anti-Keratin 8 (KRT8) Antikörper

Human Keratin 8 (KRT8) Interaktionspartner

1. 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.

2. 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.

3. KRT8 mRNA and protein are upregulated in anaplastic thyroid carcinoma. KRT8 protein binds to annexin A2.

4. K8/K18 variants are overrepresented in Chinese NAFLD patients and might accelerate liver fat storage through insulin resistance.

5. regulated enhancement of autophagy with concurrent increased expression of KRT8 and the inhibition of KRT8 phosphorylation serve to inhibit oxidative stress-induced epithelial-mesenchymal transitionof retinal pigment epithelium cells.

6. Histopathological differences between Magnetic resonance-guided high-intensity focused ultrasound (MR-HIFU)-ablated tissue and radiofrequency (RF)-ablated tissue were demonstrated. CK-8 was more reliable for cell viability assessment than H&E when used directly after ablation

7. Loss of activating transcription factor 3 (ATF3) in knockout mice promotes the emergence of keratins CK5+CK8+ epithelial cells.

8. notochord-specific marker during early intervertebral disc development

9. Data show that the filament elongation of both desmin and keratin K8/K18 proceeds very similar to that of vimentin.

10. New insights into interactions between the nucleotide-binding domain of CFTR and keratin 8.

11. We present results of a multicentre study measuring UBC((R)) Rapid Test(test that detects fragments of cytokeratins 8 and 18 in urine) in bladder cancer patients and healthy controls with focus on carcinoma in situ (CIS) and high-grade bladder cancer.

12. Data show that after siRNA transfection, TGF-beta1 protein level was decreased, and CK18 proteins was decreased, while CK8 proteins was increased, and TERT protein expression was slightly increased at 96 h.

13. The interplay between Solo protein and keratin 8/keratin 18 filaments plays a crucial role in tensile force-induced RhoA activation and consequent actin cytoskeletal reinforcement in endothelial cells.

14. K8/18 filaments provide resistance to apoptosis in granulosa cell tumor cells by impairing FAS expression.

15. These metastatic tumors revealed no detectable expression of CK8/18, E-cadherin, VCAM-1, and ICAM-1

16. Data show that loss of epithelial membrane protein 2 (EMP2) is involved in sphingosylphosphorylcholine (SPC)-induced phosphorylation of keratin 8 (K8) via ubiquitination of protein phosphatase 2 (PP2A) through alpha4 phosphoprotein by caveolin-1 (cav-1).

17. The reactivity of rheumatoid arthritis (RA) serum IgG antibodies against K8 was significantly higher than healthy controls and systemic lupus erythematosus patients, confirming K8 as a novel autoantigen of RA.

18. Variants in highly conserved residues of K8 Lys393Arg (ezetimibe/simvastatin-related) was found in patients with fatal Drug-induced liver injury.

19. Keratins 8 and 18 are type II acute-phase responsive genes overexpressed in human liver disease.

20. In human failing myocardium, where TNF-alpha expression is upregulated, K8/K18 were also ectopically expressed

Mouse (Murine) Keratin 8 (KRT8) Interaktionspartner

1. The authors found that keratin 8 suppressed toll-like receptor-induced nuclear factor (NF)-kappaB activation and interacted with the adaptor tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) to prevent its polyubiquitination.

2. K8/K18 interact with Notch1 and regulate Notch1 signalling activity during differentiation of the colonic epithelium.

3. Mitochondria in K8 wild-type beta cells and MIN6 insulinoma cells overexpressing K8 and 18 are more stationary compared with mitochondria in keratin-deficient cells

4. 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.

5. DRA mRNA levels were decreased by three- to fourfold and DRA protein was almost entirely lost in K8-/- cecum and proximal and distal colon compared with K8+/+.

6. Upregulation of IL-22 in combination with a complete loss of its negative regulator IL-22BP, and increased downstream STAT3-signaling in K8(-/-) and K8(-/-)Apc(Min/+) colonic epithelia confirmed that the IL-22 pathway, important in inflammation, proliferation and tissue regeneration

7. Krt8 deletion (Krt8(-/-)) in a mouse model of cystic fibrosis (F508del-Cftr mice) increased the levels of circulating markers of bone formation, corrected the expression of osteoblast phenotypic genes, promoted trabecular bone formation and improved bone mass and microarchitecture. Krt8 deletion corrected overactive NF-kappaB signaling & decreased Wnt-beta-catenin signaling induced by F508del-Cftr mutation in osteoblasts.

8. Autoantibodies to several antigens were identified in 81% of K8-null male mice 8 mo or older. Similar autoantibodies were detected in aging K18-null male mice that had a related liver phenotype but normal colon compared with K8-null mice

9. The regulation of the SCFA-MCT1-HMGCS2 axis is disrupted in K8(-/-) colonocytes, suggesting a role for keratins in colonocyte energy metabolism and homeostasis.

10. using knockout mice, we show K8+/- colon expresses ~50% less keratins compared to K8 wild type. In experimental colitis, K8+/- mice showed higher disease sensitivity and delayed recovery compared to K8+/+ littermates.

11. In several liver stress models epiplakin and K8 genes displayed identical expression patterns and transgenic K8 overexpression resulted in elevated hepatic epiplakin levels.

12. In human failing myocardium, where TNF-alpha expression is upregulated, K8/K18 were also ectopically expressed

13. 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.

14. Directed expression of a chimeric type II keratin partially rescues keratin 5-null mice.

15. Our data demonstrate that HF diet triggers aggregate formation and development of liver injury in susceptible individuals through misfolding and crosslinking of excess K8.

16. K8 inactivation leads to reduced fasting blood glucose levels and resistance to hyperglycaemia after glucose challenge.

17. Keratin 8 is required for the maintenance of architectural structure in thymus epithelium.

18. A conserved rod domain phosphotyrosine that is targeted by the phosphatase PTP1B promotes keratin 8 protein insolubility and filament organization.

19. K8 acetylation at Lys-207, a highly conserved residue among type II keratins, is up-regulated upon hyperglycemia and down-regulated by SIRT2.

20. Data indicate that cyclin D1 is expressed exclusively in luminal keratin 8 immunoreactive tumor cells and is dependent on the adipose secreted hormone leptin.

Cow (Bovine) Keratin 8 (KRT8) Interaktionspartner

1. Results did not support that K8/K18 filaments influence the expression of Fas on the surface of luteal cells.

Zebrafish Keratin 8 (KRT8) Interaktionspartner

1. Data identify Danio rerio keratins 8/18 as the true orthologs of the human keratin pair 8/18.

Pig (Porcine) Keratin 8 (KRT8) Interaktionspartner

1. This study reveals clear genetic-statistical evidence for a link of KRT8, FAF1 and PTH1R with some of leg weakness related traits in pigs.

2. Mechanical injury of vascular smooth muscle up-regulated keratin 8.