Disease relevance of NAT9

• It also suggests defective regulation of SLC9A3R1 or NAT9 by RUNX1 as a susceptibility factor for psoriasis [1].
• No association between atopic dermatitis and the SLC9A3R1-NAT9 RUNX1 binding site polymorphism in Japanese patients [2].

High impact information on NAT9

• Associated single-nucleotide polymorphisms (SNPs) in the proximal peak lie in or near SLC9A3R1 (also called EBP50 and NHERF1) and NAT9, a new member of the N-acetyltransferase family [1].
• A disease-associated SNP lying between SLC9A3R1 and NAT9 leads to loss of RUNX1 binding [1].
• Two peaks of association here contain the psoriasis candidate genes SLC9A3R (solute carrier family 9, isoform 3 regulatory factor), NAT9 (N-acetyltransferase superfamily), and RAPTOR (rapamycin (TOR)) [3].
• Furthermore, decreased numbers of mature myeloid cells (defined by Mab NAT-9 II:3F-6F [NAT-9]) (P less than 0.001) were demonstrated in all French-American-British (FAB) subtypes except refractory anaemia with sideroblasts (RA-S) [4].
• NAT-9 II:3F-6F did not bind to circulating monocytes, T and B cells, erythrocytes and a variety of different human cell culture lines [5].

Anatomical context of NAT9

• A monoclonal antibody, designated NAT-9 II:3F-6F (IgM), was generated by hybridization of mouse myeloma cells with spleen cell from mice immunized with normal human bone marrow cells [5].

Analytical, diagnostic and therapeutic context of NAT9

• Scanning electron microscopy and electron backscattered patterns, EBSP, have been employed to reveal both the grain structure and texture of 90% cold-rolled polycrystalline nickel after 1-hour anneals at a variety of temperatures [6].

References