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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.
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K8/K18 interact with Notch1 and regulate Notch1 signalling activity during differentiation of the colonic epithelium.
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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
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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.
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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+/+.
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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
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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.
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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
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The regulation of the SCFA-MCT1-HMGCS2 axis is disrupted in K8(-/-) colonocytes, suggesting a role for keratins in colonocyte energy metabolism and homeostasis.
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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.
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In several liver stress models epiplakin and K8 genes displayed identical expression patterns and transgenic K8 overexpression resulted in elevated hepatic epiplakin levels.
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In human failing myocardium, where TNF-alpha expression is upregulated, K8/K18 were also ectopically expressed
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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.
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Directed expression of a chimeric type II keratin partially rescues keratin 5-null mice.
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Our data demonstrate that HF diet triggers aggregate formation and development of liver injury in susceptible individuals through misfolding and crosslinking of excess K8.
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K8 inactivation leads to reduced fasting blood glucose levels and resistance to hyperglycaemia after glucose challenge.
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Keratin 8 is required for the maintenance of architectural structure in thymus epithelium.
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A conserved rod domain phosphotyrosine that is targeted by the phosphatase PTP1B promotes keratin 8 protein insolubility and filament organization.
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K8 acetylation at Lys-207, a highly conserved residue among type II keratins, is up-regulated upon hyperglycemia and down-regulated by SIRT2.
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Data indicate that cyclin D1 is expressed exclusively in luminal keratin 8 immunoreactive tumor cells and is dependent on the adipose secreted hormone leptin.
