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APOBEC1 encodes a member of the cytidine deaminase enzyme family. Additionally we are shipping APOBEC1 Antibodies (58) and APOBEC1 Proteins (7) and many more products for this protein.
The observations demonstrate that A1CF (show A1CF ELISA Kits) does not act as the APOBEC1 complementation factor (show A1CF ELISA Kits) in vivo under normal physiological conditions and suggest new roles for A1CF (show A1CF ELISA Kits), specifically within the male adult kidney.
Apobec-1-dependent C-to-U RNA editing exerts broad functional effects in a tissue-specific manner.
RBM47 and APOBEC1 constitute the basic machinery for C to U RNA editing.
In contrast to in vitro results, APOBEC1 neither inhibited nor significantly drove the molecular evolution of Friend retrovirus in wild type or APOBEC1 knockout mice.
Individual genetic variability at the Apobec1 locus results in differential rates of C-to-U(T) editing in murine macrophages; with mouse strains expressing mostly a truncated alternative transcript isoform of Apobec1 exhibiting lower rates of editing.
The transgenic rescue of intestinal apobec-1 expression restores C-to-U RNA editing of apoB (show APOB ELISA Kits) mRNA in vivo, including the canonical site at position 6666 and also at approximately 20 other newly identified downstream sites present in WT mice.
Results suggest that apo (show C9orf3 ELISA Kits) B mRNA editing protein (Apobec1 cytidine deaminase (show CDA ELISA Kits)) plays a central role in controlling testicular germ cell tumors susceptibility in both a conventional and a transgenerational manner.
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.
LDL receptor (show LDLR ELISA Kits) and the apolipoprotein B (show APOB ELISA Kits) 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
studies establish the existence of preferential degradation of intestinal apolipoprotein B-100 (show APOB ELISA Kits) and subtle defects in triglyceride secretion in apolipoprotein B editing complex 1-/- mice
Luciferase-fused 3' untranslated region of human Dickkopf1 (show DKK1 ELISA Kits) activity was highly upregulated in A1CF (show A1CF ELISA Kits)-overexpressed MCF7 cells, but this upregulation can be inhibited by mutating conserved binding motifs of Dickkopf1 (show DKK1 ELISA Kits) 3' untranslated region. A1CF (show A1CF ELISA Kits) played a crucial role in cell migration and survival through affecting 3' untranslated region of Dickkopf1 (show DKK1 ELISA Kits) to upregulate its expression in MCF7 cells.
AICDA (show AICDA ELISA Kits)/APOBEC family of cytidine deaminases is significant in innate immunity, as it restricts numerous viruses, including HBV, through hypermutationdependent and independent mechanisms. (Review)
Results show that expression of APOBEC1 induces a mutator phenotype in 2 different cellular models.
hnRNPQ6 is required for APOBEC1-enhanced IL8 (show IL8 ELISA Kits) production.
Studies indicate the APOBEC family consists of 11 members: APOBEC-1 (Apo1), APOBEC-2 (Apo2), activation induced cytidine deaminase (AID), APOBEC- 3A, -3B, -3C, -3DE, -3F, -3H (Apo3A-H) and APOBEC- 4 (Apo4).
The hypermutation activity of APOBEC-1 was decreased to background levels by a single point APOBEC-1 mutation of P29F or E181Q, while 50% of wild-type control editing at the normal site was retained.
The data presented in this report suggested that similar regulatory mechanisms controlling the functional interaction of APOBEC-1 with ACF (show A1CF ELISA Kits) might be operational during enterocyte differentiation.
Identified two novel variants, rs1349411 (APOBEC1) and rs1424032, for serum apoB (show APOB ELISA Kits) levels in Mexicans.
C-->U editing of neurofibromatosis 1 (show NF1 ELISA Kits) mRNA occurs in tumors that express both the type II transcript and apobec-1, the catalytic subunit of the apolipoprotein B (show APOB ELISA Kits) mRNA-editing enzyme
expression of two proteins essential for apolipoprotein B (show APOB ELISA Kits) mRNA editing from a single gene through alternative splicing
A moderate reduction of the APOBEC1 dependent editing induces a lean phenotype at least in the rabbit species.
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.
apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1
, C->U-editing enzyme APOBEC-1
, apolipoprotein B mRNA editing enzyme complex 1
, apolipoprotein B mRNA-editing enzyme 1
, APOBEC1 complementation factor
, apobec-1 complementation factor
, APOBEC1-stimulating protein
, apobec-1 complementation factor-like
, APOBEC1 complementation factor-like
, apolipoprotein B editing complex 1
, apolipoprotein B mRNA editing enzyme complex-1
, apolipoprotein B mRNA editing protein
, Apolipoprotein B editing protein
, Apolipoprotein B mRNA-editing enzyme 1
, apolipoprotein B mRNA editing catalytic subunit-1