APOBEC-1 Deaminase

An APOBEC deaminase catalytic subunit of the apolipoprotein B (APOB) MESSENGER RNA (mRNA) editing enzyme complex that is involved in post-transcriptional editing of a CAA codon for GLYCINE to a UAA STOP CODON in the ApoB mRNA. It also functions in CGA (ARGININE) to UGA STOP CODON editing of NEUROFIBROMIN 1 mRNA and EPIGENETIC PROCESSES.

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Networked: 154 relevant articles (4 outcomes, 9 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Davidson, Nicholas O: 6 articles (09/2010 - 01/2002)
2.	Lindner, Jonathan R: 4 articles (01/2021 - 01/2010)
3.	Xie, Aris: 4 articles (01/2021 - 01/2010)
4.	Takaori-Kondo, Akifumi: 3 articles (01/2020 - 03/2006)
5.	Malim, Michael H: 3 articles (12/2011 - 11/2003)
6.	Blanc, Valerie: 3 articles (09/2010 - 09/2007)
7.	Kennedy, Susan: 3 articles (06/2009 - 01/2002)
8.	Anant, Shrikant: 3 articles (10/2004 - 01/2002)
9.	Mukhopadhyay, Debnath: 3 articles (10/2004 - 01/2002)
10.	Zhang, Hui: 2 articles (06/2022 - 12/2017)

Related Diseases

1.	Infections 01/01/2022 - "By using HBV infection cell models and in vitro and in vivo recombinant cccDNA (rcccDNA) and HBVcircle models, the reduction rate of HBV cccDNA and the efficacy of apolipoprotein B mRNA editing enzyme catalytic subunit 3A (APOBEC3A)-mediated and CRISPR/CRISPR-associated 9 (Cas9)-mediated cccDNA targeting were compared between cccDNAs with distinct transcriptional activities. " 09/01/1996 - "An increase of VLDL was observed in NZW and WHHL rabbits after infection with Ad APOBEC-1 as well as Ad LacZ. " 10/27/2021 - "Apolipoprotein B mRNA editing enzyme catalytic subunit 3 (APOBEC3) proteins are critical for the control of infection by retroviruses. " 12/07/2015 - "Apolipoprotein B mRNA-editing enzyme 3G (APOBEC3G, A3G) and bone marrow stromal cell antigen 2 (BST2) are host resistance factors that potentially inhibit HIV-1 infection. " 02/25/2010 - "We have identified a post-entry CCR6-dependent mechanism of inhibition of HIV occurring at an early stage of infection mediated by the induction of the host restriction factor apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G). "
2.	Hypercholesterolemia 02/01/2002 - "Although initially promising, enthusiasm for apobec-1 gene therapy for hypercholesterolemia was blunted by the finding that uncontrolled transgenic expression of APOBEC-1 led to nonspecific editing of mRNAs and pathology. " 05/20/1996 - "Hepatic expression of the catalytic subunit of the apolipoprotein B mRNA editing enzyme (apobec-1) ameliorates hypercholesterolemia in LDL receptor-deficient rabbits." 07/01/1999 - "We used this physiologic hypercholesterolemia model to study the effect of adenovirus-mediated hepatic gene transfer of rat apolipoprotein B mRNA editing enzyme (Apobec1) on modulation of plasma cholesterol levels. " 05/01/1998 - "In contrast, in apoE-/- mice, inactivation of apobec-1 caused a massive increase (from <0.5 to 55.5+/-16.4 mg/dL) in plasma apoB-100 concentration but an approximately 55% reduction in hypercholesterolemia due to partial amelioration of the marked VLDL+IDL elevation. "
3.	Hyperlipidemias (Hyperlipidemia) 05/01/2010 - "These data suggest that nonspecific hypermutation induced by overexpressing APOBEC-1 can be virtually eliminated by site-specific mutation, while maintaining specific editing activity at the normal site, reopening the potential use of APOBEC-1 gene therapy for hyperlipidemia."
4.	Neoplasms (Cancer) 01/01/2023 - "Background: Family members of Apolipoprotein B mRNA-editing enzyme catalytic 3 (APOBEC3) play critical roles in cancer evolution and development. " 08/02/2022 - "Although there have been some recent cell and animal experiments indicating that expression of the gene encoding apolipoprotein B mRNA editing enzyme catalytic subunit 3B (APOBEC3B) is closely related to cancer, it still lacks pan-cancer analysis. " 08/02/2022 - "Multiple roles of apolipoprotein B mRNA editing enzyme catalytic subunit 3B (APOBEC3B) in human tumors: a pan-cancer analysis." 01/01/2022 - "Preventable mutations associated with pathogen exposure and apolipoprotein B mRNA-editing enzyme activity account for a large proportion of the cancer effect within head-and-neck, bladder, cervical, and breast cancers. " 01/01/2021 - "We applied SKIT to The Cancer Genome Atlas (TCGA) mutational signatures data for over 9,000 tumors across 32 cancer types, and identified a novel association between signature 17 curated in the Catalogue Of Somatic Mutations In Cancer (COSMIC) and apolipoprotein B mRNA editing enzyme (APOBEC) signatures in gastrointestinal cancers. "
5.	Hepatocellular Carcinoma (Hepatoma) 06/01/1998 - "However, high-level expression of APOBEC-1 in transgenic mouse and rabbit livers causes liver dysplasia and hepatocellular carcinoma. " 04/01/1998 - "In comparison, over-expression of APOBEC-1 in HepG2 (HepG2-APOBEC) human hepatoma cells, induced promiscuous editing primarily 5' of the mooring sequence, but sites 3' of the C6666 were also used more efficiently. " 10/10/1999 - "This report quantifies for the first time the effect of altering APOBEC-1 protein abundance on the proportion of edited apoB mRNAs using transfected McArdle rat hepatoma cells which had been sorted by flow cytometry into populations expressing different levels of green fluorescent protein-APOBEC-1 chimera, GFP-APOBEC. " 06/01/1997 - "Promoter-luciferase reporter constructions using regions flanking exon A and exon 1 of the rat apobec-1 gene identified two functional regions upstream of exon 1 that independently promote luciferase expression in transfected hepatoma and colon cancer cells. " 12/01/2000 - "In human hepatoma cells which lack apobec-1 activity, apo B-100 mRNA levels remained the same in cells treated with or without the agent. "

Related Drugs and Biologics

1.	Peptides (Polypeptides)
2.	Proteins (Proteins, Gene)
3.	LDL Receptors (LDL Receptor)
4.	Cytidine Deaminase
5.	Interferons
6.	Thymine
7.	Janus Kinases
8.	Small Interfering RNA (siRNA)
9.	Cholesterol
10.	Adenine

Related Therapies and Procedures

1.	Hepatectomy
2.	Aftercare (After-Treatment)
3.	Therapeutics
4.	Drug Therapy (Chemotherapy)