ArticleHuman molecular genetics2010
Genetic studies on the functional relevance of the protein prenyltransferases in skin keratinocytes.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Farnesylated prelamin A induces fibroblast polarity defects in premature aging disorders by inhibiting nesprin-2-SUN2 LINC complex function.Journal of cell science · 2026Article
- Roles of the lamin A-specific tail region in the localization to sites of nuclear envelope rupture.PNAS nexus · 2024Article
- Protein lipidation in health and disease: molecular basis, physiological function and pathological implication.Signal transduction and targeted therapy · 2024Review
- A small-molecule ICMT inhibitor delays senescence of Hutchinson-Gilford progeria syndrome cells.eLife · 2021Article
- Targeting RAS-converting enzyme 1 overcomes senescence and improves progeria-like phenotypes of ZMPSTE24 deficiency.Aging cell · 2020Article
- Deficiency in ZMPSTE24 and resulting farnesyl-prelamin A accumulation only modestly affect mouse adipose tissue stores.Journal of lipid research · 2020Article
- Mevalonate metabolism-dependent protein geranylgeranylation regulates thymocyte egress.The Journal of experimental medicine · 2020Article
- Tipifarnib prevents development of hypoxia-induced pulmonary hypertension.Cardiovascular research · 2017Article
- A mutation abolishing the ZMPSTE24 cleavage site in prelamin A causes a progeroid disorder.Journal of cell science · 2016Article
- Prelamin A processing, accumulation and distribution in normal cells and laminopathy disorders.Nucleus (Austin, Tex.) · 2016Article
- Review
- 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
- Understanding the roles of nuclear A- and B-type lamins in brain development.The Journal of biological chemistry · 2012Review
- Regulation of prelamin A but not lamin C by miR-9, a brain-specific microRNA.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Defining the nature of human pluripotent stem cell progeny.Cell research · 2012Article
- Severe hepatocellular disease in mice lacking one or both CaaX prenyltransferases.Journal of lipid research · 2012Article
- An absence of both lamin B1 and lamin B2 in keratinocytes has no effect on cell proliferation or the development of skin and hair.Human molecular genetics · 2011Article
- Absence of progeria-like disease phenotypes in knock-in mice expressing a non-farnesylated version of progerin.Human molecular genetics · 2011Article
- Direct synthesis of lamin A, bypassing prelamin a processing, causes misshapen nuclei in fibroblasts but no detectable pathology in mice.The Journal of biological chemistry · 2010Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
The modification of proteins with farnesyl or geranylgeranyl lipids, a process called protein prenylation, facilitates interactions of proteins with membrane surfaces. Protein prenylation is carried out by a pair of cytosolic enzymes, protein farnesyltransferase (FTase) and protein geranylgeranyltransferase type I (GGTase-I). FTase and GGTase-I have attracted interest as therapeutic targets for both cancer and progeria, but very little information exists on the importance of these enzymes for homeostasis of normal tissues. One study actually suggested that FTase is entirely dispensable. To explore the importance of the protein prenyltransferases for normal tissues, we used conditional knockout alleles for Fntb and Pggt1b (which encode the beta-subunits of FTase and GGTase-I, respectively) and a keratin 14-Cre transgene to create mice lacking FTase or GGTase-I in skin keratinocytes. Keratinocyte-specific Fntb knockout mice were viable but developed severe alopecia. Although hair follicles appeared normal during development, they were morphologically abnormal after birth, and ultrastructural and immunohistochemical studies revealed many apoptotic cells. The interfollicular epidermis of Fntb-deficient mice appeared normal; however, keratinocytes from these mice could not proliferate in culture. As expected, non-farnesylated prelamin A and non-farnesylated DNAJA1 accumulated in Fntb-deficient keratinocytes. Keratinocyte-specific Pggt1b knockout mice survived development but died shortly after birth. Like Fntb-deficient keratinocytes, Pggt1b-deficient keratinocytes did not proliferate in culture. Thus, both FTase and GGTase-I are required for the homeostasis of skin keratinocytes.
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