Name | keratin 18 |
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Synonyms | CK 18; CYK18; Cytokeratin 18; K18; KRT18; Keratin 18; Keratin 18 type I cytoskeletal; Cytokeratin 18s… |
Name | griseofulvin |
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CAS |
PubMed | Abstract | RScore(About this table) | |
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8770877 | Ku NO, Michie SA, Soetikno RM, Resurreccion EZ, Broome RL, Oshima RG, Omary MB: Susceptibility to hepatotoxicity in transgenic mice that express a dominant-negative human keratin 18 mutant. J Clin Invest. 1996 Aug 15;98(4):1034-46. The phosphorylation increase in normal K18 after griseofulvin feeding appears to involve sites that are different to those that increase after partial hepatectomy. |
121(1,2,3,6) | Details |
9864372 | Ku NO, Michie SA, Soetikno RM, Resurreccion EZ, Broome RL, Omary MB: Mutation of a major keratin phosphorylation site predisposes to hepatotoxic injury in transgenic mice. J Cell Biol. 1998 Dec 28;143(7):2023-32. However, exposure of S52A-expressing mice to the hepatotoxins, griseofulvin or microcystin, which are associated with K18 ser52 and other keratin phosphorylation changes, resulted in more dramatic hepatotoxicity as compared with WT K18-expressing mice. |
86(1,1,1,6) | Details |
12388748 | Nakamichi I, Hatakeyama S, Nakayama KI: Formation of Mallory body-like inclusions and cell death induced by deregulated expression of keratin 18. Mol Biol Cell. 2002 Oct;13(10):3441-51. Culture of HepG2 cells with griseofulvin has now been shown to induce both the formation of intracellular aggregates containing K18 as well as an increase in the abundance of K18 mRNA. |
12(0,0,1,7) | Details |
10952237 | Cadrin M, Hovington H, Marceau N, McFarlane-Anderson N: Early perturbations in keratin and actin gene expression and fibrillar organisation in griseofulvin-fed mouse liver. J Hepatol. 2000 Aug;33(2):199-207. BACKGROUND/AIMS: Long-term feeding of mice with a diet containing griseofulvin results in the formation of Mallory bodies, keratin K8 and K18 containing aggregates in hepatocytes. |
8(0,0,1,3) | Details |
18443813 | Strnad P, Stumptner C, Zatloukal K, Denk H: Intermediate filament cytoskeleton of the liver in health and disease. Histochem Cell Biol. 2008 Jun;129(6):735-49. Epub 2008 Apr 29. MDBs are found in various liver diseases including alcoholic and non-alcoholic steatohepatitis and can be formed in mice by feeding hepatotoxic substances griseofulvin and 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC). Adult hepatocytes contain K8 and K18 as their only cytoplasmic IF pair, whereas cholangiocytes express K7 and K19 in addition. |
6(0,0,0,6) | Details |
7536860 | Cadrin M, Anderson NM, Aasheim LH, Kawahara H, Franks DJ, French SW: Modifications in cytokeratin and actin in cultured liver cells derived from griseofulvin-fed mice. Lab Invest. 1995 Apr;72(4):453-60. The hepatocytes were labeled with [35S] or [32P] orthophosphate to study, respectively, the level of amino acid incorporation into IF proteins (CK 8 and CK 18) and their phosphorylation levels. |
3(0,0,0,3) | Details |
11434612 | Stumptner C, Fuchsbichler A, Lehner M, Zatloukal K, Denk H: Sequence of events in the assembly of Mallory body components in mouse liver: clues to the pathogenesis and significance of Mallory body formation. J Hepatol. 2001 May;34(5):665-75. BACKGROUND/AIMS: Chronic intoxication of mice with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) or griseofulvin (GF) results in appearance of Mallory bodies (MBs) and alterations of the keratin cytoskeleton, which are reversible upon drug withdrawal but recur after readministration within 2-3 days. Rapid increase of keratin 8/18 mRNA and proteins was found in all reintoxicated mice concomitant with MB formation, whereby keratin 8 prevailed over keratin 18. |
2(0,0,0,2) | Details |
15307891 | Fausther M, Villeneuve L, Cadrin M: Heat shock protein 70 expression, keratin phosphorylation and Mallory body formation in hepatocytes from griseofulvin-intoxicated mice. Comp Hepatol. 2004 Aug 12;3(1):5. RESULTS: GF-treatment induced an increase in HSP70i expression and K8 phosphorylation on serines 79 (K8 S79), 436 (K8 S436), and K18 phosphorylation on serine 33 (K18 S33) as determined by Western blotting. |
2(0,0,0,2) | Details |
18805482 | Strnad P, Zatloukal K, Stumptner C, Kulaksiz H, Denk H: Mallory-Denk-bodies: lessons from keratin-containing hepatic inclusion bodies. Biochim Biophys Acta. 2008 Dec;1782(12):764-74. Epub 2008 Sep 6. The MDB formation-underlying mechanisms include protein misfolding, chaperone alterations, disproportional protein expression with keratin 8> keratin 18 levels and subsequent keratin 8 crosslinking via transglutaminase. p62 presence is crucial for MDB formation. MDBs are induced in mice fed griseofulvin or 3,5-diethoxycarbonyl-1,4-dihydrocollidine and resolve after discontinuation of toxin administration. |
1(0,0,0,1) | Details |
10751352 | Zatloukal K, Stumptner C, Lehner M, Denk H, Baribault H, Eshkind LG, Franke WW: Cytokeratin 8 protects from hepatotoxicity, and its ratio to cytokeratin 18 determines the ability of hepatocytes to form Mallory bodies. Am J Pathol. 2000 Apr;156(4):1263-74. In alcoholic hepatitis, a severe form of -induced toxic liver injury, as well as in experimental intoxication of mice with the porphyrinogenic drugs griseofulvin and 3,5-diethoxycarbonyl-1, 4-dihydrocollidine, hepatocytes form cytoplasmic protein aggregates (Mallory bodies; MBs) containing cytokeratins (CKs) and non-CK components. |
1(0,0,0,1) | Details |
17531973 | Zatloukal K, French SW, Stumptner C, Strnad P, Harada M, Toivola DM, Cadrin M, Omary MB: From Mallory to Mallory-Denk bodies: what, how and why? . Exp Cell Res. 2007 Jun 10;313(10):2033-49. Epub 2007 Apr 27. Helmut Denk and colleagues described the first animal model of MBs in 1975 that involves feeding mice griseofulvin. The relevant proteins and cellular processes that contribute to MDB formation and accumulation include the type of chronic stress, the extent of stress-induced protein misfolding and consequent proteasome overload, a K8-greater-than-K18 ratio, transamidation of K8 and other proteins, presence of p62 and autophagy. |
1(0,0,0,1) | Details |
9211903 | Liao J, Ku NO, Omary MB: Stress, apoptosis, and mitosis induce phosphorylation of human keratin 8 at Ser-73 in tissues and cultured cells. J Biol Chem. 1997 Jul 11;272(28):17565-73. Simple epithelia express keratins 8 (K8) and 18 (K18) as their major intermediate filament proteins. In addition, mouse hepatotoxicity that is induced by chronic feeding with griseofulvin resulted in HK8 formation in the liver. |
1(0,0,0,1) | Details |