Switch from Mnt-Max to Myc-Max induces p53 and cyclin D1 expression and apoptosis during cholestasis in mouse and human hepatocytes.
about
Interactions between Myc and Mediators of Inflammation in Chronic Liver Diseasesc-MYC-Making Liver Sick: Role of c-MYC in Hepatic Cell Function, Homeostasis and Disease.Bile acids induce inflammatory genes in hepatocytes: a novel mechanism of inflammation during obstructive cholestasis.Activation of a novel c-Myc-miR27-prohibitin 1 circuitry in cholestatic liver injury inhibits glutathione synthesis in mice.A mouse model of cholestasis-associated cholangiocarcinoma and transcription factors involved in progression.The elements of human cyclin D1 promoter and regulation involved.AP-1 Inhibition by SR 11302 Protects Human Hepatoma HepG2 Cells from Bile Acid-Induced Cytotoxicity by Restoring the NOS-3 ExpressionProtective Effects of Guava Pulp on Cholestatic Liver Injuryp53 promotes inflammation-associated hepatocarcinogenesis by inducing HMGB1 release.p63α modulates c-Myc activity via direct interaction and regulation of MM1 protein stability.Modulation of the Unfolded Protein Response by Tauroursodeoxycholic Acid Counteracts Apoptotic Cell Death and Fibrosis in a Mouse Model for Secondary Biliary Liver Fibrosis.RNAi-nanoparticulate manipulation of gene expression as a new functional genomics tool in the liver.c-Myc induction of programmed cell death may contribute to carcinogenesis: a perspective inspired by several concepts of chemical carcinogenesis.MicroRNA-mediated regulation of glutathione and methionine metabolism and its relevance for liver disease.Integrin α1β1 expression is controlled by c-MYC in colorectal cancer cells.MNT and Emerging Concepts of MNT-MYC AntagonismInduction of avian musculoaponeurotic fibrosarcoma proteins by toxic bile acid inhibits expression of glutathione synthetic enzymes and contributes to cholestatic liver injury in mice.Bile acids induce apoptosis selectively in androgen-dependent and -independent prostate cancer cellsDeregulated methionine adenosyltransferase α1, c-Myc, and Maf proteins together promote cholangiocarcinoma growth in mice and humans(‡).Myc, Max, and Mnt: molecular mechanisms of enhancement of cholangiocarcinogenesis by cholestasis.Caspase-3 inhibition prevents the development of hepatopulmonary syndrome in common bile duct ligation rats by alleviating pulmonary injury.p53-mediated regulation of bile acid disposition attenuates cholic acid-induced cholestasis in mice.New molecular interactions of c-Myc in cholangiocarcinoma may open new therapeutic opportunities.Metabolic Reprogramming and the Recovery of Physiological Functionality in 3D Cultures in Micro-Bioreactors.
P2860
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P2860
Switch from Mnt-Max to Myc-Max induces p53 and cyclin D1 expression and apoptosis during cholestasis in mouse and human hepatocytes.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
2009年學術文章
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2009年學術文章
@zh-hant
name
Switch from Mnt-Max to Myc-Max ...... n mouse and human hepatocytes.
@en
Switch from Mnt-Max to Myc-Max ...... n mouse and human hepatocytes.
@nl
type
label
Switch from Mnt-Max to Myc-Max ...... n mouse and human hepatocytes.
@en
Switch from Mnt-Max to Myc-Max ...... n mouse and human hepatocytes.
@nl
prefLabel
Switch from Mnt-Max to Myc-Max ...... n mouse and human hepatocytes.
@en
Switch from Mnt-Max to Myc-Max ...... n mouse and human hepatocytes.
@nl
P2093
P2860
P356
P1433
P1476
Switch from Mnt-Max to Myc-Max ...... n mouse and human hepatocytes.
@en
P2093
Heping Yang
Kwang Suk Ko
Shelly C Lu
Tony W H Li
P2860
P304
P356
10.1002/HEP.22720
P407
P577
2009-03-01T00:00:00Z