Disease relevance of Krt1-18

• The results show that K18 expression in cells may result in the suppression of the motile and tumorigenic abilities of this adenocarcinoma [1].
• Moreover, as hepatic injuries developed into fibrosis, a much more prominent single band of CK18 was detected [2].

High impact information on Krt1-18

• In this study, we investigated the potential stem cell marker Thy1 and hepatocytic marker CK-18 during liver development to identify putative fetal liver stem cell candidates [3].
• In conclusion, hepatic progenitor cells (CK-18 positive) in fetal rat liver express Thy1 [3].
• All SHs at day 10 immunocytochemically showed positivity for albumin, transferrin, CK8, and CK18, which are markers for hepatocytes [4].
• The results reported here show first, that CKs are expressed before sexual differentiation in gonadal blastema in which no epithelial organization is observed, and second, that there is a CK 18/CK 19 shift in expression during morphogenesis of the testis which is not observed in the differentiating ovary [5].
• Under these growth-restrictive conditions, immunocytochemical analysis shows that NRP-152 cells acquire the luminal markers Z0-1 (a tight-junction associated protein), occludin (integral tight-junction protein), and cytokeratin 18, and lose the basal markers cytokeratins 5 and 14 [6].

Biological context of Krt1-18

• K18 mRNA expression appeared in male gonads, at 13.5 days of gestation, at the onset of testicular differentiation, as the first Sertoli cells differentiated and aggregated to form seminiferous cords [7].
• The present results indicate that K18 and K19 gene expression is regulated at the transcriptional level [7].
• Contrasting effects of K8 and K18 on stabilizing K19 expression, cell motility and tumorigenicity in the BSp73 adenocarcinoma [1].
• Phosphopeptide maps of keratins phosphorylated in vivo and in vitro indicate that Ca2+/calmodulin-dependent kinase may be involved in regulating the serine-specific phosphorylation of both keratin 8 and keratin 18, while cAMP-dependent protein kinase does not seem to play a major role in this context [8].
• We labled additional sections with anti-M30, directed against an epitope formed by caspase 6 digestion of cytokeratin 18 during apoptosis [9].

Anatomical context of Krt1-18

• In the anterior nasal cavity level 1 (NL1), changes in CK expression patterns were observed in the respiratory epithelium of the lateral wall and the maxilloturbinate (CK14, CK15, and CK18) and in the squamous epithelium of the ventral meatus (CK13) [10].
• Cytokeratin 19 mRNA and protein expression were also significantly decreased when desmosome formation was inhibited in reduced calcium medium, while calcium content of the medium had little effect on cytokeratin 18 [11].
• No significant changes were seen in the overall polyribosome profiles or in the distribution of mRNAs encoding beta and gamma subunits of ENaC or cytokeratin 18, indicating specific modulation of alphaENaC mRNA translation [12].
• The expression of cytokeratin 14 (a marker for basal myoepithelial cells) was reduced, but the expression of cytokeratin 18 (a marker for the luminal epithelial cells) was unaffected by estrogen [13].
• Here we show that brush cells (identified by villin antibodies) can be discriminated from the neighbouring simple epithelium of the stomach, pancreatic duct and duodenum by particularly strong immunoreactivity with antibodies specific for cytokeratin 18 [14].

Associations of Krt1-18 with chemical compounds

• Keratin 8, keratin 18 and desmoplakin I/II are the major cytoskeleton-associated targets for microcystin-LR-induced phosphorylation [8].
• Thy1-enriched cells expressed CK-18 at all times, albumin in the early, and AFP in the late stages [15].
• Feeding ethanol to rats results in dephosphorylation of one site on keratin 8 and one site on keratin 18 at all time points beginning with 6 weeks of ethanol treatment [16].
• T51B-Ni, a subclone selected by prolonged exposure of the parental clone to nickel subsulfide contains CK8 and CK18 (its usual partner in simple epithelium), as well as CK14, at a lower level [17].
• A positive PTTG immunoreactive co-localizing with 5-bromo-2'-deoxyuridine (BrdU) in the hepatocyte nucleus was found and there was a concurrent sister chromatin itself by the immunofluorescent labeling of PTTG with cytokeratin 18 (CK18) [18].

Other interactions of Krt1-18

• Switch in the expression of the K19/K18 keratin genes as a very early evidence of testicular differentiation in the rat [7].
• At the onset of testicular differentiation, when the first Sertoli cells differentiate in the gonad of 13.5-day old male fetuses, positive staining for CK 18 became evident, in addition to CK 8 and CK 19 expression [5].
• Immunohistochemistry was performed on the induced tumors using four commercially available monoclonal antibodies specific for CK 18 (TR1031), CK 13 (K8.12), CK 19 (K4.62), and the CKs 5, 7, and 8 (K8.13) [19].
• These results suggest that expression of cytokeratin 18, a later phenotypic change in foci than induction of GST-P and GGT, correlates more closely with tumour outcome in this model [20].
• Lung specimens from all animals were examined for the presence of apoptosis in type II pneumocytes by an in situ apoptosis assay and for proliferative nuclear antigen, cytokeratin-18, Fas, and Fas ligand with an immunohistochemical stain [21].

Analytical, diagnostic and therapeutic context of Krt1-18

• PCR products were cloned, sequenced and used as species-specific K18 and K19 riboprobes for in situ hybridization [7].
• Immunofluorescence of cytokeratin 18 was performed on extracted cryostat sections which were also used for electron microscopy [22].
• Comparative Northern blot analyses of nuclear and cytoplasmic mRNAs further suggested that the control of CK18 gene expression in T51B cells is post-transcriptionally mediated by nuclear events [17].
• RT-PCR for liver specific markers CK-18 and albumin were performed on the different cell populations [23].
• After 2 weeks, the specified culture conditions led to the expression of albumin and CK-18 RNA in GFP-positive sorted MSCs from the cocultures, whereas MSCs cultured without liver cells did not express the studied genes [23].

References