NARG1L Blocking Peptide
- Known as:
- NARG1L Blocking Peptide
- Catalog number:
- 33r-1516
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- NARG1L Blocking Peptide
Related genes to: NARG1L Blocking Peptide
- Gene:
- NAA16 NIH gene
- Name:
- N(alpha)-acetyltransferase 16, NatA auxiliary subunit
- Previous symbol:
- NARG1L
- Synonyms:
- FLJ22054, MGC40612, PRO2435
- Chromosome:
- 13q14.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-12-01
- Date modifiied:
- 2015-04-24
Related products to: NARG1L Blocking Peptide
Related articles to: NARG1L Blocking Peptide
- Mosquitoes, especially Aedes aegypti, transmit major human diseases such as dengue, Zika, and chikungunya. Epigenetic regulation, including histone acetylation, plays a key role in controlling Ae. aegypti development. However, the specific roles of histone acetyltransferases (HATs) and N-terminal acetyltransferases (NATs) in mosquito development remain poorly understood. In this study, we investigated 25 HAT/NAT genes functions by knocking them down via feeding Ae. aegypti larvae with dsRNA nanoformulations. Gene expression analysis confirmed that target gene expression was reduced by more than 50% in dsRNA-treated larvae. Knocking down 18 of these HATs/NATs resulted in over 50% mortality. Silencing KAT7, NATSCAN, NAT9, ATAT1, and TADA3 caused larval death, whereas knockdown of NAA80, NAA-Eco, GNPNAT1, HAT-B, and MCM3AP led to pupal mortality. Knockdown of NATSCAN, NF, TFIID, GNPNAT1, and NAA16 resulted in molting and metamorphic defects, characterized by untanned cuticles and failure to complete successful larval-pupal metamorphosis. Phylogenetic analysis of conserved domains of HATs and NATs revealed that evolutionarily conserved members cluster into distinct clades associated with larval- or pupal-specific functions. Developmental expression analysis showed stage-specific expression of these genes. Further, stage-specific expression analysis revealed that dynamic expression patterns of KAT7, RNACAT, NAT9, and NF are linked to larval growth and pupal metamorphosis. Treatment with 20-hydroxyecdysone (20E) or an ecdysone agonist increased mRNA levels of NAA30,NAA40,NAT9, and GNAT8, indicating hormonal control of histone acetylation. Ecdysone-induced HATs/NATs regulated the expression of primary ecdysone response genes: E75A and E93. These results demonstrate that HATs/NATs play key roles in Ae. aegypti development and therefore could serve as potential targets for mosquito control. - Source: PubMed
Publication date: 2026/04/27
Gaddelapati Sharath ChandraPalli Subba Reddy - N-terminal acetylation, catalyzed by N-terminal acetyltransferase (NAT) complexes, is one of the most prevalent protein modifications in eukaryotic cells, yet its role in heart development remains poorly understood. Here, we use as an in vivo platform to investigate the functions of NAT complex components in cardiac development and congenital heart disease (CHD). Focusing on the NatA complex, we showed that cardiac-specific knockdown of each of its three subunits (, , and ) led to developmental lethality, structural disorganization, fibrosis, and impaired cardiac function in . Remarkably, human NAA16 completely rescued the cardiac defects in silenced , whereas a CHD-associated variant (NAA16-R70C) failed to do so, providing direct functional evidence of its pathogenicity. Together, these findings suggest the NatA complex as a critical regulator of heart development and provide functional validation linking variants in NatA complex genes to CHD. Further studies in mammalian models will be required to provide additional supporting evidence. - Source: PubMed
Publication date: 2025/10/14
Zhu Jun-YiSeah HannahLee HangnohLiu HanhanHan Zhe - Histone acetyltransferases (HATs) catalyse the addition of acetyl groups to histones and other proteins. In contrast, histone deacetylases remove acetyl groups from core histones, and the activity of these enzymes maintains the acetylation levels of these proteins. Histone acetylation levels influence chromatin accessibility and gene expression and regulate many biological processes, including development and reproduction. Recent reports suggest that some N-terminal acetyltransferases (NATs) also regulate gene expression. We identified 29 HAT and NAT genes in the red flour beetle, Tribolium castaneum, and studied their functions in female reproduction using RNA interference (RNAi). Knockdown of seven out of 13 HAT genes (N-acetyltransferase ESCO2) (ESCO1/2), Elongator complex protein 3 (ELP3), Histone acetyltransferase type B catalytic subunit 1 (HAT1), Transcription initiation factor TFIID subunit 1 (TAF1), Protein x-mas-2 (MCM3AP), Histone acetyltransferase Tip60 (KAT5), and Cysteine-rich protein 2-binding protein (KAT14) and 12 out of 16 NAT genes Probable glucosamine 6-phosphate N-acetyltransferase (GNPNAT1), N-alpha-acetyltransferase 10 (NAA10), N-alpha-acetyltransferase 20 (NAA20), N-alpha-acetyltransferase 30 (NAA30), N-alpha-acetyltransferase 40 (NAA40), N-alpha-acetyltransferase 60 (NAA60), N-acetyltransferase 6 (NAA80), RNA cytidine acetyltransferase (NAT10), Diamine acetyltransferase 2 (SATL1), N(alpha)-acetyltransferase 16 (NAA16), Phagocyte signalling-impaired protein (NAA25), N(alpha)-acetyltransferase 35 (NAA35) caused a significant reduction in eggs laid by females compared to the eggs laid by control females injected with dsGFP. Also, knockdown of nine (KAT5, ATAT1, ELP3, HAT1, KAT8A, NAA10, NAA20, GNPNAT1 and TAF1) HAT/NAT genes caused a significant decrease in egg hatching. Parental RNAi of ATAT1 and KAT8 blocked embryogenesis. These data suggest that the acetylation of proteins plays an important role in female reproduction and embryogenesis. - Source: PubMed
Publication date: 2025/05/29
Sengodan KarthiPalli Subba Reddy - The gut microbiome (GM) has been reported to play a role in traumatic brain injury (TBI). To investigate the causal relationship between GMs, inflammatory mediators, and TBI, a comprehensive Mendelian randomization (MR) analysis was conducted. We utilized Genome-Wide Association Study (GWAS) summary statistics to examine the causal relationships between GM and TBI. To assess the potential causal associations between GM and TBI, we employed the inverse-variance-weighted, MR-Egger, and weighted median methods. Mediation analysis was used to assess the possible mediating factors. Several sensitivity analyses methods were implemented to verify the stability of the results. Additionally, we utilized FUMA GWAS to map single-nucleotide polymorphisms to genes and conduct transcriptomic MR analysis. We identified potential causal relationships between nine bacterial taxa and TBI. Notably, class , family , and order ( = 0.0003) maintained a robust positive correlation with TBI. This causal association passed false discovery rate (FDR) correction (FDR < 0.05). Genetically determined 1 inflammatory protein, 30 immune cells and 3 inflammatory factors were significantly causally related to TBI. None of them mediated the relationship between GMs and TBI. The outcome of the sensitivity analysis corroborated the findings. Regarding the mapped genes of significant GMs, genes such as , , , , and in class showed a significant causal correlation with TBI. Our study reveals the potential causal effects of nine GMs, especially on TBI, and there was no link between TBI and GM through inflammatory protein, immune cells, and inflammatory factors, which may offer fresh insights into TBI biomarkers and therapeutic targets through specific GMs. - Source: PubMed
Publication date: 2025/03/20
Song BingyiQiu YoujiaWang ZilanTao YuchenWang MenghanDuan AojieXie MinjiaYin ZiqianChen ZhouqingMa ChaoWang Zhong - Genome-wide association studies (GWAS) have identified more than a thousand loci for blood pressure (BP). Functional genes in these loci are cell-type specific. The aim of this study was to elucidate potentially functional genes associated with BP in the aorta through the utilization of RNA modification-associated single-nucleotide polymorphisms (RNAm-SNPs). - Source: PubMed
Publication date: 2024/04/30
Zhang HuanChen YuxiXu PengLiu DanWu NaqiongWang LaiyuanMo Xingbo