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APOBEC1 encodes a member of the cytidine deaminase enzyme family. Additionally we are shipping APOBEC1 Proteins (7) and many more products for this protein.
Showing 10 out of 58 products:
Mouse (Murine) Polyclonal APOBEC1 Primary Antibody for ELISA, WB - ABIN449571
Lau, Chan: Involvement of a chaperone regulator, Bcl2-associated athanogene-4, in apolipoprotein B mRNA editing. in The Journal of biological chemistry 2003
Luciferase-fused 3' untranslated region of human Dickkopf1 (show DKK1 Antibodies) activity was highly upregulated in A1CF (show A1CF Antibodies)-overexpressed MCF7 cells, but this upregulation can be inhibited by mutating conserved binding motifs of Dickkopf1 (show DKK1 Antibodies) 3' untranslated region. A1CF (show A1CF Antibodies) played a crucial role in cell migration and survival through affecting 3' untranslated region of Dickkopf1 (show DKK1 Antibodies) to upregulate its expression in MCF7 cells.
AICDA (show AICDA Antibodies)/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 Antibodies) 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 Antibodies) might be operational during enterocyte differentiation.
Identified two novel variants, rs1349411 (APOBEC1) and rs1424032, for serum apoB (show APOB Antibodies) levels in Mexicans.
C-->U editing of neurofibromatosis 1 (show NF1 Antibodies) mRNA occurs in tumors that express both the type II transcript and apobec-1, the catalytic subunit of the apolipoprotein B (show APOB Antibodies) mRNA-editing enzyme
expression of two proteins essential for apolipoprotein B (show APOB Antibodies) mRNA editing from a single gene through alternative splicing
Here, we show that partial loss of either APOBEC1 complementation factor (A1CF (show A1CF Antibodies)), the RNA-binding cofactor of APOBEC1 in RNA editing, or Argonaute 2 (AGO2 (show EIF2C2 Antibodies)), a key factor in the biogenesis of certain noncoding RNAs, modulates risk for TGCTs and testicular abnormalities in both parent-of-origin and conventional genetic manners.
substantial rearrangement/duplication of transgene elements is present, and transgene integration was accompanied by the deletion of a 19,500 bp fragment of genomic DNA that contains the promoter, exon 1 and part of intron 1 of the APOBEC1 complementation factor (A1cf (show A1CF Antibodies)) gene, as well as several elements that are predicted to regulate chromosomal architecture
The observations demonstrate that A1CF (show A1CF Antibodies) does not act as the APOBEC1 complementation factor (show A1CF Antibodies) in vivo under normal physiological conditions and suggest new roles for A1CF (show A1CF Antibodies), 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 Antibodies) 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 Antibodies) B mRNA editing protein (Apobec1 cytidine deaminase (show CDA Antibodies)) 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.
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.
C->U-editing enzyme APOBEC-1
, apolipoprotein B mRNA editing enzyme complex-1
, apolipoprotein B mRNA-editing enzyme 1
, apolipoprotein B editing complex 1
, Apolipoprotein B editing protein
, apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1
, apolipoprotein B mRNA editing enzyme complex 1
, apolipoprotein B mRNA editing protein
, APOBEC1 complementation factor
, apobec-1 complementation factor
, APOBEC1-stimulating protein
, apobec-1 complementation factor-like
, APOBEC1 complementation factor-like
, Apolipoprotein B mRNA-editing enzyme 1
, apolipoprotein B mRNA editing catalytic subunit-1