Disease relevance of Lpt1

• RESULTS: Liver-specific TfR2-KO mice develop significant iron overload comparable to complete TfR2-KO mice [1].
• In vivo Color-Coded Imaging of the Interaction of Colon Cancer Cells and Splenocytes in the Formation of Liver Metastases [2].
• BACKGROUND/AIMS: Liver regeneration following chronic injury is associated with inflammation, the proliferation of liver progenitor (oval) cells and fibrosis [3].
• METHODS: Liver tumors were established by direct injection of CT26, a murine adenocarcinoma, into the livers of BALB/c mice, followed by three transfections with either murine IL-12, murine granulocyte-macrophage colony-stimulating factor, or luciferase cDNA using particle-mediated gene transfer [4].
• The mouse model (Cftr(tm1UNC)/Cftr(tm1UNC)) for cystic fibrosis (CF) shows mucus accumulation and increased Muc1 mucin mRNA levels due to altered splicing (Hinojosa-Kurtzberg AM, Johansson MEV, Madsen CS, Hansson GC, and Gendler SJ. Am J Physiol Gastrointest Liver Physiol 284: G853-G862, 2003) [5].

High impact information on Lpt1

• METHODS: Liver fibrosis was induced either by feeding mice with the 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet or by injecting them with carbon tetrachloride [6].
• BACKGROUND & AIMS: Liver development, regeneration, and oncogenesis involve signaling events mediated by a number of proteins, such as ras and the related small guanosine triphosphatases [7].
• BACKGROUND & AIMS: Liver regeneration after loss of hepatic tissue leads to hepatocyte and nonparenchymal cell proliferation and rapid restoration of liver parenchyma [8].
• Nuclear Pregnane X Receptor Cross-talk with FoxA2 to Mediate Drug-induced Regulation of Lipid Metabolism in Fasting Mouse Liver [9].
• Restoration of Glucokinase Expression in the Liver Normalizes Postprandial Glucose Disposal in Mice With Hepatic Deficiency of PDK1 [10].

Chemical compound and disease context of Lpt1

• METHODS: Liver injury was induced in mice by delayed-type hypersensitivity to picryl chloride [11].
• MATERIALS AND METHODS: Liver metastases were induced by the intrasplenic injection of dimethylhydrazine induced colon cancer cells in mice [12].
• 3. Liver weights were increased (P > 0.001) by +90% of control mean weights; hepatocyte hypertrophy and increased fat and glycogen were seen by light microscopy, and hyperplasia of smooth endoplasmic reticulin by transmission electron microscopy [13].
• METHODS: Liver metastases were produced in male CBA mice by intrasplenic injection of a dimethyl hydrazine induced MoCR colon cancer murine cell line [14].
• 5. Liver toxicity in patients receiving relatively high daily doses of coumarin is very rare [15].

Biological context of Lpt1

• METHODS: Liver phenotype and gene expression were assessed in APOE2 knock-in mice that were fed a western-type high fat diet with or without co-administration of fenofibrate [16].
• BACKGROUND: Liver allografts are accepted across major histocompatibility complex (MHC) barriers in mice and induce donor-specific tolerance without requirement for immunosuppressive therapy [17].
• The homologous mammalian ALR(Augmenter of Liver Regeneration) genes from man, mouse and rat are important at different developmental stages of the organism as, for example, in spermatogenesis and liver regeneration [18].
• Suppression of Apoptosis in the Liver by Systemic and Local Delivery of Small-Interfering RNAs [19].
• Circadian rhythms. Liver regeneration clocks on [20].

Anatomical context of Lpt1

• BACKGROUND/AIMS: Liver natural killer 1.1 antigen (NK1)+ T cells and IL-4 play a crucial role in concanavalin-A (Con-A)-induced hepatic injury in mice, and a T helper (Th) 2 immune response was thus suggested to be involved [21].
• METHODS: Liver dendritic cell progenitors were enriched from normal C57BL/6 mice by culturing non-parenchymal cells with granulocyte-macrophage colony stimulating factor for 7 days [22].
• BACKGROUND/AIMS: Liver regeneration is dependent upon coordinated proliferation of hepatocytes and endothelial cells [23].
• METHODS: Liver fibrosis was induced in rats by bile duct resection (BDR), and by intraperitoneal injections of carbon tetrachloride (CCl4) or porcine serum, and in mice by intragastric administrations of CCl4, and BDR [24].
• CONCLUSION: Liver and spleen pathology of AGU was corrected by bone marrow transplantation, but there was no effect on lysosomal accumulation in the CNS and in the kidneys [25].

Associations of Lpt1 with chemical compounds

• Acetaminophen-induced Liver Injury Is Attenuated in Male Glutamate-cysteine Ligase Transgenic Mice [26].
• METHODS: Liver cirrhosis and fulminant hepatitis were induced by intraperitoneal administration of thioacetamide and D-galactosamine followed by lipopolysaccharide, respectively [27].
• METHODS: Liver fibrosis was induced in mice by administering carbon tetrachloride (CCl4) continuously for 10 weeks [28].
• METHODS: Liver injury and cytokine activation induced by BCG and by LPS upon BCG infection (BCG/LPS) were compared in wild-type and iNOS-/- mice [29].
• 1. Liver tryptophan pyrrolase exists as holoenzyme and apoenzyme in rat, mouse, pig, turkey, chicken and possibly man [30].

Regulatory relationships of Lpt1

• METHODS:: Liver injury was induced by intravenous injection of Con A [31].
• CONCLUSIONS: Liver-infiltrating T lymphocytes may be triggered by hepatocytes via LFA-1/ICAM-1 interaction to release toxic substances, such as proteases and oxygen radicals, which consequently lead to the hepatocyte damage [32].
• BuChE activity in females was only slightly influenced even at 300 p.p.m. Liver weight was increased in a time and concentration dependent manner in both sexes [33].

Other interactions of Lpt1

• Zonal Gene Expression in Mouse Liver Resembles Expression Patterns of Ha-ras and {beta}-Catenin Mutated Hepatomas [34].
• Hematopoietic Cells Are a Source of Nidogen-1 and Nidogen-2 during Mouse Liver Development [35].
• (v) Liver fibrosis was induced in wild-type mice with TAA, and mice received additional leptin or a control solution [36].
• The opposite hepatic outcomes in Liver mt PPARgamma Tg as a result of fasting and high-fat feeding may indicate distinct roles of PPARalpha and PPARgamma in 2 different types of nutritionally provoked steatosis [37].
• CONCLUSIONS: Liver-derived IGF-I is permissive for ovx-induced trabecular bone loss [38].

Analytical, diagnostic and therapeutic context of Lpt1

• Pseudo-hydrodynamic Delivery of Helper-dependent Adenoviral Vectors into Non-human Primates for Liver-directed Gene Therapy [39].
• BACKGROUND/AIMS: Liver regeneration following hepatectomy is complicated and involves a variety of interacting factors [40].
• BACKGROUND: Liver function after transplantation is determined by the quality of the donor organ and the influences of preservation, flush, and reperfusion injury [41].
• BACKGROUND/AIMS: Liver failure is a life threatening condition currently treated by palliative measures and, when applicable, organ transplantation [42].
• BACKGROUND: Liver allografts transplanted between MHC-disparate mice, rats, and swine are spontaneously accepted in most strain combinations without requirement for immunosuppression [43].

References