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Cumulatively, these data indicate that altered CK14 (high) and CK18 (low) expression is perhaps an early event in bladder cancer tumorigenesis in females at least and is characteristic of both urothelial superficial pre-neoplastic and neoplastic lesions.
K18 deficiency of hepatocytes leads to steatosis, increasing with age, and finally to SH. K18 deficiency and age promote liver tumor development in mice, frequently on the basis of chromosomal instability, resembling human HCC with stemness features.
K8/K18-dependent PKCdelta- and ASMase-mediated modulation of lipid raft size can explain the more prominent FasR-mediated signaling resulting from K8/K18 loss.
autoantibodies were detected in aging K18-null male mice that had a related liver phenotype but normal colon compared with K8-null mice, suggesting that the autoantibodies are linked to liver rather than colonic disease
In human failing myocardium, where TNF-alpha expression is upregulated, K8/K18 were also ectopically expressed
The findings demonstrate the near complete loss of K8/K18 with concomitant high levels of vimentin in CT26 cells, a chemically-induced mouse colonic tumor.
in contrast to its importance as luminal cell marker, CK18 is dispensable for the prostate morphogenesis but contributes to adult prostate regeneration
Keratin 18 increases CFTR expression by binding to its C-terminal hydrophobic domain.
Oxidative stress, Nrf2 and keratin 18 up-regulation associate with Mallory-Denk body formation in mouse erythropoietic protoporphyria
Keratin 8 and keratin 18 mice on the same genetic background show similar sensitivity to DDC intoxication.
These findings reveal the potential for cytokeratin 18 to be used as a diagnostic marker for early detection of hepatosplenic schistosomiasis.
K18 glycosylation provides a unique protective role in epithelial injury by promoting the phosphorylation and activation of cell-survival kinases.
Krt18 may be a useful immunohistochemical marker for detecting hepatocellular proliferative lesions in mice.
Keratin 8 and keratin 18 play roles in regulating the shape and function of mitochondria.
Data show that inhibition of extracellular signal-regulated kinase 1 and 2 (ERK1/2) activation sensitizes wild-type but not keratin 8 (K8)-null mouse hepatocytes to apoptosis, and is associated with a reduction in c-Flip protein, part of a K8/K18 complex.
loss of the keratin cytoskeleton causes defects in the trophoblast giant cell layer
K18 overexpression protects mice from Mallory body (MB) formation and from DDC-induced liver injury, which supports the importance of the K8-to-K18 ratio in MB formation.
Study demonstrates here that, in the developing placenta of the mouse, the absence of the Mrj co-chaperone prevents proteasome degradation of keratin 18 intermediate filaments, resulting in the formation of keratin inclusion bodies.
study shows that dominant mutation hK18 R89C, leads to cell type-specific lethality in mice, depending on ratio of mutant to endogenous keratins; a single, endogenous K18 allele rescued embryonic lethality but caused aggregation of keratins
Keratin absence or mutation is well tolerated after pancreatic but not liver injury, whereas excessive overexpression is toxic to the pancreas but not the liver when induced under basal conditions.
Study revealed that the expression of CK18 was significantly downregulated in breast cancer tissues and in multiple drug resistance cell line overexpressing breast cancer resistance protein BCRP, and the presence of low levels of CK18 was associated with TNM stage, lymph node metastasis, and unfavorable survival. CK18 knockdown increased BCRP expression and induced the EMT process in human breast cancer MCF7 cells.
CK18F and highlights tCK18 as specific biomarkers.
CK-18 serum levels were lower in longstanding type 1 diabetes patients compared to healthy controls
Subacute elevation of plasma caspase-cleaved cytokeratin-18 levels is associated with unfavorable early and late stroke outcome.
FGF21 and CK18 might play differential roles and have complementary value in non-invasive identification and monitoring the outcome of nonalcoholic fatty liver disease patients.
We found close association between changes in K8/K18 expression and cell death/cell survival events in the human granulosa cell lineage. Large secondary and early antral follicles and regressing corpora lutea showed low/absent K8/K18 expression. Conversely, early growing antral follicles, functional menstrual corpora lutea, as well as corpus luteum of pregnancy, where cell death was scarce, showed high K8/K18 expression.
Changes in the expression of cytokeratin18 by the cancer prostate are heterogeneous. The increase in local variability of ck18 immunoexpression can be related to the increase in heterogeneity of shape and size of the tumor acini.
the present study demonstrated that CK18 might be served as a novel biomarker to predict clinicopathological features and the outcome of breast cancer.
Cytokeratin 5/6 and CK8/18 immunohistochemistry on 150 cases of triple negative breast cancers was performed and association with various clinicopathological features was evaluated.
This study analyzed phase III data comparing basal insulin peglispro (BIL) and insulin glargine in type 1 (T1D), and type 2 diabetes (T2D) (insulin-naive and insulin-treated). Alanine aminotransferase (ALT), K-18, enhanced liver fibrosis scores and liver fat content.
Results found that CK18, MMP-9, and TIMP1 averages of those with positive clinical lymph nodes and those in clinical stage 3 were higher than the averages of those with negative clinical lymph nodes and those in clinical stage 2.
non-surviving severe malignant middle cerebral artery infarction patients had higher serum CCCK-18 levels than surviving patients
Plasma M30-M65 levels are higher in serum of patients with placental abruption.
results show that the caspase digestion-resistant K18 helps to maintain keratin filament organization and delays apoptosis, thereby resulting in protection from liver injury.
K8/K18 variants are overrepresented in Chinese NAFLD patients and might accelerate liver fat storage through insulin resistance.
The plasma keratin-18 (K18) values of nonsurviving alcoholic hepatitis (AH) patients were significantly elevated above their surviving counterparts and healthy controls
Evidence suggested that the modification of histone H3 was highly correlated with the modulation of cytokeratin 18 and probably plays an important role in tumorigenesis of hepatocytes
K8/K18 interact with Notch1 and regulate Notch1 signalling activity during differentiation of the colonic epithelium.
FIB-4 index and CK-18F have good diagnostic abilities not only for nonalcoholic steatohepatitis (NASH) overall, but also for NASH with mild fibrosis.
In children with nonalcoholic fatty liver disease, CK18 levels were found to be significantly higher in subjects with any fibrosis compared with those without fibrosis (304.6 +/- 124.8 vs 210.4 +/- 70.9, P < 0.001).
Data identify Danio rerio keratins 8/18 as the true orthologs of the human keratin pair 8/18.
krt18 is maternally inherited and its tissue distribution is reported. Its expression is established during early embryogenesis.
Ezrin and CK18 are downregulated during implantation in cattle. The expression changes represent a temporal depolarization, which could be important for an establishment of bovine pregnancy.
Results did not support that K8/K18 filaments influence the expression of Fas on the surface of luteal cells.
Data indicate that CK18 may be a molecular marker for bovine M cells in follicule-associated epithelium of Peyer's patches.
KRT18 knockdown in preimplantation embryos results in reduced blastocyst formation, but no further morphological aberrations were observed with regard to the biological function of KRT18.
Mechanical injury of vascular smooth muscle up-regulated keratin 18.
KRT18 encodes the type I intermediate filament chain keratin 18. Keratin 18, together with its filament partner keratin 8, are perhaps the most commonly found members of the intermediate filament gene family. They are expressed in single layer epithelial tissues of the body. Mutations in this gene have been linked to cryptogenic cirrhosis. Two transcript variants encoding the same protein have been found for this gene.
, Endo B
, cytokeratin endo B
, keratin D
, keratin complex 1, acidic, gene 18
, keratin, type I cytoskeletal 18
, cell proliferation-inducing gene 46 protein
, cell proliferation-inducing protein 46
, cytokeratin 18
, dorsal aorta proneprin kinesin-1
, keratin 18
, simple type I keratin
, Keratin, type I cytoskeletal 18
, keratin, type I cytoskeletal 18-like
, keratin 18, type I