ArticleJournal of lipid research2012
Severe hepatocellular disease in mice lacking one or both CaaX prenyltransferases.
Article in Journal of lipid research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Shared Plant-human Biology: Herbicide Effects and New Biomarkers Perspectives.Current environmental health reports · 2026Review
- Evaluating protein prenylation of human and viral CaaX sequences using a humanized yeast system.Disease models & mechanisms · 2024Article
- In vivo evaluation of combination therapy targeting the isoprenoid biosynthetic pathway.Pharmacological research · 2021Article
- Depletion of essential isoprenoids and ER stress induction following acute liver-specific deletion of HMG-CoA reductase.Journal of lipid research · 2020Article
- Mevalonate metabolism-dependent protein geranylgeranylation regulates thymocyte egress.The Journal of experimental medicine · 2020Article
- Inhibition of farnesyl pyrophosphate synthase improves pressure overload induced chronic cardiac remodeling.Scientific reports · 2016Article
- Mass spectrometry captures off-target drug binding and provides mechanistic insights into the human metalloprotease ZMPSTE24.Nature chemistry · 2016Article
- Targeting GGTase-I activates RHOA, increases macrophage reverse cholesterol transport, and reduces atherosclerosis in mice.Circulation · 2013Article
- Targeting protein prenylation in progeria.Science translational medicine · 2013Review
- Inhibitors of protein geranylgeranyltransferase-I lead to prelamin A accumulation in cells by inhibiting ZMPSTE24.Journal of lipid research · 2012Article
- Disruption of lamin B1 and lamin B2 processing and localization by farnesyltransferase inhibitors.Nucleus (Austin, Tex.)Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Protein farnesyltransferase (FTase) and protein geranylgeranyltransferase-I (GGTase-I) add 15- or 20-carbon lipids, respectively, to proteins that terminate with a CaaX motif. These posttranslational modifications of proteins with lipids promote protein interactions with membrane surfaces in cells, but the in vivo importance of the CaaX prenyltransferases and the protein lipidation reactions they catalyze remain incompletely defined. One study concluded that a deficiency of FTase was inconsequential in adult mice and led to little or no tissue pathology. To assess the physiologic importance of the CaaX prenyltransferases, we used conditional knockout alleles and an albumin-Cre transgene to produce mice lacking FTase, GGTase-I, or both enzymes in hepatocytes. The hepatocyte-specific FTase knockout mice survived but exhibited hepatocellular disease and elevated transaminases. Mice lacking GGTase-I not only had elevated transaminases but also had dilated bile cannaliculi, hyperbilirubinemia, hepatosplenomegaly, and reduced survival. Of note, GGTase-I-deficient hepatocytes had a rounded shape and markedly reduced numbers of actin stress fibers. Hepatocyte-specific FTase/GGTase-I double-knockout mice closely resembled mice lacking GGTase-I alone, but the disease was slightly more severe. Our studies refute the notion that FTase is dispensable and demonstrate that GGTase-I is crucial for the vitality of hepatocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.