Human ARD1A ELISA Matched Antibody Pair

Name: Human ARD1A ELISA Matched Antibody Pair
SKU: ABPR-0070
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Species Reactivity

Human

Intended Use

This antibody pair set comes with matched antibody pair to detect and quantify protein level of human ARD1A.

General Description

N-alpha-acetylation is among the most common post-translational protein modifications in eukaryotic cells. This process involves the transfer of an acetyl group from acetyl-coenzyme A to the alpha-amino group on a nascent polypeptide and is essential for normal cell function. This gene encodes an N-terminal acetyltransferase that functions as the catalytic subunit of the major amino-terminal acetyltransferase A complex. Mutations in this gene are the cause of Ogden syndrome. Alternate splicing results in multiple transcript variants.

Reconstitution And Storage

Store reagents of the antibody pair set at -20°C or lower. Please aliquot to avoid repeated freeze thaw cycle. Reagents should be returned to -20°C storage immediately after use.

Citations

Have you cited ABPR-0070 in a publication? Let us know and earn a reward for your research.

Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Fine Mapping of Xq28: Both MECP2/IRAK1 and NAA10/RENBP Contribute to Risk for SLE in Multiple Ancestral Groups

ARTHRITIS AND RHEUMATISM

Authors: Kaufman, Kenneth M.; Kelly, Jennifer A.; Hughes, Travis; Adler, Adam; Sanchez, Elena; Ojwang, Joshua O.; Langefeld, Carl D.; Ziegler, Julie T.; James, Judith A.; Brown, Elizabeth E.; Kimberly, Robert P.; Edberg, Jeffrey C.; Criswell, Lindsey A.; Chang, Deh-Ming; Gilkeson, Gary S.; Niewold, Timothy B.; Bae, Sang-Cheol; Alarcon-Riquelme, Marta E.; Jacob, Chaim O.; Moser, Kathy L.; Gaffney, Patrick M.; Harley, John B.; Sawalha, Amr H.; Tsao, Betty P.

Abstract

The Role of N-alpha-acetyltransferase 10 Protein in DNA Methylation and Genomic Imprinting

MOLECULAR CELL

Authors: Lee, Chen-Cheng; Peng, Shih-Huan; Shen, Li; Lee, Chung-Fan; Du, Ting-Huei; Kang, Ming-Lun; Xu, Guo-Liang; Upadhyay, Anup K.; Cheng, Xiaodong; Yan, Yu-Ting; Zhang, Yi; Juan, Li-Jung

Abstract

Genomic imprinting is an allelic gene expression phenomenon primarily controlled by allele-specific DNA methylation at the imprinting control region (ICR), but the underlying mechanism remains largely unclear. N-alpha-acetyltransferase 10 protein (Naa10p) catalyzes N-alpha-acetylation of nascent proteins, and mutation of human Naa10p is linked to severe developmental delays. Here we report that Naa10-null mice display partial embryonic lethality, growth retardation, brain disorders, and maternal effect lethality, phenotypes commonly observed in defective genomic imprinting. Genome-wide analyses further revealed global DNA hypomethylation and enriched dysregulation of imprinted genes in Naa10p-knockout embryos and embryonic stem cells. Mechanistically, Naa10p facilitates binding of DNA methyltransferase 1 (Dnmt1) to DNA substrates, including the ICRs of the imprinted allele during S phase. Moreover, the lethal Ogden syndrome-associated mutation of human Naa10p disrupts its binding to the ICR of H19 and Dnmt1 recruitment. Our study thus links Naa10p mutation-associated Ogden syndrome to defective DNA methylation and genomic imprinting.