| Name | keratin (protein family or complex) |
|---|---|
| Synonyms | Keratin; Keratins |
| Name | griseofulvin |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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 Biol Chem. 1997 Jul 11;272(28):17565-73. Keratin glycosylation decreased in all griseofulvin-fed mice, whereas keratin phosphorylation increased dramatically preferentially in mice expressing normal K18. |
85(1,1,1,5) | 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. Exp Cell Res. 2007 Jun 10;313(10):2033-49. Epub 2007 Apr 27. |
82(1,1,1,2) | Details |
| 8315060 | Meinhof W: Kinetics and spectrum of activity of oral antifungals: the therapeutic implications. J Am Acad Dermatol. 1993 Jul;29(1):S37-41. Griseofulvin has a low affinity and ketoconazole a high affinity for keratin, but both require long-term administration to be effective. |
81(1,1,1,1) | 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. |
36(0,1,1,6) | Details |
| 7521318 | Salmhofer H, Rainer I, Zatloukal K, Denk H: Posttranslational events involved in griseofulvin-induced keratin cytoskeleton alterations. 11-20. Epub 2008 May 7. |
33(0,0,5,8) | 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 Clin Invest. 1996 Aug 15;98(4):1034-46. |
25(0,0,4,5) | Details |
| 7504119 | Hutter H, Zatloukal K, Winter G, Stumptner C, Denk H: Disturbance of keratin homeostasis in griseofulvin-intoxicated mouse liver. Hepatology. 1987 Nov-Dec;7(6):1215-23. |
13(0,0,1,8) | 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. |
8(0,0,1,3) | Details |
| 1573853 | Zatloukal K, Denk H, Spurej G, Hutter H: Modulation of protein composition of nuclear lamina. Curr Drug Targets. 2005 Dec;6(8):849-62. Chronic griseofulvin (GF) intoxication of mice leads to severe alterations of the hepatocytic intermediate filament cytoskeleton similar to that found in alcoholic hepatitis in humans (i.e., derangement and diminution of the keratin filament network and appearance of cytoplasmic aggregates of keratin-containing material, termed Mallory bodies). |
7(0,0,1,2) | Details |
| 2143740 | Arenas R: [Onychomycosis. Hepatology. 1994 Sep;20(3):731-40. Treatment includes the removal of the infested keratin and use of local or systemic antimycotics, such as griseofulvin, ketoconazole and itraconazole. |
6(0,0,1,1) | Details |
| 6168037 | Wessely Z, Shapiro SH, Klavins JV, Tinberg HM: Identification of Mallory bodies with rhodamine B fluorescence and other stains for keratin. Stain Technol. 1981 May;56(3):169-76. Mallory body morphology, localization, and distribution in hepatocytes from griseofulvin-fed mice, human hepatoma, and human alcoholics were similar to those observed in the same tissues after conventional staining methods for Mallory bodies. |
3(0,0,0,3) | Details |
| 6184592 | Denk H, Krepler R, Lackinger E, Artlieb U, Franke WW: Immunological and biochemical characterization of the keratin-related component of Mallory bodies: a pathological pattern of hepatocytic cytokeratins. Liver. 1982 Sep;2(3):165-75. Mallory bodies induced by long-term griseofulvin feeding in mouse liver were isolated and analyzed by one- and two-dimensional gel electrophoresis and reaction of the separated polypeptides with cytokeratin antibodies using the blotting technique. |
3(0,0,0,3) | Details |
| 10386017 | Singh CJ, Singh BG: Antimycotic effects of some antibiotics on the growth of some dermatophytes and other keratin degrading fungi. Lab Invest. 1993 Nov;69(5):576-82. All, but griseofulvin observed to inhibit > 50% mycelial weight even at a lower concentration of 50 ppm. |
2(0,0,0,2) | Details |
| 8707270 | Preisegger KH, Stumptner C, Riegelnegg D, Brown PC, Silverman JA, Thorgeirsson SS, Denk H: Experimental Mallory body formation is accompanied by modulation of the expression of multidrug-resistance genes and their products. Hepatology. 1996 Jul;24(1):248-52. MBs can be produced in mouse liver by chronic administration of the porphyrinogenic drugs griseofulvin (GF) and 3,5-diethoxy-carbonyl-1,4-dihydrocollidine (DDC). However, after approximately 4 weeks of DDC and approximately 8 weeks of GF feeding, when the first small MBs appeared and loosening and diminution of keratin intermediate filament (KIF) cytoskeleton occurred in some hepatocytes, a decrease or loss of Pgp staining in affected hepatocytes was observed. |
2(0,0,0,2) | Details |
| 9306253 | Mertin D, Lippold BC: In-vitro permeability of the human nail and of a keratin membrane from bovine hooves: prediction of the penetration rate of antimycotics through the nail plate and their efficacy. Gac Med Mex. 1990 Mar-Apr;126(2):84-9; discussion 90-1. The maximum flux of ten antimycotics (amorolfine, bifonazole, ciclopirox, econazole, griseofulvin, ketoconazole, naftifine, nystatin and through the nail plate was predicted on the basis of their penetration rates through the hoof membrane and their water solubilities. |
2(0,0,0,2) | 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. Histochem Cell Biol. 2008 Jun;129(6):735-49. Epub 2008 Apr 29. 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. |
2(0,0,0,2) | Details |
| 8759055 | Yuan QX, Marceau N, French BA, Fu P, French SW: Heat shock in vivo induces Mallory body formation in drug primed mouse liver. J Pharm Pharmacol. 1997 Sep;49(9):866-72. Perturbations in keratin intermediate filament organization and Mallory body (MB) formation are associated with alcoholic hepatitis. Mice were primed by a 5-month feeding of griseofulvin (GF) or diethyl 1,4-dehydro-2,4,6-trimethyl-3,5-pyridinedicarboxylate (DDC) followed by drug withdrawal for 1 month. |
1(0,0,0,1) | 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. Mice fed long term with griseofulvin are an animal model of MB formation. Coexpression of K8 with K18 restored the normal fibrous pattern of keratin distribution and reduced the toxicity of K18. |
1(0,0,0,1) | Details |
| 16375669 | Borgers M, Degreef H, Cauwenbergh G: Fungal infections of the skin: infection process and antimycotic therapy. J Hepatol. 2000 Aug;33(2):199-207. These filamentous fungi have a high affinity for keratin, an important component of hair, skin and nails, which are the primary areas of infection by dermatophytes. The antifungal agents currently marketed for dermatomycoses are mainly inhibitors of biosynthesis, except for griseofulvin, which interferes with the cytoplasmic and nuclear microtubular system. |
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 Mol Pathol. 1995 Aug;63(1):63-76. Helmut Denk and colleagues described the first animal model of MBs in 1975 that involves feeding mice griseofulvin. The major constituents of MDBs include keratins 8 and 18 (K8/18), ubiquitin, and p62. |
1(0,0,0,1) | 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. 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 |
| 18479501 | Korting HC, Schollmann C: The significance of itraconazole for treatment of fungal infections of skin, nails and mucous membranes. J Dtsch Dermatol Ges. 2009 Jan;7(1):11-9 Itraconazole accumulates in the stratum corneum and in nail material due to its high affinity to keratin, as well as in sebum and vaginal mucosa. Itraconazole constitutes an important therapy option, along with fluconazole, terbinafine, ketoconazole and griseofulvin, for the treatment of dermatophyte infections of glabrous skin (tinea pedis, tinea manuum, tinea corporis and tinea cruris) in adults following unsuccessful topical therapy. |
1(0,0,0,1) | Details |
| 12956205 | Gupta AK, Cooper EA, Ginter G: Efficacy and safety of itraconazole use in children. Dermatol Clin. 2003 Jul;21(3):521-35. This safety of use, in combination with itraconazole's wide antifungal spectrum and pharmacokinetic properties, which allow for shorter dosing regimens, may make itraconazole a suitable alternative to griseofulvin for pediatric superficial fungal infections. Itraconazole has a high affinity for keratin, and accumulates to high levels at the site of superficial fungal infections. |
1(0,0,0,1) | Details |
| 18443813 | Strnad P, Stumptner C, Zatloukal K, Denk H: Intermediate filament cytoskeleton of the liver in health and disease. Hindustan Antibiot Bull. 1997 Feb-Nov;39(1-4):61-3. 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). Acidic (type I) and basic keratins (type II) build obligatory type I and type II heteropolymers and are expressed in epithelial cells. |
1(0,0,0,1) | Details |
| 14693542 | Sobue S, Sekiguchi K, Nabeshima T: Intracutaneous distributions of fluconazole, itraconazole, and griseofulvin in Guinea pigs and binding to human stratum corneum. Comp Hepatol. 2004 Aug 12;3(1):5. The extent of binding of FLC to human corneous keratin in vitro was about 10%, which is lower than those of ITC (94 to 97%) and GRF (36 to 38%). |
1(0,0,0,1) | Details |
| 2445643 | Katsuma Y, Swierenga SH, Khettry U, Marceau N, French SW: Changes in the cytokeratin intermediate filament cytoskeleton associated with Mallory body formation in mouse and human liver. Antimicrob Agents Chemother. 2004 Jan;48(1):216-23. Frozen sections of griseofulvin-fed mouse liver and human liver of primary biliary cirrhosis and primary sclerosing cholangitis were extracted by Triton X-100 and nuclease. Indirect immunofluorescent staining was performed by using anticow hoof keratin antibody for mouse liver and anti-human epidermal keratin antibody (AE1 and AE3) for human liver. |
1(0,0,0,1) | Details |
| 12537173 | Hainer BL: Dermatophyte infections. Lab Invest. 1992 May;66(5):589-97. Orally administered griseofulvin remains the standard treatment for tinea capitis. Dermatophytes are fungi that require keratin for growth. |
1(0,0,0,1) | Details |