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Apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1

APOBEC-1, APOBEC, apobec-1 complementation factor
This gene encodes a member of the cytidine deaminase enzyme family. The encoded protein forms a multiple-protein editing holoenzyme with APOBEC1 complementation factor (ACF) and APOBEC1 stimulating protein (ASP). This holoenzyme is involved in the editing of C-to-U nucleotide bases in apolipoprotein B and neurofibromatosis-1 mRNAs. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, apolipoprotein B, APOBEC3G, APOBEC3, Apo
Papers on APOBEC-1
APOBEC-induced mutations in human cancers are strongly enriched on the lagging DNA strand during replication.
Nikolaev et al., Moscow, Russia. In Genome Res, Feb 2016
UNASSIGNED: APOBEC3A and APOBEC3B, cytidine deaminases of the APOBEC family, are among the main factors causing mutations in human cancers.
DNA Editing by APOBECs: A Genomic Preserver and Transformer.
Levanon et al., Ramat Gan, Israel. In Trends Genet, Jan 2016
The unique AID (activation-induced cytidine deaminase)/APOBEC (apolipoprotein B mRNA editing enzyme, catalytic polypeptide) family comprises proteins that alter DNA sequences by converting deoxycytidines to deoxyuridines through deamination.
Chromothripsis and Kataegis Induced by Telomere Crisis.
de Lange et al., New York City, United States. In Cell, Jan 2016
Post-crisis clones showed chromothripsis and kataegis, presumably resulting from DNA repair and APOBEC editing of the fragmented chromatin bridge DNA.
Genetic heterogeneity of actionable genes between primary and metastatic tumor in lung adenocarcinoma.
Chang et al., Seoul, South Korea. In Bmc Cancer, Dec 2015
out of 213 non-synonymous mutations were developed in the context of APOBEC signature.
Creation of chimeric human/rabbit APOBEC1 with HIV-1 restriction and DNA mutation activities.
Koito et al., Kumamoto, Japan. In Sci Rep, Dec 2015
APOBEC1 (A1) proteins from lagomorphs and rodents have deaminase-dependent restriction activity against HIV-1, whereas human A1 exerts a negligible effect.
Clusters of Multiple Mutations: Incidence and Molecular Mechanisms.
Gordenin et al., Durham, United States. In Annu Rev Genet, Dec 2015
In addition to being a fascinating phenomenon, clustered mutagenesis also became an indispensable tool for identifying a previously unrecognized major source of mutation in cancer, APOBEC cytidine deaminases.
Invasive Bladder Cancer: Genomic Insights and Therapeutic Promise.
Kwiatkowski et al., Boston, United States. In Clin Cancer Res, Nov 2015
About 65% of all mutations are due to APOBEC-mediated mutagenesis.
An APOBEC3A hypermutation signature is distinguishable from the signature of background mutagenesis by APOBEC3B in human cancers.
Gordenin et al., United States. In Nat Genet, Sep 2015
Single-strand DNA-specific APOBEC cytidine deaminase(s) are major source(s) of mutation in several cancer types.
Genomic spectra of biliary tract cancer.
Shibata et al., Tokyo, Japan. In Nat Genet, Sep 2015
Gradient spectra of mutational signatures with a higher burden of the APOBEC-associated mutation signature were observed in gallbladder cancer and ECC.
Evolution of vertebrate adaptive immunity: immune cells and tissues, and AID/APOBEC cytidine deaminases.
Hirano, Atlanta, United States. In Bioessays, Aug 2015
All surviving jawed vertebrate representatives achieve diversity in immunoglobulin-based B and T cell receptors for antigen recognition through recombinatorial rearrangement of V(D)J segments.
APOBEC Enzymes: Mutagenic Fuel for Cancer Evolution and Heterogeneity.
Harris et al., London, United Kingdom. In Cancer Discov, Jul 2015
One emerging mechanism fueling tumor diversity and subclonal evolution is genomic DNA cytosine deamination catalyzed by APOBEC3B and at least one other APOBEC family member.
Effect of apolipoprotein B mRNA-editing catalytic polypeptide-like protein-3G in cervical cancer.
Dong et al., Jinan, China. In Int J Clin Exp Pathol, 2014
APOBEC-3G serves as a suppressor of cervical cancer cell proliferation and invasion.
Integrative genomic analysis reveals functional diversification of APOBEC gene family in breast cancer.
Long et al., Nashville, United States. In Hum Genomics, 2014
BACKGROUND: The human APOBEC protein family plays critical but distinct roles in host defense.
AID/APOBEC deaminases and cancer.
Geisberger et al., Salzburg, Austria. In Oncoscience, 2014
Common non-random mutations comprise DNA strand-biased mutation showers and mutations restricted to certain DNA motifs, which recently have become attributed to the activity of the AID/APOBEC family of DNA deaminases.
Hypermutation in human cancer genomes: footprints and mechanisms.
Gordenin et al., In Nat Rev Cancer, 2014
This major expansion of cancer mutation data sets has provided unprecedented statistical power for the analysis of mutation spectra, which has confirmed several classical sources of mutation in cancer, highlighted new prominent mutation sources (such as apolipoprotein B mRNA editing enzyme catalytic polypeptide-like (APOBEC) enzymes) and empowered the search for cancer drivers.
Hypermutation of ApoB mRNA by rat APOBEC-1 overexpression mimics APOBEC-3 hypermutation.
Patterson et al., Bethesda, United States. In J Mol Biol, 2012
It was found that rat APOBEC-1 overexpression had a hypermutation pattern similar to that of APOBEC-3s on its substrate apolipoprotein B mRNA.
Loss of ASP but not ROPN1 reduces mammalian ciliary motility.
Carr et al., Portland, United States. In Cytoskeleton (hoboken), 2012
The beat frequency of cilia from mice lacking ASP is significantly slower than wild type, indicating that ASP signaling may regulate ciliary motility.
APOBEC1-mediated editing and attenuation of herpes simplex virus 1 DNA indicate that neurons have an antiviral role during herpes simplex encephalitis.
Koyanagi et al., Kyoto, Japan. In J Virol, 2011
Taken together, these results demonstrate a model in which APOBEC1 induction during encephalitis in neurons may aid in thwarting HSV-1 infection.
Transcriptome-wide sequencing reveals numerous APOBEC1 mRNA-editing targets in transcript 3' UTRs.
Papavasiliou et al., New York City, United States. In Nat Struct Mol Biol, 2011
The transcriptomics approach to RNA editing presented in this study dramatically expands the list of APOBEC1 mRNA editing targets and reveals a novel cellular mechanism for the modification of transcript 3' UTRs.
Differential expression of genes in the calcium-signaling pathway underlies lesion development in the LDb mouse model of atherosclerosis.
Hixson et al., Houston, United States. In Atherosclerosis, 2010
LDL receptor and the apolipoprotein B mRNA editing enzyme Apobec1 are regulated via calcium signaling in mechanistic response to genetic, mechanical, and environmental insults that trigger an imbalance of intracellular calcium homeostasis
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