Disease relevance of NARG1

• NATH (N-acetyl transferase human) is overexpressed at the mRNA level in papillary thyroid carcinomas relative to non-neoplastic thyroid tissue [1].
• Heterologous expression of NATH in the papillary carcinoma cell line (NPA) and 293 cells did not alter the cellular proliferation rate [2].
• Increased NATH expression was seen especially in a Burkitt lymphoma cell line and in adult human testis [2].
• Suppressed expression of tubedown-1 in retinal neovascularization of proliferative diabetic retinopathy [3].
• Resistance to nourseothricin is conferred by the product of the nourseothricin acetyltransferase gene (nat1) from Streptomyces noursei [4].

Psychiatry related information on NARG1

• OBJECTIVE: To use Nath et al.'s (1991) conceptual model of adolescent parenting to examine the relationship between resiliency factors measured shortly after delivery and maternal parenting behavior at 6 months [5].

High impact information on NARG1

• Recombinant protein from a selected clone catalyzed the three-step conversions of GA12 to GA25 and of GA53 to GA17, as well as the formation of the C19-GAs, GA1, GA9, and GA20, from their respective aldehyde precursors, GA23, GA24, and GA19 [6].
• Plants treated with BX-112 had reduced levels of GA1 and GA8 and accumulated GA53, GA44, GA19, and GA20 [7].
• The results provide the first direct evidence that vertebrate homologues of NAT1 and ARD1 form an evolutionarily conserved N-terminal acetyltransferase and suggest that expression and down-regulation of this enzyme complex plays an important role in the generation and differentiation of neurons [8].
• FGF2 treatment regulates Ku, but not Tbdn100, protein accumulation [9].
• Northern and Western blot analyses demonstrate expression of Ku and Tbdn100 in MC3T3E1 osteoblasts [9].

Chemical compound and disease context of NARG1

• Likewise, it is equally effective as tiadenol in preventing Triton-induced hyperlipidemia and Nath diet induced hypercholesterolemia; in addition tiadenol-disulfoxide is slightly more effective than tiadenol in increasing HDL-cholesterol in hypercholesterolemic rats [10].

Biological context of NARG1

• Induction of apoptosis in human cells by RNAi-mediated knockdown of hARD1 and NATH, components of the protein N-alpha-acetyltransferase complex [11].
• Our results argue for an essential role of the NATH-hARD1 complex in cell survival and underscore the importance of protein N-alpha-acetylation in mammalian cells [11].
• NATH has two mRNA species, 4.6 and 5.8 kb, both harboring the same open reading frame encoding a putative protein of 866 amino acids [2].
• In the NAT1 gene we found two SNPs and a 3-bp insertion/ deletion polymorphism that corresponded to the NAT1*3, *10, and *18A/*18B alleles reported in other populations [12].
• Haloarchaeal N-terminal acetyltransferase reveals narrow substrate specificity, which is limited to cleaved N termini starting with serine or alanine residues [13].

Anatomical context of NARG1

• Here, we demonstrate that knockdown of NATH and/or hARD1 triggers apoptosis in human cell lines [11].
• A novel acetyltransferase subunit, tubedown-1 (tbdn-1), has been isolated, the expression of which is regulated during blood vessel development [3].
• The most abundant gibberellins identified in exudates were GA19 and GA44, as well as other members of the early 13-hydroxylation pathway [14].

Associations of NARG1 with chemical compounds

• Knockdown of hARD1 also sensitized cells to daunorubicin-induced apoptosis, potentially pointing at the NATH-hARD1 acetyltransferase complex as a novel target for chemotherapy [11].
• In NB4 cells undergoing retinoic acid mediated differentiation, the level of endogenous hARD1 and NATH protein decreases while the level of hARD2 protein is stable [15].
• These data support the hypothesis that the conversion of GA19 to GA20 in pea pericarp is seed regulated and that the auxin 4-CI-IAA can substitute for the seeds in the stimulation of pericarp growth and the conversion of GA19 to GA20 [16].
• Nath and Rydon [Nath, R. L., & Rydon, H. N. (1954) Biochem. J. 57, 1-10] examined the kinetics of the beta-glucosidase-catalyzed hydrolysis of a series of substituted phenyl glucosides [17].
• N-(2,2,5,7,8-Pentamethylchroman-6-sulfonyl)-N'-3- (N-9-fluorenylmethoxycarbonyl-glycinyl)propylguanidine (1) was prepared and utilized as an arginine surrogate (Narg) building block compatible with solid-phase synthesis according to the Fmoc methodology [18].

Other interactions of NARG1

• These observations suggest that the association of APP with hARD1 and hNAT1 and/or their N-acetyltransferase activity contributes to the regulation of A beta generation [19].

Analytical, diagnostic and therapeutic context of NARG1

• Taken together, these results suggest that NATH positively affects the level of hARD1 protein both in vivo and in cell cultures [1].
• Immunoprecipitation experiments show that hARD2 protein potentially interacts with NATH, suggesting that hARD2-NATH complexes may be responsible for protein N-alpha-acetylation in human cells [15].
• Gel supershift studies confirm sequence-specific DNA binding of Ku in the OCFRE complex; chromatin immunoprecipitation assays confirm association of Ku and Tbdn100 with the endogenous OC promoter [9].
• Overlapping RT-PCR fragments from several PTC biopsies confirmed the NATH mRNA sequence [2].
• Northern blots, semiquantitative RT-PCR experiments, TaqMan real-time RT-PCR experiments, and in situ hybridization verified the overexpression of NATH mRNA localized to tumor cells in PTC biopsies [2].

References