Results 31 to 40 of about 9,367 (212)

Genomic instability and DNA replication defects in progeroid syndromes [PDF]

open access: yes, 2018
Progeroid syndromes induced by mutations in lamin A or in its interactors – named progeroid laminopathies – are model systems for the dissection of the molecular pathways causing physio- logical and premature aging.
Chiara Merigliano   +4 more
core   +1 more source

Increasing the length of progerin's isoprenyl anchor does not worsen bone disease or survival in mice with Hutchinson-Gilford progeria syndrome

open access: yesJournal of Lipid Research, 2009
Hutchinson-Gilford progeria syndrome (HGPS) is caused by the synthesis of a truncated prelamin A, commonly called progerin, that contains a carboxyl-terminal farnesyl lipid anchor.
Brandon S.J. Davies   +10 more
doaj   +1 more source

HDV can constrain HBV genetic evolution in hbsag: Implications for the identification of innovative pharmacological targets [PDF]

open access: yes, 2018
Chronic HBV + HDV infection is associated with greater risk of liver fibrosis, earlier hepatic decompensation, and liver cirrhosis hepatocellular carcinoma compared to HBV mono-infection.
Andreoni, Massimo   +34 more
core   +2 more sources

C-Terminal Farnesylation of UCH-L1 Plays a Role in Transport of Epstein-Barr Virus Primary Oncoprotein LMP1 to Exosomes

open access: yesmSphere, 2018
Increasing evidence shows that exosomes are key regulators in cancer cell-to-cell communication. Several reports on Epstein-Barr virus (EBV)-related malignancies demonstrate that latent membrane protein 1 (LMP1) secreted by exosomes derived from EBV- or ...
E. Kobayashi   +6 more
doaj   +1 more source

Statins and protein prenylation in cancer cell biology and therapy [PDF]

open access: yes, 2012
El pdf del artículo es la versión post-print.The use of statins has scaled up to become one of the most prescribed medicines in the world and have been very useful in the manegement of cardiovascular diseases and related mortality.
Fernández-Checa, José C.   +2 more
core   +2 more sources

Age-dependent changes of nuclear morphology are uncoupled from longevity in Caenorhabditis elegans IGF/insulin receptor daf-2 mutants [PDF]

open access: yes, 2016
Nuclear envelope (NE) architecture and aging have been associated since the discovery that certain human progeria diseases are due to perturbations in processing of lamin A protein, generating alterations in NE morphology. However, whether changes in the
Askjaer, Peter   +4 more
core   +1 more source

K-Ras-Independent Effects of the Farnesyl Transferase Inhibitor L-744,832 on Cyclin B1/Cdc2 Kinase Activity, G2/M Cell Cycle Progression and Apoptosis in Human Pancreatic Ductal Adenocarcinoma Cell

open access: yesNeoplasia: An International Journal for Oncology Research, 2000
Pancreatic ductal adenocarcinoma is a highly lethal malignancy that is resistant to traditional cytotoxic therapy. High rates of activating codon 12 K-Ras mutations in this disease have generated considerable interest in the therapeutic application of ...
Si Young Song   +4 more
doaj   +1 more source

The effector domain of Rab6, plus a highly hydrophobic C terminus, is required for Golgi apparatus localization [PDF]

open access: yes, 1994
C-terminal lipid modifications are essential for the interaction of Ras-related proteins with membranes. While all Ras proteins are farnesylated and some palmitoylated, the majority of other Ras-related proteins are geranylgeranylated.
Beranger, F.   +4 more
core   +1 more source

Thematic review series: Lipid Posttranslational Modifications CAAX modification and membrane targeting of Ras

open access: yesJournal of Lipid Research, 2006
Proteins that terminate with a consensus sequence known as CAAX undergo a series of posttranslational modifications that include polyisoprenylation, endoproteolysis, and carboxyl methylation.
Latasha P. Wright, Mark R. Philips
doaj   +1 more source

Mutations in the SHR5 gene of Saccharomyces cerevisiae suppress Ras function and block membrane attachment and palmitoylation of Ras proteins [PDF]

open access: yes, 1995
We have identified a gene, SHR5, in a screen for extragenic suppressors of the hyperactive RAS2Val-19 mutation in the budding yeast Saccharomyces cerevisiae. SHR5 was cloned, sequenced, and found to encode a 23-kDa protein not significantly homologous to
Jung, V.   +4 more
core   +1 more source

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