datasets, gastric cancer cell lines, patient-derived organoids and xenografts (PDOs and PDXs), mouse models, and de-identified human tissue samples. We found a strong association between AURKA and LGR5 expression levels in gastric cancer tissues. In vitro and in vivo analyses showed increased AURKA and LGR5 protein levels in response to H. pylori infection. Using cell models and PDOs, we demontrated an AURKA-dependent induction of LGR5, whereas genetic knockdown or pharmacologic inhibition of AURKA abolished the H. pylori-induced increase in LGR5 by enhancing LGR5 ubiquitination. Mechanistically, AURKA interacted with STAMBP, suppressing LGR5 deubiquitination and thereby promoting its stabilization. Using a tamoxifen-induced conditional knockout (CKO) mouse model of Aurka (Krt19/Aurka), we detected a lower baseline expression of LGR5 in gastric glands, with reduced induction following H. pylori infection, compared to controls. The Aurka CKO mouse model was crossed with the Tff1 model of gastric tumorigenesis to create the Krt19/Aurka /Tff1 mouse model. AURKA knockout, after tamoxifen treatment, significantly reduced the LGR5 protein level and led to a marked decrease in antral thickness. In PDX models, the use of a combination treatment of AMG900 (a pan-AURORA inhibitor) with docetaxel was more effective than monotherapy, lowering LGR5 levels and suppressing tumor growth. In summary, there is a functional link between AURKA and LGR5, mediated by STAMBP to promote stem-like properties and enhance cell survival in gastric tumorigenesis. Targeting the AURKA-LGR5 axis is a potential therapeutic strategy. - Source: PubMed
Publication date: 2026/07/11
Gomaa AhmedMaacha SelmaSoutto MohammedGiordano SilviaBhat NadeemKumar ShriaMcDonald Oliver GEl-Rifai Wael